modulação hormonal

Transcrição

modulação hormonal
SOBRAF
DIRETRIZES PARA A UTILIZAÇÃO DE HORMÔNIOS
HOMÓLOGOS HUMANOS POR MÚLTIPLAS
ESPECIALIDADES MÉDICAS NA PRÁTICA CLÍNICA
A- INTRODUÇÃO:
As diretrizes aqui elencadas representam a posição oficial da Sociedade
Brasileira Para Estudos da Fisiologia – SOBRAF - com relação ao uso de
hormônios homólogos humanos por múltiplas especialidades médicas na prática
clínica, e estão fundamentadas no Projeto Diretrizes, iniciativa conjunta da
Associação Médica Brasileira e Conselho Federal de Medicina, que tem por
objetivo conciliar informações da área médica a fim de padronizar condutas que
auxiliem o raciocínio e a tomada de decisão do médico.
As informações contidas neste documento devem ser submetidas à avaliação e à
crítica do médico, responsável pela conduta a ser seguida, frente à realidade e ao
estado clínico de cada paciente.
B- DESCRIÇÃO DO MÉTODO DE COLETA DE EVIDÊNCIA:
A revisão bibliográfica de artigos científicos destas diretrizes foi realizada na
base de dados MEDLINE.
A busca de evidências partiu de cenários clínicos reais, e utilizou palavras-chaves
(MeSH terms): (aging hormone replacement therapy) OR (gynecology hormone
replacement therapy) OR (endocrinology hormone replacement therapy)
(hormones OR Estradiol OR Testosterone OR Progesterone OR Thyroid Hormones
OR DHEA OR Pregnenolone OR Melatonin OR Growth Hormone OR IGF-1 OR
deficiency OR therapeutic OR replacement) AND quality of life AND risk factors
AND bone density AND osteoporosis AND osteopenia, (hormone replacement
therapy OR hormones) AND (cancer) AND (Monitoring) AND (sexual function) AND
glucose metabolism AND plasma lipids AND inflammatory factors AND visceral fat)
AND cardiovascular disease AND antioxidant activity AND immune function AND
fatigue AND depression AND sleep disorders AND anxiety AND hypertension AND
obesity AND body composition AND lean mass AND muscle mass AND sarcopenia
AND longevity AND alzheimer´s disease AND cancer risk AND cancer prevention
AND low hormone levels .
C- GRAU DE RECOMENDAÇÃO E FORÇA DE EVIDÊNCIA:
A: Estudos experimentais e observacionais de melhor consistência.
B: Estudos experimentais e observacionais de menor consistência.
C: Relatos de casos (estudos não controlados).
D: Opinião desprovida de avaliação crítica, baseada em consensos, estudos
fisiológicos ou modelos animais.
D- OBJETIVOS:
Estabelecer a definição, interferências do uso de hormônios no metabolismo
lipoproteico, na vida sexual, na baixa densidade mineral óssea, nas mamas, na
redução do percentual de gordura corporal, na redução dos riscos de
hipertensão arterial sistêmica, na redução dos riscos de diabetes, na redução do
risco de demência de Alzheimer, na melhora da massa muscular, na promoção
de bem estar físico e mental, na redução dos riscos de doenças, na melhora da
qualidade de vida, na prevenção das perdas funcionais da velhice, na melhora da
capacidade laboral, física e funcional, na melhora da libido, na melhora da
qualidade do sono, na melhora da depressão, na melhora da ansiedade, na
melhora do estresse, na atenuação da formação de espécies oxigênio-reativas, na
redução do estresse oxidativo celular, na preservação da integridade celular, na
preservação da integridade mitocondrial, na otimização metabólica, na
otimização imunológica, na redução e ou reversão da placa ateromatosa, na
redução do risco cardiovascular, na prevenção de doenças crônicas, na
prevenção do câncer, na redução do risco de câncer e na promoção de um
envelhecimento saudável e determinar as indicações da terapêutica hormonal
baseadas nas melhores evidências atuais.
E- CONFLITO DE INTERESSE:
Nenhum conflito de interesse declarado.
1. MENOPAUSA
a. Quadro clínico
i. Amenorréia secundária em mulheres com mais de 35 anos
ou amenorréia secundária em mulheres, por período
superior a seis meses;
ii. Fogachos, sudorese noturna, insônia, labilidade emocional,
secura vaginal, dispareunia, declínio cognitivo, fragilidade
imunológica, ressecamento da pele, queda de cabelos,
aumento do peso total, aumento do percentual de gordura,
perda de massa magra, perda de massa óssea, redução da
libido e comprometimento da qualidade de vida.
b.
Quadro Laboratorial
i. FSH > 15 u/L
ii. LH > 8 u/L
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da menopausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de menopausa será confirmado
tomando-se como referência as manifestações e o quadro
clínico apresentados pelo paciente e devidamente avaliados
e registrados pelo médico. Tal conduta se justifica pela
baixa acurácia dos métodos de diagnóstico laboratorial das
deficiências hormonais, falhas de técnicas intrínsecas aos
métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a menopausa, a SOBRAF recomenda que seus médicos associados
utilizem-se do termo de consentimento padrão adotado pela
mesma e que deverá ser devidamente assinado pelo médico e pelo
seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA MENOPAUSA
i. Após criteriosa revisão da literatura científica, discussões
com médicos representantes de todos os continentes e
discussões entre médicos brasileiros, todos profissionais
versados e adequadamente qualificados em utilizar e
prescrever hormônios em seres humanos com a
finalidade primária de promoção da saúde e, ainda, em
total consonância com os preceitos e diretrizes da
Sociedade Brasileira Para Estudos da Fisiologia – SOBRAF,
da International Hormone Society e da World Society of
Anti-Aging Medicine, nós, médicos membros da SOBRAF,
concluímos haver chegado o momento de reconsiderar os
conceitos atualmente vigentes acerca da reposição
hormonal na menopausa.
A presente controvérsia acerca da reposição hormonal na
menopausa, teve início após a publicação dos resultados
do chamado estudo WHI ( Women’s Health Iniciative ),
publicado em 2002, bem como do British One Million
Women Study, publicado em 2003. Em ambos os estudos,
o uso de hormônios em mulheres na pós-menopausa foi
associado a uma maior incidência de câncer de mama,
quando comparadas ao grupo placebo-controle ou ao de
não usuárias. No estudo WHI, o uso de hormônios em
mulheres foi associado a um aumento no risco de doenças
cardiovasculares e cerebrovasculares. Para os médicos
membros da SOBRAF, ambos os estudos apresentam,
dentre outras, duas falhas graves de desenho que
consistem, respectivamente, em primeiro lugar: estas
mulheres estavam utilizando estrogênios conjugados de
urina equina. Consiste em um coquetel de 38 hormônios
obtidos da urina de éguas prenhes, portanto, um dejeto
animal, sendo que nenhum destes hormônios existe em
seres humanos ou é produzido pelos mesmos, tendo,
portanto, propriedades farmacológicas e comportamento
completamente distintos do 17-beta-estradiol, hormônio
que deixa de ser produzido por mulheres na fase pósmenopausal. Em segundo lugar, à esta combinação, foi
associado o acetato de medroxiprogesterona, molécula
que consiste em um progestogênio sintético, igualmente
não existente em seres humanos, e, consequentemente,
substância com propriedades químicas e fisiológicas
diferentes da progesterona humana.
Revisando
cuidadosamente a literatura científica existente, é
possível encontrar vários outros estudos que
demonstram, de maneira inquestionável, a potencial
toxicidade e os riscos inerentes ao uso destas substâncias.
De acordo com as recentes recomendações de um grupo
cada vez maior de sociedades médicas ao redor de todo o
mundo, nós, igualmente, não recomendamos o uso de
hormônios não-homólogos humanos a reposição
hormonal da menopausa. Em contraste com as
recomendações de algumas sociedades, que não
recomendam a reposição hormonal na menopausa, ou
ainda, algumas outras que a recomendam por um período
limitado a cinco anos, no máximo, nós recomendamos o
uso de hormônios em mulheres antes e após a
menopausa, por tanto tempo quanto se fizer necessário,
desde que as indicações e as necessidades clínicas
justifiquem e que nenhum evento adverso ocorra que
contraindique o seu uso.
Contudo, nós recomendamos o uso da combinação de
estradiol e estriol homólogos humanos, associados à
progesterona homóloga humana para a correção da
deficiência ovariana da menopausa, exceto para casos
específicos e bem pontuais e por um período de tempo
limitado, aonde o uso de hormônios não-homólogos
humanos possa apresentar resultados clínicos melhores,
com é o caso de algumas metrorragias e sangramentos da
perimenopausa. A via de administração , é, igualmente,
parâmetro de considerável importância. A via
transdérmica, é, sem dúvida bem mais segura e fisiológica
do que a via oral. Esta via não oferece risco de elevação
do câncer de mama, e, quando se associa progesterona
homóloga humana à reposição de estradiol e estriol,
vários estudos, na verdade, demonstram uma clara
redução dos riscos para aquela patologia.
A mulher que teve câncer de mama, pode fazer reposição
hormonal? A tendência observada na atualidade é de se
evitar a administração de hormônios em mulheres que
tiveram câncer de mama. Esta observação pode não se
justificar nas mulheres em que a lesão foi removida
cirurgicamente de
forma completa. Revendo
cuidadosamente todos os estudos científicos atuais que
envolvem mulheres que tiveram câncer de mama e
receberam reposição hormonal na menopausa, nenhum
risco de recorrência foi reportado ou identificado. Ao
contrário, a reposição hormonal na menopausa está
associada a uma notória redução do risco de recorrência
do câncer, bem como uma clara diminuição das taxas
gerais de mortalidade na maioria dos estudos. Mesmo a
despeito de fartas evidências em contrário, ainda é muito
cedo para recomendar-se a reposição hormonal para
mulheres em menopausa portadoras de câncer de mama.
Nós recomendamos que estudos em larga escala placebocontrole sejam efetivados com a finalidade de identificar
com a maior clareza possível, em quais mulheres que
tiveram câncer de mama a terapia de reposição hormonal
da menopausa estaria mais indicada.
Nós recomendamos aos médicos que fazem a reposição
hormonal da menopausa, que submetam suas clientes à
propedêutica e monitoração mamária periódicos, antes e
durante o período de duração da reposição, obedecendo
aos intervalos regulares preconizados e consensuados,
consistindo de inspeção, palpação e mamografia de alta
resolução,
acompanhada
de
ultrassonografia
complementar de alta resolução. Importante, igualmente,
ressaltar a necessidade de vigilância periódica do
endométrio, através de monitoramento ultrassonográfico
transvaginal.
CONCLUSÃO DO CONSENSO:
Tendo em vista as enormes repercussões biopsicossociais
da menopausa e os crescentes e exorbitantes gastos para
o tratamento e controle das doenças chamadas
“inevitáveis” da velhice, nós recomendamos aos médicos
estimularem a reposição hormonal da menopausa,
sempre observando os bons preceitos da prática médica e
utilizando-se de hormônios homólogos humanos,
preferencialmente administrados pela via transdérmica,
no caso da associação estradiol-estriol, e, no caso da
progesterona, via transdérmica ou transvaginal. Para os
casos anteriores, a via oral também pode ser uma
alternativa, desde que os hormônios administrados sejam,
igualmente, homólogos humanos.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
6.
7.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
2. ANDROPAUSA
a. Quadro clínico
i. Cansaço, redução da libido e do desempenho sexual,
redução da força muscular, adinamia, fragilidade
imunológica, ginecomastia, redução da capacidade física,
ressecamento da pele, déficit de memória, aversão ao
convívio social, aumento da circunferência abdominal,
queda de cabelos, aumento do percentual de gordura
corporal, alterações do sono, alterações do humor, perda
de massa óssea, e comprometimento da qualidade de vida.
b.
Quadro Laboratorial
i.
ii.
iii.
iv.
v.
FSH > 5 u/L
LH > 8 u/L
Testosterona Total < 700 ng/dL
Índice de Androgênio Livre < 0,7
Testosterona livre < 2%
vi. Testosterona biodisponível < 400 ng/dL
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da andropausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de andropausa será confirmado
tomando-se como referência as manifestações e o quadro
clínico apresentados pelo paciente e devidamente avaliados
e registrados pelo médico. Tal conduta se justifica pela
baixa acurácia dos métodos de diagnóstico laboratorial das
deficiências hormonais, falhas de técnicas intrínsecas aos
métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a andropausa, a SOBRAF recomenda que seus médicos associados
utilizem-se do termo de consentimento padrão adotado pela
mesma e que deverá ser devidamente assinado pelo médico e pelo
seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA ANDROPAUSA
Após criteriosa revisão da literatura científica, discussões com
médicos representantes de todos os continentes e discussões
entre médicos brasileiros, todos profissionais versados e
adequadamente qualificados em utilizar e prescrever
hormônios em seres humanos com a finalidade primária de
promoção da saúde e, ainda, em total consonância com os
preceitos e guidelines diretrizes da Sociedade Brasileira Para
Estudos da Fisiologia – SOBRAF, da International Hormone
Society e da World Society of Anti-Aging Medicine, nós,
médicos membros da SOBRAF, concluímos haver chegado o
momento de considerar a deficiência hormonal masculina, e o
conseqüente
andropausa.
tratamento
de
reposição
hormonal
da
Desde que a estrutura química da testosterona e a técnica de
obtê-la de forma sintética foram descobertos na década de 30,
um grande número de estudos têm demonstrado, de forma
indubitável, ser a testosterona um hormônio indispensável
para a manutenção de um estado ótimo de saúde na população
masculina. Na medida em que os homens envelhecem, as
frações biodisponíveis da testosterona e de outros androgênios
declinam crônica e cumulativamente. O declínio gradual da
testosterona biodisponível responde por uma vasta e
multivariada gama de sinais e sintomas, tais como fadiga,
depressão, mudanças do humor, labilidade emocional,
irritabilidade, perda de massa muscular, aumento da gordura
corporal total, aumento da gordura intra-abdominal, perda do
desejo e da performance sexual, fragilidade imunológica,
ginecomastia, perda de massa óssea e muitas outras
manifestações que são, invariavelmente, atribuídas a achados
normais da idade. A persistência da deficiência hormonal
masculina pode aumentar os riscos das comorbidades
associadas ao envelhecimento, tais como obesidade, depressão,
diabetes, osteoporose e doenças cardiovasculares. Embora o
declínio hormonal não afete de maneira tão aguda e incisiva os
homens como a queda hormonal da menopausa, de todo modo,
compromete, pela sua cronicidade e efeito cumulativo, a sua
qualidade de vida, sua saúde e, muito provavelmente, a sua
própria expectativa de vida. O declínio androgênico masculino
recebe uma vasta sinonímia: distúrbio androgênico do
envelhecimento masculino (DAEM ), andropausa, climatério
masculino, menopausa masculina, partial androgen deficiency
in aging men ( PADAM ), hipogonadismo relacionado à idade,
penopausa, dentre outros tantos.
A quantidade de homens que recebe atenção e tratamento no
transcurso da deficiência hormonal é incomparavelmente
menor do que a quantidade de mulheres que recebe reposição
e tratamento na menopausa. Isto se deve, principalmente, ao
fato de que, ao contrário do declínio feminino, o declínio
hormonal masculino ainda não é um fato plenamente aceito
por boa parte da medicina tradicional. Com base na fisiologia
do envelhecimento hormonal, nós acreditamos não haver
qualquer justificativa válida para tal discriminação.
Os oponentes da reposição hormonal da andropausa amparamse em estudos conflitantes e com sérios erros de desenho
existentes na literatura, que demonstram diferenças não
significativas entre os níveis séricos hormonais de homens
jovens e homens velhos, outros sugerem que a testosterona
pode aumentar a incidência de câncer de próstata, enquanto
outros sugerem que a reposição de testosterona não apresenta
efeitos clínicos significativos. Estes estudos atípicos são
fartamente contrapostos por um imenso número de estudos
que são claros e unânimes em demonstrar exatamente o
oposto, destacando-se, principalmente, um indubitável efeito
protetor da testosterona contra o câncer de próstata.
Uma revisão global da literatura corrente não consegue
fornecer qualquer evidência de que a reposição com
testosterona ou seus derivados possa aumentar os riscos de
câncer de próstata in vivo. Ao contrário, homens com baixos
níveis de testosterona biodisponível são exatamente os que
apresentam não só os maiores riscos de câncer de próstata,
como a ocorrência de tumores de comportamento muito mais
agressivo, aumento do processo de deposição aterosclerótica
das artérias e piora gradual e cumulativa da qualidade de
saúde. Além do mais, pacientes portadores de câncer de
próstata que têm os seus níveis circulantes de testosterona
drasticamente reduzidos por conta das terapias antiandrogênicas, não apresentam qualquer aumento ou melhora
da sobrevivência.
Com a finalidade de detectar com o maior grau de precisão
possível a deficiência hormonal masculina, nós recomendamos
não somente uma detalhada avaliação clínica, levando-se em
conta os sinais e sintomas físicos e mentais sugestivos do
declínio masculino, como a realização de testes laboratoriais
que auxiliem e quantifiquem o diagnóstico, dentre os quais:
dosagem da testosterona total, testosterona livre, SHBG,
proteinograma, DHT, testosterona biodisponível, FSH, LH, e o
índice de androgênio livre. Igualmente importante é avaliar os
níveis séricos de estradiol, uma vez que a elevação destes
níveis pode provocar um bloqueio da ação da testosterona nos
homens.
Levando-se em consideração o enorme impacto para a saúde
masculina oriundo da queda de testosterona, nós
recomendamos aos médicos que estimulem o tratamento desta
deficiência para todos os casos, utilizando-se da testosterona
homóloga humana ou de seus derivados quimicamente mais
semelhantes possíveis, excetuando-se alguma contraindicação
absoluta. Todos os homens que avançam na idade, devem
expectar, cedo ou tarde, declínio dos seus níveis ótimos de
testosterona, sendo, portanto, potenciais candidatos à terapia
de reposição. A maioria dos homens irá experimentar declínio
entre os 30 e 45 anos de idade. Vale, entretanto, salientar, que
exceções a esta regra podem ocorrer, fazendo com que alguns
homens venham a necessitar da reposição hormonal abaixo ou
acima daquela faixa etária.
Somente doses fisiológicas de testosterona devem ser
administradas, objetivando-se manter os níveis séricos
comparáveis ao de adultos jovens e saudáveis, na faixa etária
dos 25 a 30 anos.
As melhores vias de administração para este hormônio são a
transdérmica e a intramuscular.
Níveis excessivos de estradiol devem ser evitados durante o
tratamento de reposição com testosterona, por conta do efeito
biológico neutralizador e além de responder pela ocorrência de
ginecomastia, hipertrofia prostática benigna e, possivelmente
infarto agudo do miocárdio. Ajustes no padrão alimentar, evitar
álcool e cafeína, além da prática regular de atividade física são
importantes medidas de suporte para redução dos níveis
excessivos de estradiol. Evitar a obesidade é um ponto
importantíssimo neste contexto, uma vez que o tecido adiposo
é rico em aromatase, enzima que catalisa a transformação de
testosterona em estradiol. Quando estas medidas não surtirem
o efeito desejado, o uso de inibidores da aromatase ou de
pequenas doses de progesterona podem estar indicados. A
progesterona aumenta a transformação de estradiol em
estrona, diminuindo, portanto, as suas concentrações séricas.
O câncer de próstata em atividade pode ser considerado como
uma contraindicação para o uso de testosterona. Contudo, ao se
rever cuidadosamente a literatura atual, parece haver uma
inconsistente base de evidências para dar suporte a esta
afirmação. Muitos estudos, ao contrário, demonstram que
portadores de câncer de próstata que também possuem
deficiência hormonal masculina têm a sua qualidade de saúde
severamente comprometida e podem ser beneficiados com a
reposição de doses pequenas de testosterona, trazendo
benefícios suplementares que em muito superam qualquer
suposto risco de estimulo ao crescimento tumoral.
CONCLUSÃO DO CONSENSO:
Nós não conseguimos identificar na literatura atual qualquer
evidência de que repor doses fisiológicas de testosterona
deponha contra ou traga riscos à saúde de homens portadores
de declínio nos níveis daquele hormônio. Ao contrário. Uma vez
que são múltiplos e multivariados os benefícios advindos da
reposição hormonal masculina, nós recomendamos o uso de
doses fisiológicas de testosterona ou de seu derivado químico
mais próximo possível, com o intuito de corrigir esta
deficiência, submetendo este homem em reposição a um
programa de acompanhamento clínico periódico e regular.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1. Professora Doutora Ana Cristina Vendramini, PhD
2. Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
3. Professora Doutora Andrea Thomaz Soccol, PhD
4.
5.
6.
7.
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
3. SOMATOPAUSA
a. Quadro clínico
i. Deterioração da composição corporal, redução da massa
muscular, aumento do percentual de gordura corporal
total, aumento do percentual de gordura visceral, cansaço,
redução do desempenho sexual, redução da força muscular,
adinamia, fragilidade imunológica, redução da capacidade
física, ressecamento e enrugamento da pele, déficit de
memória, baixa autoestima, alterações do sono, alterações
do humor, perda de massa óssea, e comprometimento da
qualidade de vida.
b.
Quadro Laboratorial
i. IGF-1 < 300 ng/dL em homens
ii. IGF-1 < 280 ng/dL em mulheres
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da somatopausa. Por outro
lado, nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de somatopausa será
confirmado tomando-se como referência as manifestações e
o quadro clínico apresentados pelo paciente e devidamente
avaliados e registrados pelo médico. Tal conduta se justifica
pela baixa acurácia dos métodos de diagnóstico laboratorial
das deficiências hormonais, falhas de técnicas intrínsecas
aos métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a somatopausa, a SOBRAF recomenda que seus médicos
associados utilizem-se do termo de consentimento padrão adotado
pela mesma e que deverá ser devidamente assinado pelo médico e
pelo seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA SOMATOPAUSA
Após criteriosa revisão da literatura científica, discussões
com médicos representantes de todos os continentes e
discussões entre médicos brasileiros, todos profissionais
versados e adequadamente qualificados em utilizar e
prescrever hormônios em seres humanos com a finalidade
primária de promoção da saúde e, ainda, em total
consonância com os preceitos e guidelines da Sociedade
Brasileira Para Estudos da Fisiologia – SOBRAF, da
International Hormone Society e da World Society of AntiAging Medicine, nós, médicos membros da SOBRAF,
concluímos haver chegado o momento de considerar a
reposição com o hormônio do crescimento humano
recombinante não só em adultos portadores de patologias
que impeçam ou dificultem a sua produção, como nos
adultos que estão envelhecendo e decaindo a sua
capacidade inata de síntese endógena. Nós concordamos e
aprovamos os consensos já estabelecidos e consagrados em
muitos países, que aconselham a reposição com o hormônio
do crescimento humano recombinante em adultos
portadores de patologias que impeçam ou dificultem a sua
produção. Nestas situações, existe história pregressa de
remoção, trauma, radiação, tumores ou severa inativação
da hipófise, fatos que impedem a produção endógena do
hormônio do crescimento.
Pensamos já haver na literatura científica atual uma base
suficiente de dados que demonstram e confirmam os
múltiplos benefícios e segurança do uso clínico do
hormônio do crescimento. Desta forma, tornou-se uma
necessidade médica estendermos a indicação de reposição
também aos adultos que estão envelhecendo e decaindo a
sua capacidade inata de síntese endógena, por conta da
progressiva redução funcional, consequente ao processo de
envelhecimento.
A evidência é de que o hormônio do crescimento é essencial
não apenas para o crescimento de crianças, mas também
essencial para a saúde física e mental de adultos,
particularmente na manutenção da integridade dos
sistemas muscular, adiposo, ósseo, imunológico e
cardiovascular. A deficiência do hormônio do crescimento é
frequentemente acompanhada de fadiga, ansiedade e
depressão, além de um progressivo e cumulativo
comprometimento da qualidade de vida. Por outro lado, a
reposição com o hormônio do crescimento nestes casos tem
demonstrado ser capaz de promover a parada e, por muitas
vezes reversão da progressão de todos aqueles processos.
A falta da reposição do hormônio do crescimento nos
adultos que estão envelhecendo e decaindo a sua
capacidade inata de síntese endógena, ao contrário do que
se imagina, pode trazer consequências verdadeiramente
desastrosas. Aumento considerável da velocidade de
deposição da placa ateromatosa, aumento das taxas de
mortalidade cardiovascular, deterioração da composição
corporal através da perda de massa muscular e
concomitante aumento da deposição de gordura corporal
total e gordura intra-abdominal, fragilidade imunológica,
perda de massa óssea, depressão, distúrbios progressivos
do sono e redução da síntese de proteínas são, dentre
outros, alguns dos fenômenos que se sucedem ao declínio
da capacidade de manutenção da síntese de níveis
fisiológicos do hormônio do crescimento, e que são parcial
ou totalmente reversíveis através da reposição do mesmo.
Nós recomendamos aos médicos submeterem os clientes
em uso do hormônio do crescimento a um regime de
avaliações regulares e aprazados. Isto inclui: anamnese,
exame físico e exames laboratoriais complementares
obedecendo a um intervalo de um a doze meses,
dependendo da necessidade individual de cada cliente.
Em relação a um eventual aumento no risco de
desenvolvimento de certos tipos de câncer com o uso do
hormônio do crescimento, os estudos mais sérios e
respeitados realizados em pacientes que receberam o
hormônio, comparados ao grupo controle de indivíduos
não-tratados,
mostram
uma
clara
redução
de
aproximadamente 50% na incidência de câncer e na
mortalidade por câncer no grupo de indivíduos que
receberam o hormônio. Na realidade, inexiste qualquer
argumento consistente ou fundamentação razoável para se
acreditar que repor o hormônio do crescimento possa
elevar o risco de câncer.
De qualquer forma, uma pesquisa de rotina a cada seis a 12
meses para o câncer de próstata e mama, complementadas
por ultrassom e mamografia quando necessário, constitui
conduta essencial, segundo este grupo de consenso. Além
do mais, nós também recomendamos que o tratamento de
reposição seja programado de modo a se respeitar as doses
fisiológicas preconizadas. Em casos clínicos muito
específicos e pontuais, como, por exemplo, os grandes
obesos e indivíduos com grande superfície corporal, pode
ser justificável o uso de doses maiores, que deverão ser
mantida por período de tempo não superior a 90 dias.
Doses acima dos limites fisiológicos não são recomendadas
por esta sociedade e fogem t ao escopo deste protocolo de
consenso.
Desta forma e seguindo estes princípios, o médico estará
assegurando não só a eficácia como a segurança do
tratamento.
CONCLUSÃO DO CONSENSO:
Na atualidade inexiste qualquer base científica de dados
que contraindique a reposição do hormônio do crescimento
humano recombinante em adultos que estão envelhecendo
e decaindo a sua capacidade inata de síntese endógena. Ao
contrário, uma multiplicidade de sinais, sintomas e
problemas adversos e deletérios à saúde humana tem sido
abundantemente reportada em indivíduos portadores de
níveis endógenos infra fisiológicos do hormônio do
crescimento, bem como tem sido fartamente reportada
melhora, desaparecimento ou mesmo reversão dos
problemas aludidos ao se promover a adequada reposição
do mesmo.
Ressaltamos, mais uma vez, a importância de se observar as
doses fisiológicas do hormônio, bem como a realização de
avaliações clínico-laboratoriais periódicas.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
6.
7.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
4. TIREOPAUSA
a. Quadro clínico
i. Deterioração da composição corporal, redução da massa
muscular, aumento do percentual de gordura corporal
total, aumento do percentual de gordura visceral, cansaço,
depressão marcadamente matinal, apatia, incapacidade de
concentração, dificuldade de perder peso, unhas fracas,
queda de cabelos, dislipidemia, hipercolesterolemia,
ateromatose precoce, intolerância ao frio, adinamia,
fragilidade imunológica, constipação, redução da
capacidade física, zumbidos, ressecamento e enrugamento
da pele, déficit de memória, alterações do sono, alterações
do humor, e comprometimento da qualidade de vida.
b.
Quadro Laboratorial
i.
ii.
iii.
iv.
c.
TSH ultrassensível > 2,0 pg/mL
T3 livre < 0,37 ng/dL
T4 livre < 0,7 ng/mL
Média da Temperatura Basal < 36,5o C em cinco aferições
matinais consecutivas.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da tireopausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de somatopausa será
confirmado tomando-se como referência as manifestações e
o quadro clínico apresentados pelo paciente e devidamente
avaliados e registrados pelo médico. Tal conduta se justifica
pela baixa acurácia dos métodos de diagnóstico laboratorial
das deficiências hormonais, falhas de técnicas intrínsecas
aos métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a tireopausa, a SOBRAF recomenda que seus médicos associados
utilizem-se do termo de consentimento padrão adotado pela
mesma e que deverá ser devidamente assinado pelo médico e pelo
seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA TIREOPAUSA
Após criteriosa revisão da literatura científica, discussões
com médicos representantes de todos os continentes e
discussões entre médicos brasileiros, todos profissionais
versados e adequadamente qualificados em utilizar e
prescrever hormônios em seres humanos com a finalidade
primária de promoção da saúde e, ainda, em total
consonância com os preceitos e guidelines da Sociedade
Brasileira Para Estudos da Fisiologia – SOBRAF, da
International Hormone Society e da World Society of AntiAging Medicine, nós, médicos membros da SOBRAF,
concluímos existir um sólido conjunto de evidências de
ordem clínica, prática e teórica que já permitem expandir o
tratamento do hipotireoidismo além dos parâmetros
correntes convencionais.
Existe, na atualidade, uma controvérsia entre grupos de
médicos. Um grupo essencialmente define o diagnóstico do
hipotireoidismo baseado em testes de laboratório,
enquanto o outro toma como base parâmetro
essencialmente clínicos. Uma sólida base de evidências
científicas não dá suporte à ideia de que o diagnóstico do
hipotireoidismo deva ou possa ser baseado apenas em
testes laboratoriais. Isto implica em que a existência do
hipotireoidismo só se confirma quando os níveis séricos de
TSH encontram-se acima dos limites superiores atuais de
referência, e os níveis séricos de tiroxina (T4) e
triiodotireonina (T4), encontram-se abaixo dos limites
inferiores atuais de referência, negligenciando os sinais e
sintomas clínicos.
Esta sociedade adota a posição intermediária. A decisão de
iniciar a reposição com o hormônio tireoidiano deve ser
baseada tanto em achados clínicos quanto laboratoriais, e
não somente em resultados de um simples teste
laboratorial, como se encontra atualmente expresso nos
jornais JAMA e Thyroid, conduta que representa o atual
consenso da Sociedade Americana de Tireoide.
Entendemos que achados e informações clínicas são
essenciais no diagnóstico de deficiências hormonais. Os
dados necessários ao diagnóstico do hipotireoidismo
incluem a pesquisa das queixas físicas e emocionais dos
pacientes, sinais físicos e coleta de história pregressa
pessoal e familiar sugestivas de deficiência tireoidiana, bem
como eventuais anormalidades no volume glandular,
expressos pela presença de hipertrofia ou bócio e/ou
tireoidite autoimune.
As seguintes evidências dão suporte à existência de
hipotireoidismo clínico, em indivíduos erroneamente
considerados laboratorialmente normais, e que são
candidatos ao tratamento de reposição hormonal
tireoidiana:
Os níveis de referencia da normalidade são excessivamente
largos e ignoram e existência dos níveis ótimos de
referência. Estes níveis incluem largas margens de
referência de normalidade para os níveis de T3, T4 e TSH,
que são, na realidade, plenamente compatíveis com
múltiplas disfunções tireoidianas. Não existe qualquer
evidência atual que dê suporte à persistência do uso destes
parâmetros, uma vez que são completamente incapazes de
definir e diferenciar de maneira clara e adequada os
estados de eutireoidismo e hipotireoidismo. A base de
dados atuais sugere que sejam utilizados níveis de
referencia incomparavelmente mais estreitos e específicos
para esta situação. Os níveis convencionais de referência
para detecção do hipotireoidismo sofrem variação de mais
de 30 vezes ( 0.2 a 6.5 mUI/L ).
Em muitos estudos clínicos atuais, níveis séricos de TSH
acima de 1.5 a 2.0 mUI/L tem sido associados com
dislipidemia, inflamação crônica subclínica, níveis elevados
de homocisteína, proteína C reativa, hipercolesterolemia,
depressão, pobre resposta ao tratamento com
antidepressivos, maiores índices de massa corpórea, maior
incidência de hipertensão arterial sistêmica, elevação dos
triglicérides e hiperglicemia. Do mesmo modo, aqueles
níveis tem sido associados a anormalidades cardíacas e
vasculares, que incluem ateromatose acelerada e perda da
elasticidade vascular. Neonatos com baixo peso e partos
prematuros tem sido relatados em mães com TSH acima de
2.0 mUI/L. Mais importante, iniciar o tratamento do
hipotireoidismo nestes casos, tem demonstrado ser uma
medida capaz de minimizar ou reverter aqueles problemas.
Com base ainda nestes múltiplos estudos, existem
evidências que dão suporte a adoção de níveis de referencia
bem mais estreitos para o TSH, cujos valores devem se
situar entre 0.4 a 2.0 mUI/L. Torna-se importante ressaltar
que 95% da população de indivíduos saudáveis e com a
atividade tireoidiana normal exibem níveis séricos de TSH
dentro do intervalo de 0.4 a 2.0 mUI/L.
Um outro ponto de capital importância, é que os estudos
demonstram resultados clínicos incomparavelmente
superiores quando se utiliza no tratamento a associação
entre T3 e T4, ao invés do tratamento isolado com T4. Isto
se deve ao fato de que uma boa parte do T4 administrado
isoladamente, sofre conversão para T3 reverso, forma
hormonal inativa biologicamente. Além do mais, para que o
estado de eutireoidismo seja alcançado, o organismo
humano necessita de ambos os hormônios, T4, que tem a
finalidade principal de atrair moléculas de TBG ( thyroid
binding globulin ) e T3, que, livre do atrelamento da TBG,
pode ligar-se rapidamente aos receptores celulares do
hormônio tireoidiano nas células-alvo. A combinação
fisiológica entre T3 e T4, obedecendo às proporções de uma
parte de T3 para cinco partes de T4 , produz resultados
clínicos inequivocamente superiores.
Nós recomendamos aos médicos que excluam
cuidadosamente outras patologias ou estados clínicos que
produzam sintomatologia semelhante ao hipotireoidismo
antes de iniciar a reposição do hormônio tireoidiano. Ao se
iniciar o tratamento, utilizar doses menores e programar
elevação gradual, de acordo com a necessidade clínica,
visando evitar a presença de superdosagem, e,
consequentemente,
um
possível
quadro
de
hipertireoidismo iatrogênico, efeito adverso mais frequente
no tratamento do hipotireoidismo.
Intolerância ao
tratamento pode ser causada por excessiva conversão de T4
em T3, acelerando, desta forma, a atividade tireoidiana.
Devemos lembrar que a principal causa deste problema é a
deficiência não diagnosticada de outros hormônios,
principalmente a hipocortisolemia e a deficiência de
estradiol na menopausa. Os médicos devem dedicar
especial atenção aos níveis de cortisol. A fadiga adrenal
crônica, que leva à queda excessiva dos níveis de cortisol
provoca uma baixa tolerância ao tratamento do
hipotireoidismo, principalmente quando a opção foi pela
combinação T4/T3. A deficiência de cortisol provoca
hiperatividade do sistema nervoso ortossimpático e uma
excessiva e rápida conversão de T4 em T3. Desta forma, em
pacientes com fadiga adrenal crônica, nós recomendamos
que os médicos tratem a deficiência de cortisol antes de
iniciarem o tratamento do hipotireoidismo ou, no mínimo,
de forma concomitante ao início do mesmo. A segurança do
tratamento do hipotireoidismo pode ser aumentada se o
iniciarmos com doses menores, promovendo um aumento
gradual nos casos em que tais ajustes se fizerem
necessários.
CONCLUSÃO DO CONSENSO:
Hipotireoidismo clínico, em indivíduos erroneamente
considerados laboratorialmente normais, constitui, sem
nenhuma dúvida uma racional justificativa para se
promover a inclusão destas pessoas no grupo de candidatos
ao tratamento com os hormônios tireoidianos. Estes
indivíduos podem se beneficiar com um programa de
reposição com baixas dosagens, em que estejam associados
T4 e T3 em proporções fisiológicas. Avaliação clínica e
laboratorial aprazados, utilizando-se parâmetros mais
estreitos para os níveis de referência do TSH, além de um
cuidadoso monitoramento individual de cada caso, são as
bases que conduzem a resultados clínicos favoráveis.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
6.
7.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
5. FADIGA ADRENAL CRÔNICA
a. Quadro clínico
i. Cansaço marcadamente matinal, apatia, incapacidade de
concentração,
adinamia,
fragilidade
imunológica,
compulsão massas e doces, irritabilidade, intolerância ao
estresse, déficit de memória, alterações do sono, alterações
do humor, e comprometimento da qualidade de vida.
b.
Quadro Laboratorial
i. Cortisol matinal < 15 mcg/dL
ii. Cortisol livre < 10 ng/ml
iii. Transcortina > 30 mg/L
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da fadiga adrenal crônica. Por
outro lado, nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico da fadiga adrenal crônica será
confirmado tomando-se como referência as manifestações e
o quadro clínico apresentados pelo paciente e devidamente
avaliados e registrados pelo médico. Tal conduta se justifica
pela baixa acurácia dos métodos de diagnóstico laboratorial
das deficiências hormonais, falhas de técnicas intrínsecas
aos métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a fadiga adrenal crônica, a SOBRAF recomenda que seus médicos
associados utilizem-se do termo de consentimento padrão adotado
pela mesma e que deverá ser devidamente assinado pelo médico e
pelo seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA FADIGA ADRENAL CRÔNICA
Após criteriosa revisão da literatura científica, discussões
com médicos representantes de todos os continentes e
discussões entre médicos brasileiros, todos profissionais
versados e adequadamente qualificados em utilizar e
prescrever hormônios em seres humanos com a finalidade
primária de promoção da saúde e, ainda, em total
consonância com os preceitos e guidelines da Sociedade
Brasileira Para Estudos da Fisiologia – SOBRAF, da
International Hormone Society e da World Society of AntiAging Medicine, nós, médicos membros da SOBRAF,
concluímos ter chegado o momento de reconsiderar os
conceitos atualmente vigentes acerca do tratamento da
deficiência adrenal, em particular a deficiência de cortisol,
não apenas nas pessoas afetadas por severas deficiências,
mas também nos portadores de fadiga adrenal crônica.
Nós concordamos plenamente e aprovamos o consenso
mundial que foi atingido no que concerne ao tratamento
com glicocorticoides para adultos portadores de severa
deficiência de cortisol. Geralmente, naquela condição, existe
uma deficiência total ou quase total da produção de cortisol,
que ocorre por conta de remoção total ou parcial ou
inativação total ou parcial das glândulas adrenais, as
estruturas responsáveis pela produção de cortisol.
Acreditamos que a quantidade de evidências existentes na
atualidade demonstrando os efeitos benéficos do cortisol,
bem como os seus eventuais efeitos adversos é suficiente
para promover a extensão da recomendação da reposição
de cortisol também para os portadores da condição clínica
conhecida como fadiga adrenal crônica.
Entre os quadros de deficiência de cortisol deve também
ser incluído a forma que incide ao longo do processo do
envelhecimento, ocasionada pela progressiva deterioração
do eixo hipofisário-adrenal.
A evidência é de que o cortisol é essencial não só para os
portadores de estados de severa depleção, como também
para a manutenção do equilíbrio físico e mental dos adultos
que estão envelhecendo e declinando a sua capacidade de
produção. Uma quantidade adequada de cortisol é essencial
para o normal funcionamento de uma multiplicidade de
órgãos e sistemas: cérebro, pele, articulações, músculos,
trato digestório, sistemas imunológico e cardiovascular. A
deficiência de cortisol encontra-se clinicamente relacionada
com fadiga, baixa tolerância ao estresse, confusão mental e
comprometimento da qualidade de vida. O tratamento com
glicocorticoides tem se mostrado capaz de melhorar a
qualidade de vida, humor e status mental dos pacientes.
Consequências adversas da deficiência de cortisol variam
desde potenciação dos efeitos debilitantes de doenças
inflamatórias ( artrite reumatoide, gastrenterite, colite,
desordens imunológicas e alergias ), até o aumento da
mortalidade em condições de alto risco como o choque
séptico. Os estados de deficiência leve de cortisol podem,
igualmente, causar mais repercussões danosas à saúde
humana do que se imaginava antes.
Como a suplementação de cortisol e de outros
glicocorticoides tem sido associada com importantes efeitos
adversos, dentre os quais: imunossupressão, osteoporose,
ganho de peso, atrofia cutânea, hipertensão, supressão
adrenal e fácies cushingóide, nós recomendamos aos
médicos que a reposição de cortisol deva ser pautada pela
observância de guidelines de segurança. Acreditamos
firmemente que os efeitos colaterais são consequentes ao
uso de doses excessivas, bem como pelo fato de que a
reposição de cortisol não pode ocorrer na ausência da
correção dos desequilíbrios nos níveis de hormônios
anabólicos (pausas humanas ), principalmente a queda dos
níveis de DHEA. e T3. A presença de níveis fisiológicos de
hormônios anabólicos pode bloquear os efeitos catabólicos
da presença de doses excessivas de glicocorticoides. Em
vários casos de deficiência de cortisol, reposição de
derivados sintéticos produz efeitos clínicos muito menos
efetivos do que a reposição do cortisol na sua forma
homóloga humana.
Em termos de diagnóstico laboratorial, pode-se lançar mão
das dosagens séricas de cortisol total matinal, cortisol livre,
transcortina ( CBG= cortisol binding globulin ), ACTH, bem
como dosagens dos 17-hidroxiesteróides em urina de 24
horas, pela técnica de cromatografia a gás.
O tratamento de reposição com cortisol nas formas leves
pode ser feito observando-se os limites diários das doses
fisiológicas. Em casos mais severos, as doses recomendadas
podem sofrer um acréscimo de até 30-50%.
Lembramos que os homens necessitam de doses maiores
porque fisiologicamente secretam quantidades diárias
cerca de 50% maiores do que as mulheres. Apenas 50 % da
dose diária administrada é absorvida pelo trato
gastrintestinal. Em situações de agravamento das condições
de estresse, como: infecções, procedimentos cirúrgicos e
abalo emocional intenso, recomendamos que as doses
sejam temporariamente aumentadas.
Importante lembrar que a reposição com cortisol pode
agravar deficiências já existentes na produção dos
hormônios tireoidianos e DHEA. Desta forma,
recomendamos aos médicos corrigirem concomitantemente
aquelas deficiências.
CONCLUSÃO DO CONSENSO:
Com base na literatura científica atual, inexistem quaisquer
justificativas
plausíveis
que
contraindiquem
ou
desestimulem o tratamento de reposição com cortisol em
adultos com baixos níveis. Efeitos colaterais adversos
podem ser evitados seguindo-se os guidelines já propostos,
bem como utilizando-se doses fisiológicas da forma
homóloga humana do cortisol. Novamente ressaltamos a
capital importância da correção concomitante de outras
deficiências na produção de hormônios anabólicos,
particularmente DHEA e o hormônio tireoidiano. Monitorar
os pacientes através de um programa regular de
acompanhamento clínico-laboratorial.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
6.
7.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
6. ADRENOPAUSA
a. Quadro clínico
i. Depressão e cansaço em pessoas jovens, adinamia, apatia,
fragilidade imunológica, ateromatose, irritabilidade, déficit
de memória, alterações do sono, alterações do humor,
ressecamento vaginal, queda de cabelos, rarefação de pelos
pubianos, redução da libido, hipercolesterolemia,
dislipidemia, perda de massa óssea e comprometimento da
qualidade de vida.
b.
Quadro Laboratorial
i. SDHEA < 350 ug/mL em homens
ii. SDHEA < 300 ug/mL em mulheres
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da adrenopausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de adrenopausa será
confirmado tomando-se como referência as manifestações e
o quadro clínico apresentados pelo paciente e devidamente
avaliados e registrados pelo médico. Tal conduta se justifica
pela baixa acurácia dos métodos de diagnóstico laboratorial
das deficiências hormonais, falhas de técnicas intrínsecas
aos métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a adrenopausa, a SOBRAF recomenda que seus médicos associados
utilizem-se do termo de consentimento padrão adotado pela
mesma e que deverá ser devidamente assinado pelo médico e pelo
seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA ADRENOPAUSA
Após criteriosa revisão da literatura científica, discussões
com médicos representantes de todos os continentes e
discussões entre médicos brasileiros, todos profissionais
versados e adequadamente qualificados em utilizar e
prescrever hormônios em seres humanos com a finalidade
primária de promoção da saúde e, ainda, em total
consonância com os preceitos e guidelines da Sociedade
Brasileira Para Estudos da Fisiologia – SOBRAF, da
International Hormone Society e da World Society of AntiAging Medicine, nós, médicos membros da SOBRAF,
concluímos ter chegado o momento de considerar a
deficiência de dehidroepiandrosterona, bem como a sua
reposição.
Até o presente momento, as sociedades médicas
convencionais relacionadas à endocrinologia, ainda não
reconheceram a necessidade e a importância clínica de
tratar
e
repor
a
deficiência
adrenal
de
dehidroepiandrosterona
(DHEA).
Algumas
poucas
sociedades médicas convencionais ao redor do mundo, tem
expressado de forma pontual e tímida a importância da
reposição de DHEA. Em geral, se identifica a conclusão de
que ainda não existe base de dados suficiente que dê
suporte à reposição deste hormônio. Eles são da opinião de
que a literatura cientifica sobre o DHEA ainda é muito
escassa e sua eficácia clínica ainda não está suficientemente
comprovada.. Eles, igualmente, expressam a preocupação
de que a reposição de DHEA poderia estar relacionada a
uma maior incidência do câncer genital e a uma redução do
HDL – colesterol.
Após uma cuidadosa e exaustiva revisão da literatura
cientifica atual, bem como ler e discutir os relatórios
negativos institucionais, concluímos não existir qualquer
base de dados científica razoável que dê suporte à ideia de
que o uso de DHEA possa trazer riscos à saúde humana.
Nós reconhecemos e corroboramos um grande número de
estudos aonde homens e mulheres com deficiência de
DHEA tem sido tratados e tem apresentado significativa
melhora em múltiplos aspectos físicos e mentais.
Ao nos detalharmos com estudos que demonstram efeitos
“pouco significativos” no tratamento com DHEA é possível
observar que uma falha de desenho importante é
frequentemente perceptível: o tempo excessivamente curto
em que estas pessoas tem passado recebendo o hormônio,
períodos inferiores a duas semanas, em boa parte das
vezes, tempo notoriamente insuficiente para que resultados
consistentes sejam alcançados.
Ao lado de uma minoria de estudos que demonstram
resultados negativos ou não significativos, existe um grande
número de estudos que atesta de maneira inquestionável a
importância e, mais ainda, uma multivariedade de
benefícios oriundos da reposição com DHEA. Além do mais,
estes estudos não só confirmam a eficácia como chegam à
conclusão que a reposição de DHEA, o mais abundante
hormônio esteroide produzido no corpo humano, é uma das
formas de reposição mais seguras e eficientes que existem.
Estudos randomizados, placebo-controle e duplo-cego,
confirmam inexistirem quaisquer efeitos danosos à saúde
humana, quando níveis fisiológicos de DHEA são
suplementados. Efeitos colaterais porventura existentes,
encontram-se completamente vinculados ao emprego de
doses excessivas. Os sinais mais característicos de doses
excessivas de DHEA são: pele oleosa, acne e leve hirsutismo,
efeitos reversíveis através do devido ajuste nas dosagens.
Em muitos estudos que analisam a reposição de DHEA,
significativos benefícios foram obtidos no ganho de massa
óssea, qualidade da pele, sistema imunológico,
sensibilidade à glicose, sensibilidade à insulina e perfil
lipídico. Benefícios também foram evidenciados na
performance mental e emocional, qualidade de vida, fadiga,
depressão, redução do risco cardiovascular, diabetes e
obesidade.
É a opinião deste grupo que os seguintes argumentos dão
suporte e justificam plenamente o tratamento de reposição
com DHEA em adultos com baixos níveis séricos:
1. DHEA é um hormônio natural aos seres humanos,
está plenamente configurado para atender às nossas
demandas metabólicas, e, na verdade, é o hormônio
presente em maior quantidade no corpo humano.
2. DHEA exerce mais de 150 funções anabólicas no
metabolismo humano.
3. Apresenta uma multiplicidade de benefícios quando
usando em indivíduos adultos que apresentam
baixos níveis, sendo uma valiosa ferramenta no
combate
às
doenças
relacionadas
ao
envelhecimento.
4. Reposição de DHEA é segura.
5. Reposição de DHEA tem um custo acessível.
Com o intuito de elevar a segurança do tratamento de
reposição com DHEA, nós recomendamos que os médicos
submetam seus clientes a um programa de avaliações
periódicas, incluindo anamnese, exame físico e exames
laboratoriais complementares a cada 3 a 12 meses,
dependendo das necessidades individuais de cada um.
Entendemos ser igualmente relevante promover uma
rotina de avaliações clínico-laboratoriais para o câncer de
próstata e mama, obedecendo a um intervalo de seis a 12
meses, dependendo de cada caso.
Na nossa experiência, os melhores métodos para o
diagnóstico da deficiência de DHEA são a avaliação sérica
dos níveis do sulfato de dehidroepiandrosterona e a
avaliação da excreção dos metabólitos 17-cetoesteróidesDHEA em urina de 24 horas, pela técnica de cromatografia
a gás.
As doses de segurança são as chamadas doses fisiológicas,
que devem ser seguidas e observadas pelos membros da
sociedade.
Ressaltamos que nos casos em que é clinicamente
relevante evitar a conversão de DHEA para Testosterona
ou Estradiol, pode-se lançar mão da reposição de 7-KetoDHEA, principal metabólito ativo do DHEA, que possui
exatamente as mesmas propriedades do DHEA, porém, não
sofre conversão para outros hormônios. Neste caso, devese, igualmente, observar as doses fisiológicas de segurança.
CONCLUSÃO DO CONSENSO:
Com base na literatura científica atual, inexistem
justificativas
plausíveis
que
contraindiquem
ou
desestimulem o tratamento de reposição de DHEA em
adultos com baixos níveis, exceto para as mulheres que
encontram-se na pós-menopausa e não estão fazendo a
reposição hormonal da menopausa. Ao contrário, benefícios
em quantidade e intensidade suficientes já tem sido
demonstrados e servem como base para nos permitir
recomendar o uso de doses fisiológicas de DHEA para
corrigir as deficiências bem estabelecidas e previamente
diagnosticadas em adultos, submetendo-os, daí por diante,
a um programa regular de acompanhamento clínicolaboratorial. A reposição de DHEA encontra-se
especialmente justificada em indivíduos portadores de
condições de saúde tratadas com corticoides, uma vez que o
seu uso pode neutralizar com segurança os efeitos
catabólicos excessivos da corticoterapia.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
6.
7.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
Professor Doutor Marcos Renato Scholz, PhD
Dr. Ítalo Emmanuel Valeriano Rachid
7. MELATOPAUSA
a. Quadro clínico
i. Depressão, cansaço, adinamia, apatia, fragilidade
imunológica, irritabilidade, déficit de memória, alterações
do sono, alterações do humor, alterações gastrointestinais e
comprometimento da qualidade de vida.
b.
Quadro Laboratorial
i. 6-Sultatoxi-Melatonina < 40 ng/dia em urina de 24 horas
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da melatopausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de melatopausa será
confirmado tomando-se como referência as manifestações e
o quadro clínico apresentados pelo paciente e devidamente
avaliados e registrados pelo médico. Tal conduta se justifica
pela baixa acurácia dos métodos de diagnóstico laboratorial
das deficiências hormonais, falhas de técnicas intrínsecas
aos métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a melatopausa, a SOBRAF recomenda que seus médicos associados
estarão, concomitantemente, utilizem-se do termo de
consentimento padrão adotado pela mesma e que deverá ser
devidamente assinado pelo médico e pelo seu paciente.
e.
CONSENSO DA SOBRAF PARA O TRATAMENTO
HORMONAL DA MELATOPAUSA
Após criteriosa revisão da literatura científica, discussões com
médicos representantes de todos os continentes e discussões
entre médicos brasileiros, todos profissionais versados e
adequadamente qualificados em utilizar e prescrever
hormônios em seres humanos com a finalidade primária de
promoção da saúde e, ainda, em total consonância com os
preceitos e guidelines do Grupo Longevidade Saudável, da
International Hormone Society e da World Society of AntiAging Medicine, nós, médicos membros do Grupo de Consenso
do Grupo Longevidade Saudável, concluímos ter chegado o
momento de considerar o tratamento da deficiência de
melatonina em adultos.
Até o presente momento, nenhuma sociedade médica
convencional no mundo reconheceu a necessidade e a
importância de tratar a deficiência da glândula pineal através
da reposição de melatonina.
Como é de costume quando se trata do assunto reposição
hormonal, a controvérsia também não foge à regra na
reposição de melatonina. Para algumas escolas constitui-se em
um hormônio essencial, com importantes repercussões para a
saúde humana. Já para outras escolas, não passa de um placebo
sem qualquer importância clínica. Em contraste com esta
controvérsia, existe uma unanimidade completa acerca da
segurança e importância da reposição de melatonina entre
pesquisadores renomados e médicos ao redor de todo o mundo
que acumularam vasta experiência no uso e aplicações clínicas
deste hormônio em seres humanos. A melatonina tem se
mostrado tão segura, que até o presente momento não foi
possível determinar os limites de doses tóxicas para humanos e
para animais. Doses extremamente elevadas tem sido
utilizadas em experimentos com animais com o intuito de
estabelecer aqueles níveis, sem que se consiga produzir efeitos
danosos ou mesmo a morte dos animais.
Após exaustiva revisão da literatura e troca de experiências
entre grupos versados no emprego clínico da melatonina, o que
se pode concluir é que a sua reposição é capaz de produzir
consistentes e significativos benefícios à saúde humana. Os
efeitos mais notórios são observados na qualidade do sono,
controle do Jet Lag, varredura de radicais livres, metabolismo
da glicose, ossos, sistema cardiovascular, metabolismo
cerebral, melhora do perfil lipídico e manutenção da ciclicidade
e responsividade dos receptores celulares para hormônios
anabólicos.
Foram revistos mais de 350 estudos sobre o uso de melatonina
e o sono, sendo que a quase totalidade dos mesmos (98,6%)
deixa evidente uma notória melhora da qualidade do sono, por
ser a melatonina capaz de encurtar o tempo de indução do
sono, encurtar o início da fase REM do sono profundo e
provocar um relaxamento muscular e nervoso através da
estimulação do sistema parassimpático. O conjunto destas
ações facilita o sono e melhora a sua qualidade, além de
contribuir diretamente para o processo de reparo e
recuperação metabólica ao longo do período de permanência
no sono.
Com base na literatura e experiência mundial atuais, inexistem
quaisquer justificativas plausíveis de ordem científica ou
médica que contraindiquem ou desestimulem o tratamento de
reposição com melatonina. Sua segurança e eficácia clínica são
motivos mais do que suficientes para ressegurar às autoridades
de saúde a validade e aceitação do seu uso, desde de que tal
seja feito sob criteriosa prescrição e supervisão médica.
As doses de segurança são as chamadas doses fisiológicas, que
devem ser seguidas e observadas pelos membros da sociedade.
Lembramos que a melatonina pode reduzir a atividade do
cortisol, de modo que, em casos de fadiga adrenal crônica devese iniciar o tratamento com doses menores e também corrigir a
deficiência de cortisol de forma concomitante.
Na opinião deste grupo, os seguintes argumentos dão suporte e
fundamentam o tratamento de reposição de melatonina em
adultos:
 Melatonina é uma substância natural ao organismo
humano e sua presença é abundante, principalmente no
período noturno.
 Melatonina está completamente adaptada ao corpo
humano.
 Melatonina exerce uma multiplicidade de benefícios na
manutenção da saúde física e mental, bem como contra
o desenvolvimento das doenças degenerativas da
velhice.
 Melatonina é segura.
 Melatonina tem custo acessível.
O diagnóstico da deficiência de melatonina é baseado
em critérios essencialmente clínicos. Pode-se,
entretanto, em casos que se façam necessários, recorrer
à dosagem da excreção em urina de 24 horas da 6sulfatoxi-melatonina,
principal
metabólito
da
melatonina, como parâmetro diagnóstico laboratorial.
CONCLUSÃO DO CONSENSO:
Com base na literatura científica atual, inexistem
quaisquer justificativas plausíveis que contraindiquem
ou desestimulem o tratamento de reposição com
melatonina em adultos com baixos níveis. Ao contrário,
uma vasta base de dados e evidências dão suporte e
validam o seu emprego em indivíduos com deficiência e
com baixos níveis, submetendo-os a um programa
regular de acompanhamento médico.
São Paulo, 12 de Novembro de 2012
Grupo de Consensos da SOBRAF
1.
2.
3.
4.
5.
Professora Doutora Ana Cristina Vendramini, PhD
Professora Doutora Andreia Conceição Milan B. Antoniolli, PhD
Professora Doutora Andrea Thomaz Soccol, PhD
Professor Doutor Eduardo Faria, PhD
Professor Doutor Marcelo Alexandre de Mattos, PhD
6. Professor Doutor Marcos Renato Scholz, PhD
7. Dr. Ítalo Emmanuel Valeriano Rachid
8. ELETROPAUSA
a. Quadro clínico
i. Depressão, cansaço, adinamia, apatia, fragilidade
imunológica, irritabilidade, déficit de memória, alterações
do sono, alterações do humor e comprometimento da
qualidade de vida.
b.
Quadro Laboratorial
i. Dosagem do Sulfato de Pregnenolona no líquor
ii. Sulfato de pregnenolona < 90 ng/mL.
c.
Observações
complementares
diagnóstico clínico-laboratorial:
acerca
do
i. Quando o diagnóstico laboratorial mostrar-se coerente e
compatível com o quadro clínico, este será considerado na
confirmação do diagnóstico da eletropausa. Por outro lado,
nas situações em que ocorrer clara discrepância,
divergência ou distorções entre os dados clínicos e
laboratoriais, o diagnóstico de eletropausa será confirmado
tomando-se como referência as manifestações e o quadro
clínico apresentados pelo paciente e devidamente avaliados
e registrados pelo médico. Tal conduta se justifica pela
baixa acurácia dos métodos de diagnóstico laboratorial das
deficiências hormonais, falhas de técnicas intrínsecas aos
métodos, uso de metodologia inadequada na coleta da
amostra de sangue, horário em que a amostra foi colhida,
nível de hidratação do paciente no momento da coleta e
limitações técnicas dos métodos laboratoriais. A coleta de
uma amostra matinal de sangue para dosar um dado
hormônio, expressa um retrato estático de um fenômeno
intensamente dinâmico e complexo, que sofre influência de
múltiplas variáveis, o que torna
qualquer método
diagnóstico potencialmente falho, limitado e pouco
confiável, até que sejam desenvolvidas tecnologias e
métodos mais eficazes.
d. No momento da instituição da proposta terapêutica hormonal para
a eletropausa, a SOBRAF recomenda que seus médicos associados
utilizem-se do termo de consentimento padrão adotado pela
mesma e que deverá ser devidamente assinado pelo médico e pelo
seu paciente.
REFERÊNCIAS BIBLIOGRÁFICAS COMPLEMENTARES
1- ATIVIDADE ANTI-OXIDANTE
MODULAÇÃO HORMONAL
MEDIADA
PELA
Atividade Antioxidante da Melatonina
1.
2.
3.
4.
5.
6.
7.
8.
9.
Col C, Dinler K, Hasdemir O, Buyukasik O, Bugdayci G. Oxidative stress and
lipid peroxidation products: effect of pinealectomy or exogenous melatonin
injections on biomarkers of tissue damage during acute pancreatitis.
Hepatobiliary Pancreat Dis Int. 2010 Feb;9(1):78-82
Sokolovic D, Djindjic B, Nikolic J, Bjelakovic G, Pavlovic D, Kocic G, Krstic D,
Cvetkovic T, Pavlovic V. Melatonin reduces oxidative stress induced by chronic
exposure of microwave radiation from mobile phones in rat brain. J Radiat Res
(Tokyo). 2008 Nov;49(6):579-86
Rodriguez MI, Escames G, López LC, García JA, Ortiz F, López A, AcuñaCastroviejo D. Melatonin administration prevents cardiac and diaphragmatic
mitochondrial oxidative damage in senescence-accelerated mice. J Endocrinol.
2007 Sep;194(3):637-43
Pan L, Xu W, Fu JH, Xue XD. Effect of melatonin on hyperoxia-induced
oxidant/antioxidant imbalance in the lung of neonatal rats with chronic lung
disease]Zhongguo Dang Dai Er Ke Za Zhi. 2009 Jul;11(7):581-4
z A, Tasset I, Ramírez LM, Arjona A, Segura J, Túnez I, Montilla P, Muntané J,
Padillo FJ. Effect of melatonin on myocardial oxidative stress induced by
experimental obstructive jaundice. Rev Esp Enferm Dig. 2009 Jul;101(7):460-3
Fischer TW, Slominski A, Zmijewski MA, Reiter RJ, Paus R. Melatonin as a
major skin protectant: from free radical scavenging to DNA damage repair. Exp
Dermatol. 2008 Sep;17(9):713-30.
Sofic E, Rimpapa Z, Kundurovic Z, Sapcanin A, Tahirovic I, Rustembegovic A,
Cao G. Antioxidant capacity of the neurohormone melatonin. J Neural Transm.
2005 Mar;112(3):349-58
Ayata A, Mollaoglu H, Yilmaz HR, Akturk O, Ozguner F, Altuntas I. Oxidative
stress-mediated skin damage in an experimental mobile phone model can be
prevented by melatonin. J Dermatol. 2004 Nov;31(11):878-83
Baydas G, Tuzcu M. Protective effects of melatonin against ethanol-induced
reactive gliosis in hippocampus and cortex of young and aged rats. Exp Neurol.
2005 Jul;194(1):175-81
10.
11.
12.
Kerman M, Cirak B, Ozguner MF, Dagtekin A, Sutcu R, Altuntas I, Delibas N.
Does melatonin protect or treat brain damage from traumatic oxidative stress?
Exp Brain Res. 2005 Jun;163(3):406-10
Abdel-Wahhab MA, Abdel-Galil MM, El-Lithey M. Melatonin counteracts
oxidative stress in rats fed an ochratoxin A contaminated diet. J Pineal Res.
2005 Mar;38(2):130-5
Ozacmak VH, Sayan H, Arslan SO, Altaner S, Aktas RG. Protective effect of
melatonin on contractile activity and oxidative injury induced by ischemia and
reperfusion of rat ileum. Life Sci. 2005 Feb 18;76(14):1575-88
Atividade Antioxidante dos Hormônios Tideoidianos
1.
2.
3.
4.
Nanda N, Bobby Z, Hamide A. Association of thyroid stimulating hormone and
coronary lipid risk factors with lipid peroxidation in hypothyroidism. Clin Chem
Lab Med. 2008;46(5):674-9
Antipenko AYe, Antipenko YN. Thyroid hormones and regulation of cell
reliability systems. Adv Enzyme Regul. 1994;34:173-98
Tseng YL, Latham KR. Iodothyronines: oxidative deiodination by hemoglobin
and inhibition of lipid peroxidation. Lipids. 1984 Feb;19(2):96-102
Bozhko AP, Gorodetskaia IV. The role of thyroid hormones in prevention of
disorders of myocardial contractile function and antioxidant activity during heat
stress. Ross Fiziol Zh Im I M Sechenova. 1998 Mar;84(3):226-32
Atividade Antioxidante do Hormônio do Crescimento
1. Higashi Y, Sukhanov S, Anwar A, Shai SY, Delafontaine P. IGF-1, oxidative
stress and atheroprotection. Trends Endocrinol Metab 2010 Apr;21(4):245-54
2. Sukhanov S, Higashi Y, Shai SY, Vaughn C, Mohler J, Li Y, Song YH,
Titterington J, Delafontaine P. IGF-1 reduces inflammatory responses,
suppresses oxidative stress, and decreases atherosclerosis progression in ApoEdeficient mice. Arterioscler Thromb Vasc Biol. 2007 Dec;27(12):2684-90
3. Kajstura J, Fiordaliso F, Andreoli AM, Li B, Chimenti S, Medow MS, Limana F,
Nadal-Ginard B, Leri A, Anversa P. IGF-1 overexpression inhibits the
development of diabetic cardiomyopathy and angiotensin II-mediated oxidative
stress. Diabetes. 2001 Jun;50(6):1414-24
5.
6.
7.
Faure P, Oziol L, Artur Y, Chomard P. Thyroid hormone (T3) and its acetic
derivative (TA3) protect low-density lipoproteins from oxidation by different
mechanisms. Biochimie. 2004 Jun;86(6):411-8
Brzezinska-Slebodzinska E. Influence of hypothyroidism on lipid peroxidation,
erythrocyte resistance and antioxidant plasma properties in rabbits. Acta Vet
Hung. 2003;51(3):343-51
Oziol L, Faure P, Bertrand N, Chomard P. Inhibition of in vitro macrophageinduced low density lipoprotein oxidation by thyroid compounds. J Endocrinol.
2003 Apr;177(1):137-46
Atividade Antioxidante do DHEA
1.
Iwasaki Y, Asai M, Yoshida M, Nigawara T, Kambayashi M, Nakashima N.
Dehydroepiandrosterone-sulfate inhibits nuclear factor-kappaB-dependent
transcription in hepatocytes, possibly through antioxidant effect. J Clin
Endocrinol Metab. 2004 Jul;89(7):3449-54
2.
3.
4.
Bekesi G, Kakucs R, Varbiro S, Racz K, Sprintz D, Feher J, Szekacs B. In vitro
effects of different steroid hormones on superoxide anion production of
human neutrophil granulocytes. Steroids. 2000 Dec;65(12):889-94
Bednarek-Tupikowska G, Gosk I, Szuba A, Bohdanowicz-Pawlak A, Kosowska
B, Bidzinska B, Milewicz A. Influence of dehydroepiandrosterone on platelet
aggregation, superoxide dismutase activity and serum lipid peroxide
concentrations in rabbits with induced hypercholesterolemia. Med Sci
Monit. 2000;6(1):40-5
Brignardello E, Runzo C, Aragno M, Catalano MG, Cassader M, Perin PC,
Boccuzzi G. Dehydroepiandrosterone administration counteracts oxidative
imbalance and advanced glycation end product formation in type 2 diabetic
patients. Diabetes Care. 2007 Nov;30(11):2922-7
Atividade Antioxidante do Estradiol
1.
2.
3.
4.
5.
6.
7.
Bokov AF, Ko D, Richardson A. The effect of gonadectomy and estradiol on
sensitivity to oxidative stress. Endocr Res. 2009;34(1-2):43-58
Tasset I, Peña J, Jimena I, Feijóo M, Del Carmen Muñoz M, Montilla P, Túnez
I. Effect of 17beta-estradiol on olfactory bulbectomy-induced oxidative stress
and behavioral changes in rats. Neuropsychiatr Dis Treat. 2008 Apr;4(2):441-9
Sugishita K, Li F, Su Z, Barry WH. Anti-oxidant effects of estrogen reduce
[Ca2+]i during metabolic inhibition. J Mol Cell Cardiol. 2003 Mar;35(3):331-6
Han HJ, Park SH, Park HJ, Lee JH, Lee BC, Hwang WS. Effects of sex
hormones on Na+/glucose cotransporter of renal proximal tubular cells
following oxidant injury. Kidney Blood Press Res. 2001;24(3):159-65
Barp J, Araujo AS, Fernandes TR, Rigatto KV, Llesuy S, Bello-Klein A, Singal
P. Myocardial antioxidant and oxidative stress changes due to sex hormones.
Braz J Med Biol Res. 2002 Sep;35(9):1075-81
Azevedo RB, Lacava ZG, Miyasaka CK, Chaves SB, Curi R. Regulation of
antioxidant enzyme activities in male and female rat macrophages by sex
steroids. Braz J Med Biol Res. 2001 May;34(5):683-7
Massafra C, Gioia D, De Felice C, Picciolini E, De Leo V, M Bonifazi, Bernabei
A. Effects of estrogens and androgens on erythrocyte antioxidant superoxide
dismutase, catalase and glutathione peroxidase activities during the menstrual
cycle. J Endocrinol. 2000 Dec;167(3):447-52
Atividade Antioxidante da Progesterona
1.
Ozacmak VH, Sayan H. The effects of 17beta estradiol, 17alpha estradiol and
progesterone on oxidative stress biomarkers in ovariectomized female rat
brain subjected to global cerebral ischemia. Physiol Res. 2009;58(6):909-12
Atividade Antioxidante da Testosterona
1.
2.
Tam NN, Ghatak S, Ho SM. Sex hormone-induced alterations in the activities of
antioxidant enzymes and lipid peroxidation status in the prostate of Noble
rats. Prostate. 2003 Apr 1;55(1):1-8
102. Ahlbom E, Prins GS, Ceccatelli S. Testosterone protects cerebellar
granule cells from oxidative stress-induced cell death through a receptor
mediated mechanism. Brain Res. 2001 Feb 23;892(2):255-62
3.
4.
5.
6.
7.
8.
9.
Tam NN, Ghatak S, Ho SM. Sex hormone-induced alterations in the activities of
antioxidant enzymes and lipid peroxidation status in the prostate of Noble
rats. Prostate. 2003 Apr 1;55(1):1-8
Ahlbom E, Prins GS, Ceccatelli S. Testosterone protects cerebellar granule
cells from oxidative stress-induced cell death through a receptor mediated
mechanism. Brain Res. 2001 Feb 23;892(2):255-62
Klinger W, Lupp A, Karge E, Baumbach H, Eichhorn F, Feix A, Fuldner F,
Gernhardt S, Knels L, Kost B, Mertens G, Werner F, Oettel M, Romer W,
Schwarz S, Elger W, Schneider B. Estradiol, testosterone,
dehydroepiandrosterone and androstenedione: novel derivatives and
enantiomers. Interactions with rat liver microsomal cytochrome P450 and
antioxidant/radical scavenger activities in vitro. Toxicol Lett. 2002 Mar
10;128(1-3):129-44
Juliet PA, Hayashi T, Daigo S, Matsui-Hirai H, Miyazaki A, Fukatsu A, Funami
J, Iguchi A, Ignarro LJ. Combined effect of testosterone and apocynin on
nitric oxide and superoxide production in PMA-differentiated THP-1 cells.
Biochim Biophys Acta. 2004 Sep 17;1693(3):185-91
Tam NN, Gao Y, Leung YK, Ho SM. Androgenic regulation of oxidative stress
in the rat prostate: involvement of NAD(P)H oxidases and antioxidant
defense machinery during prostatic involution and regrowth. Am J Pathol.
2003 Dec;163(6):2513-22
Lee MN, Lee SH, Lee MY, Kim YH, Park JH, Ryu JM, Yun SP, Lee YJ, Kim
MO, Park K, Han HJ. Effect of dihydrotestosterone on mouse embryonic
stem cells exposed to H2O2-induced oxidative stress. J Vet Sci. 2008
Sep;9(3):247-56
Celec P, Jani P, Smrekova L, Mrlian A, Kudela M, Hodosy J, Boor P, Kristova
V, Jakubovsky J, Jezova D, Halcak L, Bozek P, Slamova J, Ulicna O, Hojsik
D, Jurkovicova I. Effects of anabolic steroids and antioxidant vitamins on
ethanol-induced tissue injury. Life Sci. 2003 Dec 12;74(4):419-34
2- OTIMIZAÇÃO DA IMUNIDADE MEDIADA PELA
MODULAÇÃO HORMONAL
Atividade Imunomoduladora da Melatonina
1.
2.
3.
4.
5.
Maestroni GJ. Therapeutic potential of melatonin in immunodeficiency states,
viral diseases, and cancer. Adv Exp Med Biol 1999;467:217-26
Reiter RJ, Calvo JR, Karbownik M, Qi W, Tan DX. Melatonin and its relation to
the immune system and inflammation. Ann N Y Acad Sci. 2000;917:376-86.
Akbulut KG, Gonul B, Akbulut H. The effects of melatonin on humoral immune
responses of young and aged rats. Immunol Invest. 2001 Feb;30(1):17-20
Knoferl MW, Jarrar D, Angele MK, Ayala A, Schwacha MG, Bland KI, Chaudry
IH. Echinacea purpurea and melatonin augment natural-killer cells in
leukemic mice and prolong life span. Exp Gerontol. 2001 Feb;36(2):311-26.
Maestroni GJ. The immunotherapeutic potential of melatonin. Expert Opin
Investig Drugs. 2001 Mar;10(3):467-76
Baixos Níveis de Hormônios Tireoidianos Associados Com Imunodeficiência
1.
2.
3.
4.
Kmiec Z, Mysliwska J, Rachon D, Kotlarz G, Sworczak K, Mysliwski A. Natural
killer activity and thyroid hormone levels in young and elderly persons.
Gerontology. 2001 Sep-Oct;47(5):282-8
Mariani E, Ravaglia G, Forti P, Meneghetti A, Tarozzi A, Maioli F, Boschi F,
Pratelli L, Pizzoferrato A, Piras F, Facchini A. Vitamin D, thyroid hormones
and muscle mass influence natural killer (NK) innate immunity in healthy
nonagenarians and centenarians. Clin Exp Immunol. 1999 Apr;116(1):19-27
Basso A, Piantanelli L, Rossolini G, Piloni S, Vitali C, Masera N. Role of
triiodothyronine in down-regulation and recovery of lymphocyte betaadrenoceptors in thyroidectomized patients. J Clin Endocrinol Metab. 1991
Dec;73(6):1340-4
Chow CC, Mak TW, Chan CH, Cckram CS. Euthyroid sick syndrome in
pulmonary tuberculosis before and after treatment. Ann Clin Biochem. 1995
Jul; 32 (Pt 4): 385-91
Reposição Com os Hormônios Tireoidianos Estimula a Imunidade
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Padberg S, Heller K, Usadel KH, Schumm-Draeger PM. One-year prophylactic
treatment of euthyroid Hashimoto's thyroiditis patients with levothyroxine: is
there a benefit? Thyroid. 2001 Mar;11(3):249-55
Aksoy DY, Kerimoglu U, Okur H, Canpinar H, Karaagaoglu E, Yetgin S, Kansu
E, Gedik O. Effects of prophylactic thyroid hormone replacement in
euthyroid Hashimoto's thyroiditis. Endocr J. 2005 Jun;52(3):337-43
Bloehr H, Bregengaard C, Povlsen JV. Triiodothyronine stimulates growth of
peripheral blood mononuclear cells in serum-free cultures in uremic
patients. Am J Nephrol. 1992;12(3):148-54
Paavonen T. Enhancement of human B lymphocyte differentiation in vitro by
thyroid hormone. Scand J Immunol. 1982 Feb;15(2):211-5
Botella-Carretero JI, Prados A, Manzano L, Montero MT, Escribano L, Sancho
J, Escobar-Morreale HF. The effects of thyroid hormones on circulating
markers of cell-mediated immune response, as studied in patients with
differentiated thyroid carcinoma before and during thyroxine withdrawal. Eur
J Endocrinol. 2005 Aug;153(2):223-30
Balazs C, Leovey A, Szabo M, Bako G. Stimulating effect of triiodothyronine on
cell-mediated immunity. Eur J Clin Pharmacol. 1980 Jan;17(1):19-23
Fabris N, Mocchegiani E, Mariotti S, Pacini F, Pinchera A. Thyroid function
modulates thymic endocrine activity. J Clin Endocrinol Metab. 1986
Mar;62(3):474-8
Dorshkind K, Horseman ND. The roles of prolactin, growth hormone, insulin-like
growth factor-I, and thyroid hormones in lymphocyte development and
function: insights from genetic models of hormone and hormone receptor
deficiency. Endocr Rev. 2000 Jun;21(3):292-312
Kvetny J, Matzen LE. Thyroid hormone induced oxygen consumption and
glucose-uptake in human mononuclear cells. Thyroidology. 1989
Apr;1(1):5-9
McCormack PD, Thomas J, Malik M, Staschen CM. Cold stress, reverse T3
and lymphocyte function. Alaska Med. 1998 Jul-Sep;40(3):55-62
Atividade Imunomoduladora do Hormônio do Crescimento
1.
Chu YW, Schmitz S, Choudhury B, Telford W, Kapoor V, Garfield S, Howe
D, Gress RE. Exogenous insulin-like growth factor 1 enhances
thymopoiesis predominantly through thymic epithelial cell expansion. Blood.
2008 Oct 1;112(7):2836-46
2.
3.
4.
5.
Heemskerk VH, Daemen MA, Buurman WA. Insulin-like growth factor-1
(IGF-1) and growth hormone (GH) in immunity and inflammation. Cytokine
Growth Factor Rev. 1999 Mar;10(1):5-14
Chapes SK, Simske SJ, Forsman AD, Bateman TA, Zimmerman RJ.
Effects of space flight and IGF-1 on immune function. Adv Space Res.
1999;23(12):1955-64
Savino W, de Mello-Coelho V, Dardenne M. Control of the thymic
microenvironment by growth hormone/insulin-like growth factor-I-mediated
circuits. Neuroimmunomodulation. 1995 Nov-Dec;2(6):313-8
Kudsk KA, Mowatt-Larssen C, Bukar J, Fabian T, Oellerich S, Dent DL,
Brown R. Effect of recombinant human insulin-like growth factor I and early
total parenteral nutrition on immune depression following severe head
injury. Arch Surg. 1994 Jan;129(1):66-70
Deficiência Imunológica Está Associada a Baixos Níveis de DHEA
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Martínez-Taboada V, Bartolomé MJ, Amado JA, Blanco R, García-Unzueta MT,
Rodríguez-Valverde V, López-Hoyos M. Changes in peripheral blood
lymphocyte subsets in elderly subjects are associated with an impaired
function of the hypothalamic-pituitary-adrenal axis. Mech Ageing Dev. 2002
Sep;123(11):1477-86
Doldi N, Belvisi L, Bassan M, Fusi FM, Ferrari A. Premature ovarian failure:
steroid synthesis and autoimmunity. Gynecol Endocrinol 1998;12(1):23-8
de la Torre B, von Krogh G, Svensson M, Holmberg V. Blood cortisol and
dehydroepiandrosterone sulphate (DHEAS) levels and CD4 T cell counts in
HIV infection. Clin Exp Rheumatol 1997;15(1):87-90
Fulop T Jr, Wagner JR, Khalil A, Weber J, Trottier L, Payette H. Relationship
between the response to influenza vaccination and the nutritional status in
institutionalized elderly subjects. J Gerontol A Biol Sci Med Sci
1999;54(2):M59-64
Christeff N, Nunez EA, Gougeon ML. Changes in cortisol/DHEA ratio in HIVinfected men are related to immunological and metabolic perturbations
leading to malnutrition and lipodystrophy. Ann NY Acad Sci 2000;917:96270
Jacobson MA, Fusaro RE, Galmarini M, Lang W. Decreased serum DHEA is
associated with an increased progression of human immunodeficiency virus
infection in men with CD4 cell counts of 200-499. J Infect Dis.
1991,164:864-8
Ferrando SJ, Rabkin JG, Poretsky L. Dehydroepiandrosterone sulfate (DHEAS)
and testosterone: relation to HIV illness stage and progression over one
year. J Acquir Immune Defic Syndr. 1999;22(2):146-54
Grinspoon S, Corcoran C, Miller K, Biller BM, Askari H, Wang E, Hubbard J,
Anderson EJ, Basgoz N, Heller HM, Klibanski A. Body composition and
endocrine function in women with acquired immunodeficiency syndrome
wasting. J Clin Endocrinol Metab. 1997;82(5):1332-7
Christeff N, Gherbi N, Mammes O, Dalle MT, Gharakhanian S, Lortholary O,
Melchior JC, Nunez EA. Serum cortisol and DHEA concentrations during
HIV infection. Psychoneuroendocrinology. 1997;22 Suppl 1:S11-8
Laudat A, Blum L, Guechot J, Picard O, Cabane J, Imbert JC, Giboudeau J.
Changes in systemic gonadal and adrenal steroids in asymptomatic human
immunodeficiency virus-infected men: relationship with the CD4 cell counts.
Eur J Endocrinol 1995;133(4):418-24
Centurelli MA, Abate MA. The role of dehydroepiandrosterone in AIDS. Ann
Pharmacother 1997;31(5):639-42
12.
13.
14.
Rook GA, Hernandez-Pando R. Pathogenetic role, in human and murine
tuberculosis, of changes in the peripheral metabolism of glucocorticoids and
antiglucocorticoids. Psychoneuroendocrinology. 1997;22 Suppl 1:S109-13
Mavoungou D, Lansoud-Soukate J, Dupont A. Steroid and gonadotropin
hormone levels in young African women with filarial infection. J Steroid
Biochem 1989;34(1-6):577-80
Parker CR Jr, Wendel GD. The effects of syphilis on endocrine function of the
fetoplacental unit. Am J Obstet Gynecol. 1988;159(6):1327-31
Deficiência Imunológica: A Melhora Com Reposição de DHEA
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Khorram O, Vu L, Yen SS. Activation of immune function by
dehydroepiandrosterone (DHEA) in age-advanced men. J Gerontol A Biol
Sci Med Sci. 1997;52(1):M1-7
Araneo B, Dowell T, Woods ML, Daynes R, Judd M, Evans T. DHEAS as an
effective vaccine adjuvant in elderly humans. Proof-of-principle studies. Ann
N Y Acad Sci. 1995;774:232-48
Degelau J, Guay D, Hallgren H. The effect of DHEAS on influenza vaccination
in aging adults. J Am Geriatr Soc. 1997;45(6):747-51
Solerte SB, Fioravanti M, Schifino N, Cuzzoni G, Fontana I, Vignati G, Govoni
S, Ferrari E. Dehydroepiandrosterone sulfate decreases the interleukin-2mediated overactivity of the natural killer cell compartment in senile
dementia of the Alzheimer type. Dement Geriatr Cogn Disord.
1999;10(1):21-7
Solerte SB, Fioranti M, Vignati G, Giustina A, Cravello L, Ferrari E,.
Dehydroepiandrosterone sulfate enhances natural killer cell cytotoxitcity in
humans via locally generated immunoractive insulin-like growth factor I. J
Clin Endocrinol Metab. 1999; 84 (9): 3260-7
Okabe T, Haji M, Takayanagi R, Adachi M, Imasaki K, Kurimoto F, Watanabe
T, Nawata H.Up-regulation of high-affinity dehydroepiandrosterone binding
activity by dehydroepiandrosterone in activated human T lymphocytes. J
Clin Endocrinol Metab. 1995;80(10):2993-6
Henderson E, Schwartz A, Pashko L, Abou-Gharbia M, Swern D.,
Dehydroepiandrosterone and 16 alpha-bromo-epiandrosterone: inhibitors of
Epstein-Barr virus-induced transformation of human lymphocytes.
Carcinogenesis. 1981;2(7):683-6
Diallo K, Loemba H, Oliveira M, Mavoungou DD, Wainberg MA. Inhibition of
human immunodeficiency virus type-1 (HIV-1) replication by immunor
(IM28), a new analog of dehydroepiandrosterone. Nucleosides Nucleotides
Nucleic Acids. 2000;19(10-12):2019-24
Yang JY, Schwartz A, Henderson EE. Inhibition of 3'azido-3' deoxythymidineresistant HIV-1 infection by DHEA in vitro. Biochem Biophys Res Commun.
1994 Jun 30;201(3):1424-32
Yang JY, Schwartz A, Henderson EE. Inhibition of HIV-1 latency reactivation by
dehydroepiandrosterone (DHEA) and an analog of DHEA. AIDS Res Hum
Retroviruses. 1993;9(8):747-54
Weksler ME. Immune senescence and adrenal steroids: immune dysregulation
and the action of dehydroepiandrosterone (DHEA) in old animals. Eur J Clin
Pharmacol 1993;45 Suppl 1:S21-3
Daynes RA, Dudley DJ, Araneo BA.Regulation of murine lymphokine
production in vivo. II. Dehydroepiandrosterone is a natural enhancer of
interleukin 2 synthesis by helper T cells. Eur J Immunol 1990;20(4):793-802
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
Yan CH, Jiang XF, Pei X, Dai YR. The in vitro antiapoptotic effect of
dehydroepiandrosterone sulfate in mouse thymocytes and its relation to
caspase-3/caspase-6., Cell Mol Life Sci 1999;56(5-6):543-7
Riley V, Fitzmaurice MA. DHEA and thymus integrity in the mouse. In: The
biological role of DHEA, edited by Regelson W, Kalimi M, De GruyterBerlin, 1990: 131-155
Loria RM, Inge TH, Cook SS, Szakal AK, Regelson W. Protection against acute
lethal viral infections with the native steroid dehydroepiandrosterone
(DHEA). J Med Virol 1988;26(3):301-14
Lucas JA, Ahmed SA, Casey ML, MacDonald PC. Prevention of autoantibody
formation and prolonged survival in New Zealand black/New Zealand white
F1 mice fed dehydroisoandrosterone. J Clin Invest. 1985;75(6):2091-3
Ben-Nathan D, Lustig S, Kobiler D, Danenberg HD, Lupu E, Feuerstein G.
Dehydroepiandrosterone protects mice inoculated with West Nile virus and
exposed to cold stress. J Med Virol. 1992;38(3):159-66
Ben-Nathan D, Lachmi B, Lustig S, Feuerstein G. Protection by
dehydroepiandrosterone in mice infected with viral encephalitis. Arch Virol.
1991;120(3-4):263-71
Padgett DA, Loria RM. In vitro potentiation of lymphocyte activation by DHEA,
androstenediol and androstenetriol. J Immunol. 1994, 1544-52
Carr DJ. Increased levels of IFN-gamma in the trigeminal ganglion correlate
with protection against HSV-1-induced encephalitis following subcutaneous
administration with androstenediol. J Neuroimmunol. 1998;89(1-2):160-7
Daigle J, Carr DJ. Androstenediol antagonizes herpes simplex virus type 1induced encephalitis through the augmentation of type I IFN production. J
Immunol. 1998;160(6):3060-6
Garg M, Bondada S. ReversaI of age-associated decline in immune response
to Pnu-imune vaccine by supplementation with the steroid hormone DHEA.
Infect Immun. 1993 May;61(5):2238-41
Kim HR, Ryu SY, Kim HS, Choi BM, Lee EJ, Kim HM, Chung HT.
Administration of DHEA reverses the immune suppression induced by high
dose antigen in mice. Immunol Invest. 1995;24(4):583-93
Danenberg HD, Ben-Yehuda A, Zakay-Rones Z, Friedman G.
Dehydroepiandrosterone (DHEA) treatment reverses the impaired immune
response of old mice to influenza vaccination and protects from influenza
infection. Vaccine 1995;13(15):1445-8
Loria RM, Padgett DA, Huynh PN. Regulation of the immune response by
dehydroepiandrosterone and its metabolites. J Endocrinol. 1996;150
Suppl:S209-20
Bradley WG, Kraus LA, Good RA, Day NK. Dehydroepiandrosterone inhibits
replication of feline immunodeficiency virus in chronically infected cells. Vet
Immunol Immunopathol. 1995;46(1-2):159-68
Zhang Z, Araghi-Niknam M, Liang B, Inserra P, Ardestani SK, Jiang S, Chow S,
Watson RR. Prevention of immune dysfunction and vitamin E loss by
dehydroepiandrosterone and melatonin supplementation during murine
retrovirus infection. Immunology. 1999;96(2):291-7
Lee J, Sepulveda RT, Jiang S, Zhang Z, Inserra P, Zhang Y, Hosseini S,
Watson RR. Immune dysfunction during alcohol consumption and murine
AIDS: the protective role of dehydroepiandrosterone sulfate. Alcohol Clin
Exp Res. 1999;23(5):856-62
Gianotti L, Alexander JW, Fukushima R, Pyles T. Steroid therapy can modulate
gut barrier function, host defense, and survival in thermally injured mice. J
Surg Res. 1996;62(1):53-8
30.
31.
32.
33.
34.
35.
36.
37.
Ben-Nathan
D,
Padgett
DA,
Loria
RM.
Androstenediol
and
dehydroepiandrosterone protect mice against lethal bacterial infections and
lipopolysaccharide toxicity. J Med Microbiol. 1999;48(5):425-31
Oberbeck R, Dahlweid M, Koch R, van Griensven M, Emmendorfer A,
Tscherne H, Pape HC. Dehydroepiandrosterone decreases mortality rate
and improves cellular immune function during polymicrobial sepsis. Crit
Care Med. 2001;29(2):380-4
Hernandez-Pando R, De La Luz Streber M, Orozco H, Arriaga K, Pavon L, AlNakhli SA, Rook GA. The effects of androstenediol and
dehydroepiandrosterone on the course and cytokine profile of tuberculosis
in BALB/c mice. Immunology. 1998;95(2):234-41
Rasmussen KR, Healey MC, Cheng L, Yang S. Effects of
dehydroepiandrosterone in immunosuppressed adult mice infected with
Cryptosporidium parvum. J Parasitol. 1995;81(3):429-33
Yang BC, Liu CW, Chen YC, Yu CK. Exogenous dehydroepiandrosterone
modified the expression of T helper-related cytokines in NZB/NZW F1 mice.
Immunol Invest. 1998;27(4-5):291-302
Norton SD, Harrison LL, Yowell R, Araneo BA.- Administration of
dehydroepiandrosterone sulfate retards onset but not progression of
autoimmune disease in NZB/W mice. Autoimmunity. 1997;26(3):161-71
Araneo B, Daynes R. Dehydroepiandrosterone functions as more than an
antiglucocorticoid in preserving immunocompetence after thermal injury.
Endocrinology. 1995;136(2):393-401
Casson PR, Faquin LC, Stentz FB, Straughn AB, Andersen RN, Abraham
GE, Buster JE. Replacement of dehydroepiandrosterone enhances Tlymphocyte insulin binding in postmenopausal women. Fertil Steril. 1995
May;63(5):1027-31
Atividade Imunomoduladora do Estradiol
1.
2.
3.
4.
Eriksen BC, Hunskar S. Urogenital estrogen deficiency syndrome. Investigation
and treatment with special reference to hormone substitution. Tidsskr Nor
Laegeforen. 1991 Oct 10;111(24):2949-5
Merkel SM, Alexander S, Zufall E, Oliver JD, Huet-Hudson YM. Essential role
for estrogen in protection against Vibrio vulnificus-induced endotoxic shock.
Infect Immun. 2001 Oct;69(10):6119-22
de Ruiz CS, Rey MR, de Ruiz Holgado AP, Nader-Macias ME. Experimental
administration of estradiol on the colonization of lactobacillus fermentum
and escherichia coli in the urogenital tract of mice. Biol Pharm Bull. 2001
Feb;24(2):127-34
Eriksen B. A randomized, open, parallel-group study on the preventive effect of
an estradiol-releasing vaginal ring (Estring) on recurrent urinary tract
infections in postmenopausal women. Am J Obstet Gynecol. 1999
May;180(5):1072-9
Atividade Imunomoduladora da Progesterona
1.
Vassiliadou N, Tucker L, Anderson DJ. Progesterone-induced inhibition of
chemokine receptor expression on peripheral blood mononuclear cells
correlates with reduced HIV-1 infectability in vitro. J Immunol. 1999 Jun
15;162(12):7510-8
3- OTIMIZAÇÃO DO BEM
QUALIDADE DE VIDA
MODULAÇÃO HORMONAL
ESTAR FÍSICO E
MEDIADOS PELA
Baixa Qualidade de Vida e Fadiga: Correlação Com Baixos Níveis de
Melatonina
1- Sterzl I, Fucikova T, Hrda P, Matucha P, Zamrazil V. The fatigue syndrome in
autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitr
Lek. 1998 Aug;44(8):456-60
2- Wikner J, Hirsch U, Wetterberg L, Rojdmark S. Fibromyalgia--a syndrome
associated with decreased nocturnal melatonin secretion. Clin Endocrinol
(Oxf). 1998 Aug;49(2):179-83
3- Fiorina P, Lattuada G, Silvestrini C, Ponari O, Dall'Aglio P. Disruption of
nocturnal melatonin rhythm and immunological involvement in ischaemic
stroke patients. Scand J Immunol. 1999 Aug;50(2):228-31
4- Muller HL, Handwerker G, Wollny B, Faldum A, Sorensen N. Melatonin
secretion and increased daytime sleepiness in childhood craniopharyngioma
patients. J Clin Endocrinol Metab. 2002 Aug;87(8):3993-6
Baixa Qualidade de Vida e Fadiga: Melhora Com Reposição de Melatonina
1. Luthringer R, Muzet M, Zisapel N, Staner L. The effect of prolongedrelease melatonin on sleep measures and psychomotor performance in
elderly patients with insomnia. Int Clin Psychopharmacol. 2009
Sep;24(5):239-49
2. Zisapel N. [Controlled release melatonin (Circadin) in the treatment of
insomnia in older patients: efficacy and safety in patients with history of
use and non-use of hypnotic drugs] Harefuah. 2009 May;148(5):337-41,
348
3. Wade AG, Ford I, Crawford G, McMahon AD, Nir T, Laudon M, Zisapel N.
Efficacy of prolonged relase melatonin in insomnia patients aged 55-80
years: quality of sleep and next-day alertness outcomes. Curr Med Res
Opin. 2007 Oct;23(10):2597-605
4. van Heukelom RO, Prins JB, Smits MG, Bleijenberg G. Influence of
melatonin on fatigue severity in patients with chronic fatigue syndrome
and late melatonin secretion. Eur J Neurol. 2006 Jan;13(1):55-60
5. Nagtegaal JE, Laurant MW, Kerkhof GA, Smits MG, van der Meer YG,
Coenen AM. Effects of melatonin on the quality of life in patients with
delayed sleep phase syndrome. J Psychosom Res. 2000 Jan;48(1):45-50
6. Dalton EJ, Rotondi D, Levitan RD, Kennedy SH, Brown GM. Use of slowrelease melatonin in treatment-resistant depression. J Psychiatry
Neurosci. 2000 Jan;25(1):48-52
7. Kayumov L, Brown G, Jindal R, Buttoo K, Shapiro CM. A randomzed,
double-blind, placebo-controlled crossover study of the effect of
exogenous melatonin on delayed sleep phase syndrome. Psychosom
Med. 2001 Jan-Feb;63(1):40-8
8. Siegrist C, Benedetti C, Orlando A, Beltran JM, Tuchscherr L, Noseda
CM, Brusco LI, Cardinali DP.Lack of changes in serum prolactin, FSH,
TSH, and estradiol after melatonin treatment in doses that improve sleep
and reduce benzodiazepine consumption in sleep-disturbed, middle-aged,
and elderly patients. J Pineal Res. 2001 Jan;30(1):34-42
9. Paul MA, Brown G, Buguet A, Gray G, Pigeau RA, Weinberg H, Radomski
M. Melatonin and zopiclone as pharmacologic aids to facilitate crew rest.
Aviat Space Environ Med. 2001 Nov;72(11):974-84
10. Lissoni P, Barni S, Crispino S, Tancini G, Fraschini F. Endocrine and
immune effects of melatonin therapy in metastatic cancer patients. Eur J
Cancer Clin Oncol. 1989 May;25(5):789-95
11. Lissoni P, Barni S, Tancini G, Crispino S, Paolorossi F, Lucini V, Mariani
M, Cattaneo G, Esposti D, Esposti G, et al.Clinical study of melatonin in
untreatable advanced cancer patients. Tumori. 1987 Oct 31;73(5):475-80
12. Lissoni P, Barni S, Cattaneo G, Tancini G, Esposti G, Esposti D, Fraschini
F. Clinical results with the pineal hormone melatonin in advanced cancer
resistant to standard antitumor therapies. Oncology. 1991;48(6):448-50
13. Barni S, Lissoni P, Paolorossi F, Crispino S, Archili C, Tancini G. A study
of the pineal hormone melatonin as a second line therapy in metastatic
colorectal cancer resistant to fluorouracil plus folates. Tumori. 1990 Feb
28;76(1):58-60
14. Lissoni P, Barni S, Ardizzoia A, Tancini G, Conti A, Maestroni G. A
randomized study with the pineal hormone melatonin versus supportive
care alone in patients with brain metastases due to solid neoplasms.
Cancer. 1994 Feb 1;73(3):699-701
15. Nagtegaal JE, Kerkhof GA, Smits MG, Swart AC, Van Der Meer YG.
Delayed sleep phase syndrome: A placebo-controlled cross-over study on
the effects of melatonin administered five hours before the individual dim
light melatonin onset. J Sleep Res. 1998 Jun;7(2):135-43
16. Yang CM, Spielman AJ, D'Ambrosio P, Serizawa S, Nunes J, Birnbaum J.
A single dose of melatonin prevents the phase delay associated with a
delayed weekend sleep pattern. Sleep. 2001 May 1;24(3):272-81
17. Petrie K, Dawson AG, Thompson L, Brook R. A double-blind trial of
melatonin as a treatment for jet lag in international cabin crew. Biol
Psychiatry. 1993 Apr 1;33(7):526-30
18. Suhner A, Schlagenhauf P, Johnson R, Tschopp A, Steffen R.
Comparative study to determine the optimal melatonin dosage form for
the alleviation of jet lag. Chronobiol Int. 1998 Nov;15(6):655-66
19. Brackowski R, Zubelewicz B, Romanowski W, Lissoni P, Barni S, Tancini
G, Maestroni GJ.Preliminary study on modulation of the biological effects
of tumor necrosis factor-alpha in advanced cancer patients by the pineal
hormone melatonin. J Biol Regul Homeost Agents. 1994 Jul-Sep;8(3):7780
20. Lissoni P, Barni S, Mandala M, Ardizzoia A, Paolorossi F, Vaghi M,
Longarini R, Malugani F, Tancini G. Decreased toxicity and increased
efficacy of cancer chemotherapy using the pineal hormone melatonin in
metastatic solid tumour patients with poor clinical status. Eur J Cancer.
1999 Nov;35(12):1688-92
21. Lissoni P, Tancini G, Barni S, Paolorossi F, Ardizzoia A, Conti A,
Maestroni G. Treatment of cancer chemotherapy-induced toxicity with the
pineal hormone melatonin. Support Care Cancer. 1997 Mar;5(2):126-9
Baixa Qualidade de Vida, Baixa Performance e Fadiga: Correlação Com Baixos
Níveis dos Hormônios Tireodianos
1. Okamoto I, Munakata M, Miyazaki M, Satoh T, Takahata T, Takamatsu Y,
Muto O, Koike K, Ishitani K, Mukaiyama T, Sakata Y, Nakagawa K, Tamura
K. Disturbance of the growth hormone-insulin-like growth factor-1 axis
2.
3.
4.
5.
6.
7.
8.
9.
associated with poor performance status in patients with solid tumors. Jpn J
Clin Oncol. 2010 Mar;40(3):222-6
Tagay S, Herpertz S, Langkafel M, Erim Y, Freudenberg L, Schöpper N,
Bockisch A, Senf W, Görges R. Health-related quality of life, anxiety and
depression in thyroid cancer patients under short-term hypothyroidism and
TSH-suppressive levothyroxine treatment. Eur J Endocrinol. 2005
Dec;153(6):755-63
Leclère J, Cousty C, Schlienger JL, Wémeau JL. Subclinical hypothyroidism
and quality of life of women aged 50 or more with hypercholesterolemia:
results of the HYOGA study. Presse Med. 2008 Nov;37(11):1538-46
van der Sluijs Veer L, Kempers MJ, Last BF, Vulsma T, Grootenhuis MA.
Quality of life, developmental milestones, and self-esteem of young adults
with congenital hypothyroidism diagnosed by neonatal screening. J Clin
Endocrinol Metab. 2008 Jul;93(7):2654-61
Kong WM, Sheikh MH, Lumb PJ, Naoumova RP, Freedman DB, Crook M,
Dore CJ, Finer N, Naoumova P. A 6-month randomized trial of thyroxine
treatment in women with mild subclinical hypothyroidism. Am J Med. 2002
Apr 1;112(5):348-54
Guimaraes V, DeGroot LJ. Moderate hypothyroidism in preparation for whole
body 131I scintiscans and thyroglobulin testing. Thyroid. 1996 Apr;6(2):69-73
Heitman B, Irizarry A. Hypothyroidism: common complaints, perplexing
diagnosis. Nurse Pract. 1995 Mar;20(3):54-60
Doucet J, Trivalle C, Chassagne P, Perol MB, Vuillermet P, Manchon ND,
Menard,JF, Bercoff E. Does age play a role in clinical presentation of
hypothyroidism? J Am Geriatr Soc. 1994 Sep;42(9):984-6
De Lorenzo F, Xiao H, Mukherjee M, Harcup J, Suleiman S, Kadziola Z,
Kakkar VV. Chronic fatigue syndrome: physical and cardiovascular
deconditioning. QJM. 1998 Jul;91(7):475-81
Baixa Qualidade de Vida, Baixa Performance e Fadiga: A Melhora Com a
Reposição dos Hormônios Tideoidianos
1. Mainenti MR, Vigário PS, Teixeira PF, Maia MD, Oliveira FP, Vaisman M.
Effect of levothyroxine replacement on exercise performance in subclinical
hypothyroidism. J Endocrinol Invest. 2009 May;32(5):470-3
2. Razvi S, Ingoe L, Keeka G, Oates C, McMillan C, Weaver JU. The beneficial
effect of L-thyroxine on cardiovascular risk factors, endothelial function, and
quality of life in subclinical hypothyroidism: randomized, crossover trial. J Clin
Endocrinol Metab. 2007 May;92(5):1715-23
3. Dzurec LC. Experiences of fatigue and depression before and after low-dose
L-thyroxine supplementation in essentially euthyroid individuals. Res Nurs
Health. 1997 Oct;20(5):389-98
4. Bunevicius R, Kazanavicius G, Zalinkevicius R, Prange AJ Jr. Effects of
thyroxine as compared with thyroxine plus triiodothyronine in patients with
hypothyroidism. N Engl J Med. 1999 Feb 11;340(6):424-9
5. Hertoghe T, Lo Cascio A., Hertoghe J. Considerable improvement of
hypothyroid symptoms with two combined T3-T4 medication in patients still
symptomatic with thyroxine treatment alone. Anti-Aging Medicine, Ed.
German Society of Anti-Aging Medicine-Verlag 2003- 2004; 32-43
6. Hashizume K. Supplement with target hormone in aged patients with
endocrine dysfunction: thyroid hormone replacement therapy. Nippon Ronen
Igakkai Zasshi. 2000 Nov;37(11):870-2.
7. Surkov SI, Naarov AN, Kotova GA, Artemova AM. The efficacy of
replacement therapy with L-thyroxine in manifest and latent forms of
hypothyroidism. Probl Endokrinol (Mosk). 1990 Sep-Oct;36(5):14-8.
Baixa Qualidade de Vida, Baixa Performance e Fadiga: Correlação Com Baixos
Níveis do Hormônios do Crescimento
1. Molon G, Adamo E, De Ferrari GM, Accardi F, Dalla Vecchia E, Sallusti L,
Ciaffoni S, Barbieri E. Effects of cardiac resynchronization therapy on insulinlike growth factor-1 in patients with advanced heart failure. J Cardiovasc Med
(Hagerstown). 2007 Nov;8(11):917-22
2. Lasaite L, Bunevicius R, Lasiene D, Lasas L. Psychological functioning after
growth hormone therapy in adult growth hormone deficient patients:
endocrine and body composition correlates. Medicina (Kaunas).
2004;40(8):740-4
3. Stouthart PJ, Deijen JB, Roffel M, Delemarre-van de Waal HA. Quality of life
of growth hormone (GH) deficient young adults during discontinuation and
restart of GH therapy. Psychoneuroendocrinology. 2003 Jul;28(5):612-26
Baixa Qualidade de Vida, Baixa Performance e Fadiga: A Melhora Com a
Reposição do Hormônio do Crescimento
1. Okamoto I, Munakata M, Miyazaki M, Satoh T, Takahata T, Takamatsu Y,
Muto O, Koike K, Ishitani K, Mukaiyama T, Sakata Y, Nakagawa K, Tamura
K. Disturbance of the Growth Hormone-Insulin-like Growth Factor-1 Axis
Associated with Poor Performance Status in Patients with Solid Tumors. Jpn
J Clin Oncol. 2010 Mar;40(3):222-6.
Baixa Qualidade de Vida, Baixa Performance e Fadiga: Correlação Com Baixos
Níveis de DHEA
2. Morgan CA 3rd, Rasmusson A, Pietrzak RH, Coric V, Southwick SM.
Relationships
among
plasma
dehydroepiandrosterone
and
dehydroepiandrosterone sulfate, cortisol, symptoms of dissociation, and
objective performance in humans exposed to underwater navigation stress.
Biol Psychiatry. 2009 Aug 15;66(4):334-40
3. Ahboucha S, Pomier-Layrargues G, Vincent C, Hassoun Z, Tamaz R, Baker
G, Butterworth RF. Reduced plasma dehydroepiandrosterone sulfate levels
are significantly correlated with fatigue severity in patients with primary biliary
cirrhosis. Neurochem Int. 2008 Mar-Apr;52(4-5):569-74
4. Téllez N, Comabella M, Julià E, Río J, Tintoré M, Brieva L, Nos C, Montalban
X. Fatigue in progressive multiple sclerosis is associated with low levels of
dehydroepiandrosterone. Mult Scler. 2006 Aug;12(4):487-94
5. O'Donnell AB, Travison TG, Harris SS, Tenover JL, McKinlay JB.
Testosterone, dehydroepiandrosterone, and physical performance in older
men: results from the Massachusetts Male Aging Study. . J Clin Endocrinol
Metab. 2006 Feb;91(2):425-31
6. Maes M, Mihaylova I, De Ruyter M. Decreased dehydroepiandrosterone
sulfate but normal insulin-like growth factor in chronic fatigue syndrome
(CFS): relevance for the inflammatory response in CFS. Neuro Endocrinol
Lett. 2005 Oct;26(5):487-92
7. Morales AJ, Nolan JJ, Nelson JC, Yen SS. Effects of replacement dose of
dehydroepiandrosterone in men and women of advancing age. J Clin
Endocrinol Metab 1994 Jun;78(6):1360-7
8. Arlt W, Callies F, Allolio B. DHEA replacement in women with adrenal
insufficiency - pharmacokinetics, bioconversion and clinical effects on wellbeing, sexuality and cognition. Endocr Res. 2000;26(4):505-11
9. Cawood EH, Bancroft J. Steroid hormones, the menopause, sexuality and
well-being of women. Psychol Med. 1996 Sep;26(5):925-36
10. Rigaud AS, Pellerin J. Neuropsychic effects of dehydroepiandrosterone. Ann
Med Interne (Paris). 2001 Apr;152 Suppl 3:IS43-9
11. Piketty C, Jayle D, Leplege A, Castiel P, Ecosse E, Gonzalez-Canali G,
Sabatier B, Boulle N, Debuire B, Le Bouc Y, Baulieu EE, Kazatchkine MD.
Double-blind placebo-controlled trial of oral dehydroepiandrosterone in
patients with advanced HIV disease. Clin Endocrinol (Oxf). 2001
Sep;55(3):325-30
Baixa Qualidade de Vida, Baixa Performance e Fadiga: A Melhora Com a
Reposição de DHEA
1. Alkatib AA, Cosma M, Elamin MB, Erickson D, Swiglo BA, Erwin PJ, Montori
VM. A systematic review and meta-analysis of randomized placebo-controlled
trials of DHEA treatment effects on quality of life in women with adrenal
insufficiency. . J Clin Endocrinol Metab. 2009 Oct;94(10):3676-81
2. Nordmark G, Bengtsson C, Larsson A, Karlsson FA, Sturfelt G, Rönnblom L.
Effects of dehydroepiandrosterone supplement on health-related quality of life
in glucocorticoid treated female patients with systemic lupus erythematosus.
Autoimmunity. 2005 Nov;38(7):531-40
3. Calabrese V. DHEA in multiple sclerosis: positive effects in a non-randomized
study. In: The biological role of DHEA, edited by Regelson W, Kalimi M, De
Gruyter-Berlin, 1990: 95-100
4. Bloch M, Schmidt PJ, Danaceau MA, Adams LF, Rubinow DR.
Dehydroepiandrosterone treatment of midlife dysthymia. Biol Psychiatry.
1999;45(12):1533-41
5. Hunt PJ, Gurnell EM, Huppert FA, Richards C, Prevost AT, Wass JA, Herbert
J, Chatterjee VK. Improvement in mood and fatigue after
dehydroepiandrosterone replacement in Addison's disease in a randomized,
double blind trial. J Clin Endocrinol Metab. 2000;85(12):4650-6
6. van Vollenhoven RF, Engleman EG, McGuire JL. Dehydroepiandrosterone in
systemic lupus erythematosus. Results of a double-blind, placebo-controlled,
randomized clinical trial. Arthritis Rheum. 1995 Dec;38(12):1826-31
Baixa Qualidade de Vida, Baixa Performance e Fadiga: Correlação Com Baixos
Níveis de Estradiol
1. Studer DW. Clinical symptoms of estrogen deficiency in Estrogen Deficiency:
Causes and consequence, 1996, Ed. RW Staw, The Parthenon Publishing
Group, New-York, USA
2. Freedman MA. Quality of life and menopause: the role of estrogen. J
Womens Health (Larchmt). 2002 Oct;11(8):703-18
3. Carette S, Dessureault M, Belanger A. Fibromyalgia and sex hormones. J
Rheumatol. 1992 May;19(5):831
Baixa Qualidade de Vida, Baixa Performance e Fadiga: A Melhora Com a
Reposição de Estradiol
1. Serrano D, Mariani L, Mora S, Guerrieri-Gonzaga A, Cazzaniga M, Daldoss
C, Ramazzotto F, Feroce I, Decensi A, Bonanni B. Quality of life assessment
in a chemoprevention trial: fenretinide and oral or transdermal HRT.
Maturitas. 2006 Aug 20;55(1):69-75
2. Czarnecka D, Klocek M, Betkowska-Korpala B, Jankowski P, Olszanecka A,
Kawecka-Jaszcz K. Influence of hormone replacement therapy on the quality
of life in postmenopausal women with hypertension. Przegl Lek. 2000;57(78):397-401
3. Burger HG, Hailes J, Menelaus M, Nelson J, Hudson B, Balazs N. The
management of persistent menopausal symptoms with oestradioltestosterone implants: clinical, lipid and hormonal results. Maturitas. 1984
Dec;6(4):351-8
4. Dobs AS, Nguyen T, Pace C, Roberts CP. Differential effects of oral estrogen
versus oral estrogen-androgen replacement therapy on body composition in
postmenopausal women. J Clin Endocrinol Metab. 2002 Apr;87(4):1509-16
5. Nathorst-Boos J, Wiklund I, Mattsson LA, Sandin K, von Schoultz B. Is sexual
life influenced by transdermal estrogen therapy? A double blind placebo
controlled study in postmenopausal women. Acta Obstet Gynecol Scand.
1993 Nov;72(8):656-60
6. Wendlova J. Effect of Kliogest on bone metabolism, bone mineral density and
quality of life in postmenopausal patients. Vnitr Lek 1998 Aug;44(8):464-8
7. Gorins A, Espie M, Bedairia N, Perret F, Tournant B, Novak H, LucchiAngelier E, Marty M. Hormone replacement therapy in breast cancer patients:
a study of 230 patients, with a case-control study. Gynecol Obstet Fertil. 2003
Jul-Aug;31(7-8):614-9
8. Gambacciani M, Ciaponi M, Cappagli B, Monteleone P, Benussi C,
Bevilacqua G, Genazzani AR. Effects of low-dose, continuous combined
estradiol and noretisterone acetate on menopausal quality of life in early
postmenopausal women. Maturitas. 2003 Feb 25;44(2):157-63
9. Derman RJ, Dawood MY, Stone S. Quality of life during sequential hormone
replacement therapy – a placebo-controlled study. Int J Fertil Menopausal
Stud. 1995 Mar-Apr;40(2):73-8
10. Collins A, Hanson U, Eneroth P, Hagenfeldt K, Lundberg U, Frankenhaeuser
M. Psychophysiological stress responses in postmenopausal women before
and after hormonal replacement therapy. Hum Neurobiol. 1982;1(2):153-9
11. Ulrich LG, Barlow DH, Sturdee DW, Wells M, Campbell MJ, Nielsen B, Bragg
AJ, Vessey MP. Quality of life and patient preference for sequential versus
continuous combined HRT: the UK Kliofem multicenter study experience. UK
Continuous Combined HRT Study Investigators. Int J Gynaecol Obstet. 1997
Oct;59 Suppl 1:S11-7
12. Gelfand MM, Moreau M, Ayotte NJ, Hilditch JR, Wong BA, Lau CY. Clinical
assessment and quality of life of postmenopausal women treated with a,new
intermittent progestogen combination hormone replacement therapy: a
placebo-controlled study. Menopause. 2003 Jan-Feb;10(1):29-36
13. Barrett-Connor E, Young R, Notelovitz M, Sullivan J, Wiita B, Yang HM,
Nolan J. A two-year, double-blind comparison of estrogen-androgen and
conjugated estrogens in surgically menopausal women. Effects on bone
mineral density, symptoms and lipid profiles. J Reprod Med. 1999
Dec;44(12):1012-20
14. Bech P, Munk-Jensen N, Obel EB, Ulrich LG, Eiken P, Nielsen SP. Combined
versus sequential hormonal replacement therapy: a double-blind, placebocontrolled study on quality of life-related outcome measures. Psychother
Psychosom. 1998 Jul-Oct;67(4-5):259-65
15. Wu MH, Pan HA, Wang ST, Hsu CC, Chang FM, Huang KE. Quality of life
and sexuality changes in postmenopausal women receiving tibolone therapy.
Climacteric. 2001 Dec;4(4):314-9
16. Pornel B.Efficacy and safety of Menorest in two positive-controlled studies.
Eur J Obstet Gynecol Reprod Biol. 1996 Apr;64 Suppl:S35-7
17. Karlberg J, Mattsson LA, Wiklund I. A quality of life perspective on who
benefits from estradiol replacement therapy. Acta Obstet Gynecol Scand.
1995 May;74(5):367-72
18. Limouzin-Lamothe MA, Mairon N, Joyce CR, Le Gal M. Quality of life after the
menopause: influence of hormonal replacement therapy. Am J Obstet
Gynecol. 1994 Feb;170(2):618-24
19. Iversen OE, Eid AB, Johannesen KH, Nyland B, Lovset T. Transdermal
estrogen treatment. A placebo controlled study. Tidsskr Nor Laegeforen.
1991 Aug 30;111(20):2544-6
20. Wiklund I, Karlberg J, Mattsson LA. Quality of life of postmenopausal women
on a regimen of transdermal estradiol therapy: a double-blind placebocontrolled study. Am J Obstet Gynecol. 1993 Mar;168(3 Pt 1):824-30
21. Wiklund I, Berg G, Hammar M, Karlberg J, Lindgren R, Sandin K. Long-term
effect of transdermal hormonal therapy on aspects of quality of life in
postmenopausal women. Maturitas. 1992 Mar;14(3):225-36
22. Wiklund I, Holst J, Karlberg J, Mattsson LA, Samsioe G, Sandin K, Uvebrant
M, von Schoultz B.A new methodological approach to the evaluation of
quality of life in postmenopausal women. Maturitas. 1992 Mar;14(3):211-24
23. Hilditch JR, Lewis J, Ross AH, Peter A, van Maris B, Franssen E, Charles J,
Norton P, Dunn EV.A comparison of the effects of oral conjugated equine
estrogen and transdermal estradiol-17 beta combined with an oral progestin
on quality of life in postmenopausal women. Maturitas. 1996 Jul;24(3):177-84
24. Hall G, Pripp U, Schenck-Gustafsson K, Landgren BM. Long-term effects of
hormone replacement therapy on symptoms of angina pectoris, quality of life
and compliance in women with coronary artery disease. Maturitas. 1998 Jan
12;28(3):235-42
25. Rigano A, Rigano M, Cancellieri F, Pulle C. Sexually and well-being in early
menopause. Effect of transdermal estradiol therapy. Panminerva Med. 2001
Jun;43(2):115-8.
26. Adamson DL, Webb CM, Collins P. Esterified estrogens combined with
methyltestosterone improve emotional well-being in postmenopausal women
with chest pain and normal coronary angiograms. Menopause. 2001 JulAug;8(4):233-8
27. Collins A, Hanson U, Eneroth P, Hagenfeldt K, Lundberg U, Frankenhaeuser
M. Psychophysiological stress responses in postmenopausal women before
and after hormonal replacement therapy. Hum Neurobiol. 1982;1(2):153-9
28. Best NR, Rees MP, Barlow DH, Cowen PJ. Effect of estradiol implant on
noradrenergic
function
and
mood
in
menopausal
subjects.
Psychoneuroendocrinology. 1992;17(1):87-93
29. Campbell S, Whitehead M. Oestrogen therapy and the menopausal
syndrome. Clin Obstet Gynaecol. 1977 Apr;4(1):31-47
Baixa Qualidade de Vida, Baixa Performance e Fadiga: Correlação Com Baixos
Níveis de Testosterona
1.
Salminen E, Portin R, Korpela J, Backman H, Parvinen LM, Helenius H, Nurmi
M. Androgen deprivation and cognition in prostate cancer. Br J Cancer. 2003
Sep 15;89(6):971-6
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
van Andel G, Kurth KH. The impact of androgen deprivation therapy on health
related quality of life in asymptomatic men with lymph node positive prostate
cancer. Eur Urol. 2003 Aug;44(2):209-14
Pether M, Goldenberg SL, Bhagirath K, Gleave M. Intermittent androgen
suppression in prostate cancer: an update of the Vancouver experience. Can J
Urol. 2003 Apr;10(2):1809-14
Segal RJ, Reid RD, Courneya KS, Malone SC, Parliament MB, Scott CG,
Venner PM, Quinney HA, Jones LW, D'Angelo ME, Wells GA. Resistance
exercise in men receiving androgen deprivation therapy for prostate cancer. J
Clin Oncol. 2003 May 1;21(9):1653-9
Potosky AL, Reeve BB, Clegg LX, Hoffman RM, Stephenson RA, Albertsen PC,
Gilliland FD, Stanford JL. Quality of life following localized prostate cancer
treated initially with androgen deprivation therapy or no therapy. J Natl Cancer
Inst. 2002 Mar 20;94(6):430-7
Novak A, Brod M, Elbers J. Andropause and quality of life: findings from patient
focus groups and clinical experts. Maturitas. 2002 Dec 10;43(4):231-7
Fowler FJ Jr, McNaughton Collins M, Walker Corkery E, Elliott DB, Barry MJ.
The impact of androgen deprivation on quality of life after radical prostatectomy
for prostate carcinoma. Cancer. 2002 Jul 15;95(2):287-95
Seidman SN, Araujo AB, Roose SP, Devanand DP, Xie S, Cooper TB,
McKinlay JB. Low testosterone levels in elderly men with dysthymic disorder.
Am J Psychiatry. 2002 Mar;159(3):456-9
Lubeck DP, Grossfeld GD, Carroll PR. The effect of androgen deprivation
therapy on health-related quality of life in men with prostate cancer. Urology.
2001 Aug;58(2 Suppl 1):94-100
Herr HW, O'Sullivan M. Quality of life of asymptomatic men with nonmetastatic
prostate cancer on androgen deprivation therapy. J Urol. 2000
Jun;163(6):1743-6
Wang C, Alexander G, Berman N, Salehian B, Davidson T, McDonald V,
Steiner B, Hull L, Callegari C, Swerdloff RS. Testosterone replacement therapy
improves mood in hypogonadal men - a clinical research center study. J Clin
Endocrinol Metab. 1996 Oct;81(10):3578-83
van Kemenade JF, Cohen-Kettenis PT, Cohen L, Gooren LJ. Effects of the
pure antiandrogen RU 23.903 (anandron) on sexuality, aggression, and mood
in male-to-female transsexuals. Arch Sex Behav. 1989 Jun;18(3):217-28
Baixa Qualidade de Vida, Baixa Performance e Fadiga: A Melhora Com a
Reposição de Testosterona
1. Knapp PE, Storer TW, Herbst KL, Singh AB, Dzekov C, Dzekov J, LaValley
M, Zhang A, Ulloor J, Bhasin S. Effects of a supraphysiological dose of
testosterone on physical function, muscle performance, mood, and fatigue in
men with HIV-associated weight loss. Am J Physiol Endocrinol Metab. 2008
Jun;294(6):E1135-43
2. Lu PH, Masterman DA, Mulnard R, Cotman C, Miller B, Yaffe K, Reback E,
Porter V, Swerdloff R, Cummings JL. Effects of testosterone on cognition
and mood in male patients with mild Alzheimer disease and healthy elderly
men. Arch Neurol. 2006 Feb;63(2):177-85
3. Katznelson L, Robinson MW, Coyle CL, Lee H, Farrell CE. Effects of modest
testosterone supplementation and exercise for 12 weeks on body
composition and quality of life in elderly men. Eur J Endocrinol. 2006
Dec;155(6):867-75 (“Improved quality of life with testosterone treatment if the
treatment was associated with exercise”)
4. Arver S, Dobs AS, Meikle AW, Caramelli KE, Rajaram L, Sanders SW, Mazer
NA. Long-term efficacy and safety of a permeation-enhanced testosterone
transdermal system in hypogonadal men. Clin Endocrinol (Oxf) 1997
Dec;47(6):727-37
5. Park NC, Yan BQ, Chung JM, Lee KM. Oral testosterone undecanoate
(Andriol) supplement therapy improves the quality of life for men with
testosterone deficiency. Aging Male. 2003 Jun;6(2):86-93
6. English KM, Steeds RP, Jones TH, Diver MJ, Channer KS. Low-dose
transdermal testosterone therapy improves angina threshold in men with
chronic stable angina: A randomized, double-blind, placebo-controlled study.
Circulation. 2000 Oct 17;102(16):1906-11
7. Rabkin JG, Wagner GJ, Rabkin R. A double-blind, placebo-controlled trial of
testosterone therapy for HIV-positive men with hypogonadal symptoms. Arch
Gen Psychiatry. 2000 Feb;57(2):141-7
8. Rabkin JG, Wagner GJ, Rabkin R. Testosterone therapy for human
immunodeficiency virus-positive men with and without hypogonadism. J Clin
Psychopharmacol. 1999 Feb;19(1):19-27
9. Rabkin JG, Wagner GJ, McElhiney MC, Rabkin R, Lin SH. Testosterone
versus fluoxetine for depression and fatigue in HIV/AIDS: a placebocontrolled trial. J Clin Psychopharmacol. 2004 Aug;24(4):379-85
10. O'Connor DB, Archer J, Hair WM, Wu FC. Exogenous testosterone,
aggression, and mood in eugonadal and hypogonadal men. Physiol Behav.
2002 Apr 1;75(4):557-66
11. Rozenek R, Rahe CH, Kohl HH, Marple DN, Wilson GD, Stone MH.
Physiological responses to resistance-exercise in athletes self-administering
anabolic steroids. J Sports Med Phys Fitness. 1990 Dec;30(4):354-60.
12. Wagner GJ, Rabkin JG, Rabkin R. Testosterone as a treatment for fatigue in
HIV+ men. Gen Hosp Psychiatry. 1998 Jul;20(4):209-13
13. Wagner G, Rabkin J, Rabkin R. Exercise as a mediator of psychological and
nutritional effects of testosterone therapy in HIV+ men. Med Sci Sports Exerc.
1998 Jun;30(6):811-7
14. Okun MS, McDonald WM, DeLong MR. Refractory nonmotor symptoms in
male patients with Parkinson disease due to testosterone deficiency: a
common unrecognized comorbidity. Arch Neurol. 2002 May;59(5):807-11
15. Crawford BA, Liu PY, Kean MT, Bleasel JF, Handelsman DJ. Randomized
placebo-controlled trial of androgen effects on muscle and bone in men
requiring long-term systemic glucocorticoid treatment. J Clin Endocrinol
Metab. 2003 Jul;88(7):3167-76
16. Grinspoon S, Corcoran C, Askari H, Schoenfeld D, Wolf L, Burrows B, Walsh
M, Hayden D, Parlman K, Anderson E, Basgoz N, Klibanski A. Effects of
androgen administration in men with the AIDS wasting syndrome. A
randomized, double-blind, placebo-controlled trial. Ann Intern Med. 1998 Jul
1;129(1):18-26
17. Howell SJ, Radford JA, Adams JE, Smets EM, Warburton R, Shalet SM.
Randomized placebo-controlled trial of testosterone replacement in men with
mild Leydig cell insufficiency following cytotoxic chemotherapy. Clin
Endocrinol (Oxf). 2001 Sep;55(3):315-24
18. Gruenewald DA, Matsumoto AM.Testosterone supplementation therapy for
older men: potential benefits and risks. J Am Geriatr Soc. 2003
Jan;51(1):101-15
19. van Basten JP, van Driel MF, Jonker-Pool G, Sleijfer DT, Schraffordt Koops
H, van de Wiel HB, Hoekstra HJ. Sexual functioning in testosteronesupplemented patients treated for bilateral testicular cancer. Br J Urol. 1997
Mar;79(3):461-7
Baixa Performance: A Correlação Com Baixos Níveis de Testosterona
1. Orwoll E, Lambert LC, Marshall LM, Blank J, Barrett-Connor E, Cauley J,
Ensrud K, Cummings SR; Osteoporotic Fractures in Men Study Group.
Endogenous testosterone levels, physical performance, and fall risk in older
men. Arch Intern Med. 2006 Oct 23;166(19):2124-31
2. Cardinale M, Stone MH.Is testosterone influencing explosive performance? J
Strength Cond Res. 2006 Feb;20(1):103-7
3. O'Donnell AB, Travison TG, Harris SS, Tenover JL, McKinlay JB.
Testosterone, dehydroepiandrosterone, and physical performance in older
men: results from the Massachusetts Male Aging Study. . J Clin Endocrinol
Metab. 2006 Feb;91(2):425-31
Baixa Performance: A Melhora Com a Reposição de Testosterona
1. Caminiti G, Volterrani M, Iellamo F, Marazzi G, Massaro R, Miceli M, Mammi
C, Piepoli M, Fini M, Rosano GM. Effect of long-acting testosterone treatment
on functional exercise capacity, skeletal muscle performance, insulin
resistance, and baroreflex sensitivity in elderly patients with chronic heart
failure a double-blind, placebo-controlled, randomized study. J Am Coll
Cardiol. 2009 Sep 1;54(10):919-27
2. Sattler FR, Castaneda-Sceppa C, Binder EF, Schroeder ET, Wang Y, Bhasin
S, Kawakubo M, Stewart Y, Yarasheski KE, Ulloor J, Colletti P, Roubenoff R,
Azen SP. Testosterone and growth hormone improve body composition and
muscle performance in older men. J Clin Endocrinol Metab. 2009
Jun;94(6):1991-2001
3. Srinivas-Shankar U, Roberts SA, Connolly MJ, O'Connell MD, Adams JE,
Oldham JA, Wu FC. Effects of testosterone on muscle strength, physical
function, body composition, and quality of life in intermediate-frail and frail
elderly men: a randomized, double-blind, placebo-controlled study. J Clin
Endocrinol Metab. 2010 Feb;95(2):639-50
-
CONTROLE DA ANSIEDADE ATRAVÉS DA
MODULAÇÃO HORMONAL
4
Ansiedade: Associação Com Baixos Níveis de DHEA
1- Ritsner M, Maayan R, Gibel A, Strous RD, Modai I, Weizman A. Elevation of
the cortisol/dehydroepiandrosterone ratio in schizophrenia patients. Eur
Neuropsychopharmacol. 2004 Aug;14(4):267-73
2- Ritsner M, Gibel A, Ram E, Maayan R, Weizman A. Alterations in DHEA
metabolism in schizophrenia: Two-month case-control study. Eur
Neuropsychopharmacol. 2006 Feb;16(2):137-46
3- Goyal RO, Sagar R, Ammini AC, Khurana ML, Alias AG. Negative correlation
between negative symptoms of schizophrenia and testosterone levels. Ann N
Y Acad Sci. 2004 Dec;1032:291-4
Ansiedade: Associação Com Baixos Níveis de Androgênios
1- Diamond P, Brisson GR, Candas B, Peronnet F. Trait anxiety, submaximal
physical exercise and blood androgens. Eur J Appl Physiol Occup Physiol.
1989;58(7):699-704
Ansiedade: A Melhora Com a Reposição de DHEA
1- Arlt W, Callies F, van Vlijmen JC, Koehler I, Reincke M, Bidlingmaier M,
Huebler D, Oettel M, Ernst M, Schulte HM, Allolio B. Dehydroepiandrosterone
replacement in women with adrenal insufficiency. N Engl J Med.
1999;341(14):1013-20
2- Strous RD, Maayan R, Lapidus R, Stryjer R, Lustig M, Kotler M, Weizman A.
Dehydroepiandrosterone augmentation in the management of negative,
depressive, and anxiety symptoms in schizophrenia. Arch Gen Psychiatry.
2003 Feb;60(2):133-41
3- Morales AJ, Nolan JJ, Nelson JC, Yen SS. Effects of replacement dose of
dehydroepiandrosterone in men and women of advancing age. J Clin
Endocrinol Metab. 1994 Jun;78(6):1360-7
4- Sharma AN, Chopde CT, Hirani K, Kokare DM, Ugale RR Chronic
progesterone treatment augments while dehydroepiandrosterone sulphate
prevents tolerance to ethanol anxiolysis and withdrawal anxiety in rats. Eur J
Pharmacol. 2007 Jul 19;567(3):211-22
5- Maayan R, Touati-Werner D, Ram E, Strous R, Keren O, Weizman A. The
protective effect of frontal cortex dehydroepiandrosterone in anxiety and
depressive models in mice. Pharmacol Biochem Behav. 2006 Oct;85(2):41521
6- Melchior CL, Ritzmann RF. Dehydroepiandrosterone is an anxiolytic in mice
on the plus maze. Pharmacol Biochem Behav. 1994 Mar;47(3):437-41
7- Ovsiukova MV, Kudriavtseva NN, Obut TA, Amikishieva AV. Anxiolytic effect
of the dehydroepiandrosterone sulfate: mu-opioid mechanism. Ross Fiziol Zh
Im I M Sechenova. 2003 May;89(5):598-604
Baixa Resistência Ao Estresse: A Associação Com Baixos Níveis de DHEA
1- Morgan CA 3rd, Rasmusson A, Pietrzak RH, Coric V, Southwick SM.
Relationships
among
plasma
dehydroepiandrosterone
and
dehydroepiandrosterone sulfate, cortisol, symptoms of dissociation, and
objective performance in humans exposed to underwater navigation stress.
Biol Psychiatry. 2009 Aug 15;66(4):334-40 (“DHEA and DHEAS were
significantly and negatively related to stress-induced symptoms of
dissociation during performance of the task”)
Ansiedade: A Melhora Com a Reposição de Melatonina
1- Ovanesov KB, Ovanesova IM, Arushanian EB. Effects of melatonin and
motherwort tincture on the emotional state and visual functions in anxious
subjects. Eksp Klin Farmakol. 2006 Nov-Dec;69(6):17-9
2- Acil M, Basgul E, Celiker V, Karagoz AH, Demir B, Aypar U. Perioperative
effects of melatonin and midazolam premedication on sedation, orientation,
anxiety scores and psychomotor performance. Eur J Anaesthesiol. 2004
Jul;21(7):553-7
3- Lissoni P, Barni S, Meregalli S, Fossati V, Cazzaniga M, Esposti D, Tancini
G. Modulation of cancer endocrine therapy by melatonin: a phase II study of
tamoxifen plus melatonin in metastatic breast cancer patients progressing
under tamoxifen alone Br J Cancer. 1995 Apr;71(4):854-6
4- Nelson E, Panksepp J, Ikemoto S. The effects of melatonin on isolation
distress in chickens. Pharmacol Biochem Behav. 1994 Oct;49(2):327-33Nava
F, Carta G. Melatonin reduces anxiety induced by lipopolysaccharide in the
rat. Neurosci Lett. 2001 Jul 6;307(1):57-60
5- Naranjo-Rodriguez EB, Osornio AO, Hernandez-Avitia E, MendozaFernandez V, Escobar A. Anxiolytic-like actions of melatonin, 5metoxytryptophol, 5-hydroxytryptophol and benzodiazepines on a conflict
procedure. Prog Neuropsychopharmacol Biol Psychiatry. 2000 Jan;24(1):11729
Ansiedade: Associação Com Baixos Níveis dos Hormônios Tireoidianos
1- Constant EL, Adam S, Seron X, Bruyer R, Seghers A, Daumerie C. Anxiety
and depression, attention, and executive functions in hypothyroidism. J Int
Neuropsychol Soc. 2005 Sep;11(5):535-44
2- Kikuchi M, Komuro R, Oka H, Kidani T, Hanaoka A, Koshino Y. Relationship
between anxiety and thyroid function in patients with panic disorder. Prog
Neuropsychopharmacol Biol Psychiatry. 2005 Jan;29(1):77-81
3- Bauer M, Priebe S, Kurten I, Graf KJ, Baumgartner A. Psychological and
endocrine abnormalities in refugees from East Germany: Part I. Prolonged
stress, psychopathology, and hypothalamic-pituitary-thyroid axis activity.
Psychiatry Res. 1994 Jan;51(1):61-73
4- Magliozzi JR, Maddock RJ, Gold AS, Gietzen DW. Relationships between
thyroid indices and symptoms of anxiety in depressed outpatients Ann Clin
Psychiatry. 1993 Jun;5(2):111-6
5- Sait Gonen M, Kisakol G, Savas Cilli A, Dikbas O, Gungor K, Inal A, Kaya A.
Assessment of anxiety in subclinical thyroid disorders. Endocr J. 2004
Jun;51(3):311-5
6- Larisch R, Kley K, Nikolaus S, Sitte W, Franz M, Hautzel H, Tress W, Muller
HW.. Depression and anxiety in different thyroid function states. Horm Metab
Res. 2004 Sep;36(9):650-3
7- Constant EL, Adam S, Seron X, Bruyer R, Seghers A, Daumerie C. Anxiety
and depression, attention, and executive functions in hypothyroidism. J Int
Neuropsychol Soc. 2005 Sep;11(5):535-44
8- Landen M, Baghaei F, Rosmond R, Holm G, Bjorntorp P, Eriksson E.
Dyslipidemia and high waist-hip ratio in women with self-reported social
anxiety. Psychoneuroendocrinology. 2004 Sep;29(8):1037-46 (Serum levels
of free thyroxin (14+/-2 versus. 16+/-4, P=0.04) were lower in subjects
confirming social anxiety)
Ansiedade: A Melhora Com a Reposição dos Hormônios Tireoidianos
1- Saravanan P, Simmons DJ, Greenwood R, Peters TJ, Dayan CM. Partial
substitution of thyroxine (T4) with tri-iodothyronine in patients on T4
replacement therapy: results of a large community-based randomized
controlled trial. J Clin Endocrinol Metab. 2005 Feb;90(2):805-12
2- Venero C, Guadano-Ferraz A, Herrero AI, Nordstrom K, Manzano J, de
Escobar GM, Bernal J, Vennstrom B. Anxiety, memory impairment, and
locomotor dysfunction caused by a mutant thyroid hormone receptor alpha1
can be ameliorated by T3 treatment. Genes Dev. 2005 Sep 15;19(18):215263
Ansiedade: Associação Com Baixos Níveis do Hormônio do Crescimento
1- Stouthart PJ, Deijen JB, Roffel M, Delemarre-van de Waal HA. Quality of life
of growth hormone (GH) deficient young adults during discontinuation and
restart of GH therapy. Psychoneuroendocrinology. 2003 Jul;28(5):612-26
2- Malberg JE, Platt B, Rizzo SJ, Ring RH, Lucki I, Schechter LE, RosenzweigLipson S. Increasing the levels of insulin-like growth factor-I by an IGF
binding protein inhibitor produces anxiolytic and antidepressant-like effects.
Neuropsychopharmacology. 2007 Nov;32(11):2360-8
3- Uhde TW, Malloy LC, Slate SO. Fearful behavior, body size, and serum IGF-I
levels in nervous and normal pointer dogs. Pharmacol Biochem Behav. 1992
Sep;43(1):263-9
4- Tancer ME, Stein MB, Uhde TW. Growth hormone response to intravenous
clonidine in social phobia: comparison to patients with panic disorder and
healthy volunteers. Biol Psychiatry. 1993 Nov 1;34(9):591-5
5- Cameron OG, Abelson JL, Young EA. Anxious and depressive disorders and
their comorbidity: effect on central nervous system noradrenergic function.
Biol Psychiatry. 2004 Dec 1;56(11):875-83
6- Stabler B. Impact of growth hormone (GH) therapy on quality of life along the
lifespan of GH-treated patients. Horm Res. 2001;56 Suppl 1:55-8
7- Abelson JL, Glitz D, Cameron OG, Lee MA, Bronzo M, Curtis GC. Blunted
growth hormone response to clonidine in patients with generalized anxiety
disorder. Arch Gen Psychiatry. 1991 Feb;48(2):157-62
Ansiedade: A Melhora Com a Reposição do Hormônio do Crescimento
1- Thompson JL, Butterfield GE, Gylfadottir UK, Yesavage J, Marcus R, Hintz
RL, Pearman A, Hoffman AR. Effects of human growth hormone, insulin-like
growth factor I, and diet and exercise on body composition of obese
postmenopausal women. : J Clin Endocrinol Metab. 1998 May;83(5):1477-84
2- Darnaudéry M, Perez-Martin M, Bélizaire G, Maccari S, Garcia-Segura LM.
Insulin-like growth factor 1 reduces age-related disorders induced by prenatal
stress in female rats. Neurobiol Aging. 2006 Jan;27(1):119-27
3- Arwert LI, Deijen JB, Muller M, Drent ML. Long-term growth hormone
treatment preserves GH-induced memory and mood improvements: a 10year follow-up study in GH-deficient adult men. Horm Behav. 2005
Mar;47(3):343-9
4- Lasaite L, Bunevicius R, Lasiene D, Lasas L. Psychological functioning after
growth hormone therapy in adult growth hormone deficient patients:
endocrine and body composition correlates. Medicina (Kaunas).
2004;40(8):740-4
Ansiedade: Associação Com Baixos Níveis de Pregnenolona
1.
2.
3.
4.
Ritsner M, Maayan R, Gibel A, Weizman A. Differences in blood pregnenolone
and dehydroepiandrosterone levels between schizophrenia patients and
healthy subjects. Eur Neuropsychopharmacol. 2007 Apr;17(5):358-65
Heydari B, Le Melledo JM. Low pregnenolone sulphate plasma concentrations
in patients with generalized social phobia. Psychol Med. 2002 Jul;32(5):929-33
Semeniuk T, Jhangri GS, Le Melledo JM. Neuroactive steroid levels in patients
with generalized anxiety disorder. J Neuropsychiatry Clin Neurosci. 2001
Summer;13(3):396-8
Serra M, Pisu MG, Littera M, Papi G, Sanna E, Tuveri F, Usala L, Purdy RH,
Biggio G. Social isolation-induced decreases in both the abundance of
neuroactive steroids and GABA(A) receptor function in rat brain. J Neurochem.
2000 Aug;75(2):732-40
Ansiedade: A Melhora Com a Reposição de Pregnenolona
1- Reddy DS, Kulkarni SK. Neurosteroid coadministration prevents development
of tolerance and augments recovery from benzodiazepine withdrawal anxiety
and hyperactivity in mice. Methods Find Exp Clin Pharmacol. 1997 JulAug;19(6):395-405
2- Reddy DS, Kulkarni SK. Differential anxiolytic effects of neurosteroids in the
mirrored chamber behavior test in mice. Brain Res. 1997 Mar 28;752(1-2):6171
3- Jorge JC, Gonzalez L, Fortis A, Cruz ND. Sex-specific modulation of anxiety
and locomotion after neonatal exposure to pregnenolone sulfate. Physiol
Behav. 2005 Jan 17;83(5):779-86
4- Melchior CL, Ritzmann RF. Pregnenolone and pregnenolone sulfate, alone
and with ethanol, in mice on the plus-maze. Pharmacol Biochem Behav. 1994
Aug;48(4):893-7
Ansiedade: A Melhora Com a Reposição de Estradiol e Progesterona
1- Collins A, Hanson U, Eneroth P, Hagenfeldt K, Lundberg U, Frankenhaeuser
M. Psychophysiological stress responses in postmenopausal women before
and after hormonal replacement therapy. Hum Neurobiol. 1982;1(2):153-9
Ansiedade: A Melhora Com a Reposição de Estradiol
1- Best NR, Rees MP, Barlow DH, Cowen PJ. Effect of estradiol implant on
noradrenergic
function
and
mood
in
menopausal
subjects.
Psychoneuroendocrinology. 1992;17(1):87-93
2- Campbell S, Whitehead M. Oestrogen therapy and the menopausal
syndrome. Clin Obstet Gynaecol. 1977 Apr;4(1):31-47
3- Montgomery JC, Appleby L, Brincat M, Versi E, Tapp A, Fenwick PB, Studd
JW. Effect of oestrogen and testosterone implants on psychological disorders
in the climacteric. Lancet. 1987 Feb 7;1(8528):297-9
4- Nathorst-Boos J, von Schoultz B, Carlstrom K. Elective ovarian removal and
estrogen replacement therapy - effects on sexual life, psychological well-
being and androgen status. J Psychosom Obstet Gynaecol. 1993
Dec;14(4):283-93
5- Walf AA, Paris JJ, Frye CA. Chronic estradiol replacement to aged female
rats reduces anxiety-like and depression-like behavior and enhances
cognitive performance. Psychoneuroendocrinology. 2009 Jul;34(6):909-16
6- Walf AA, Frye CA. Estradiol decreases anxiety behavior and enhances
inhibitory avoidance and gestational stress produces opposite effects. Stress.
2007 Aug;10(3):251-60
Ansiedade: A Melhora Com a Reposição de Progesterona
1- Wieland S, Lan NC, Mirasedeghi S, Gee KW. Anxiolytic activity of the
progesterone metabolite 5 alpha-pregnan-3 alpha-o1-20-one. Brain Res.
1991 Nov 29;565(2):263-8
2- Picazo O, Fernandez-Guasti A. Anti-anxiety effects of progesterone and
some of its reduced metabolites: an evaluation using the burying behavior
test. Brain Res. 1995 May 22;680(1-2):135-41.
3- Bitran D, Shiekh M, McLeod M. Anxiolytic effect of progesterone is mediated
by the neurosteroid allopregnanolone at brain GABAA receptors. J
Neuroendocrinol. 1995 Mar;7(3):171-7
4- Baker ER, Best RG, Manfredi RL, Demers LM, Wolf GC. Efficacy of
progesterone vaginal suppositories in alleviation of nervous symptoms in
patients with premenstrual syndrome. J Assist Reprod Genet. 1995
Mar;12(3):205-9
5- Bitran D, Purdy RH, Kellogg CK. Anxiolytic effect of progesterone is
associated with increases in cortical allopregnanolone and GABAA receptor
function. Pharmacol Biochem Behav. 1993 Jun;45(2):423-8
Ansiedade: Associação Com Baixos Níveis de Testosterona
13.
14.
Werner AA. The male climateric JAMA. 1946;132(4):188-94
Diamond P, Brisson GR, Candas B, Peronnet F. Trait anxiety, submaximal
physical exercise and blood androgens. Eur J Appl Physiol Occup Physiol.
1989;58(7):699-704
Ansiedade: A Melhora Com a Reposição de Testosterona
15.
16.
Cooper MA, Ritchie EC. Testosterone replacement therapy for anxiety. Am J
Psychiatry. 2000 Nov;157(11):1884
Aikey JL, Nyby JG, Anmuth DM, James PJ. Testosterone rapidly reduces
anxiety in male house mice (Mus musculus). Horm Behav. 2002 Dec;42(4):44860
-
CONTROLE DA QUALIDADE DO SONO
ATRAVÉS DA MODULAÇÃO HORMONAL
5
Distúrbios do Sono: A Correlação Com Baixos Níveis de Melatonina
1- Rahman SA, Marcu S, Kayumov L, Shapiro CM. Altered sleep architecture
and higher incidence of subsyndromal depression in low endogenous
melatonin secretors. Eur Arch Psychiatry Clin Neurosci. 2010
2- Blaicher W, Speck E, Imhof MH, Gruber DM, Schneeberger C, Sator MO,
Huber JC. Melatonin in postmenopausal females. Arch Gynecol Obstet. 2000
Feb;263(3):116-8
3- Riemann D, Klein T, Rodenbeck A, Feige B, Horny A, Hummel R, Weske G,
Al-Shajlawi A, Voderholzer U. Nocturnal cortisol and melatonin secretion in
primary insomnia. Psychiatry Res. 2002 Dec 15;113(1-2):17-27
4- Rodenbeck A, Huether G, Ruther E, Hajak G. Nocturnal melatonin secretion
and its modification by treatment in patients with sleep disorders. Adv Exp
Med Biol. 1999;467:89-93
5- Hajak G, Rodenbeck A, Staedt J, Bandelow B, Huether G, Ruther E.
Nocturnal plasma melatonin levels in patients suffering from chronic primary
insomnia. J Pineal Res. 1995 Oct;19(3):116-22
6- Hansen T, Bratlid T, Lingjarde O, Brenn T. Midwinter insomnia in the
subarctic region: evening levels of serum melatonin and cortisol before and
after treatment with bright artificial light. Acta Psychiatr Scand. 1987
Apr;75(4):428-34
Distúrbios do Sono: A Melhora Com a Reposição de Melatonina
1- Rahman SA, Kayumov L, Shapiro CM. Antidepressant action of melatonin in
the treatment of Delayed Sleep Phase Syndrome. Sleep Med. 2010
Feb;11(2):131-136
2- Bendz LM, Scates AC. Melatonin treatment for insomnia in pediatric patients
with attention-deficit/hyperactivity disorder. Ann Pharmacother. 2010
Jan;44(1):185-91
3- Aeschbach D, Lockyer BJ, Dijk DJ, Lockley SW, Nuwayser ES, Nichols LD,
Czeisler CA. Use of transdermal melatonin delivery to improve sleep
maintenance during daytime. Clin Pharmacol Ther. 2009 Oct;86(4):378-82
4- Luthringer R, Muzet M, Zisapel N, Staner L. The effect of prolonged-release
melatonin on sleep measures and psychomotor performance in elderly
patients with insomnia. Int Clin Psychopharmacol. 2009 Sep;24(5):239-49
5- Megwalu UC, Finnell JE, Piccirillo JF. The effects of melatonin on tinnitus and
sleep. Otolaryngol Head Neck Surg. 2006 Feb;134(2):210-3
6- Wade AG, Ford I, Crawford G, McMahon AD, Nir T, Laudon M, Zisapel N.
Efficacy of prolonged release melatonin in insomnia patients aged 55-80
years: quality of sleep and next-day alertness outcomes. Curr Med Res Opin.
2007 Oct;23(10):2597-605
7- Skene DJ, Arendt J. Circadian rhythm sleep disorders in the blind and their
treatment with melatonin. Sleep Med. 2007 Sep;8(6):651-5
8- Attenburrow ME, Cowen PJ, Sharpley AL. Low dose melatonin improves
sleep in healthy middle-aged subjects. Psychopharmacology (Berl). 1996
Jul;126(2):179-81
9- Garfinkel D, Laudon M, Nof D, Zisapel N. Improvement of sleep quality in
elderly people by controlled-release melatonin. Lancet. 1995 Aug
26;346(8974):541-4
10- Pawlikowski M, Kolomecka M, Wojtczak A, Karasek M. Effects of six months
melatonin treatment on sleep quality and serum concentrations of estradiol,
cortisol, dehydroepiandrosterone sulfate, and somatomedin C in elderly
women. Neuroendocrinol Lett. 2002 Apr;23 Suppl 1:17-9
11- Monti JM, Cardinali DP. A critical assessment of the melatonin effect on sleep
in humans. Biol Signals Recept. 2000 Nov-Dec;9(6):328-39
Distúrbios do Sono: A Melhora Com a Reposição dos Hormônios Tireoidianos
1- Jha A, Sharma SK, Tandon N, Lakshmy R, Kadhiravan T, Handa KK, Gupta
R, Pandey RM, Chaturvedi PK. Thyroxine replacement therapy reverses
sleep-disordered breathing in patients with primary hypothyroidism. Sleep
Med. 2006 Jan;7(1):55-61
2- Misiolek M, Marek B, Namyslowski G, Scierski W, Zwirska-Korczala K,
Kazmierczak-Zagorska Z, Kajdaniuk D, Misiolek H. Sleep apnea syndrome
and snoring in patients with hypothyroidism with relation to overweight. J
Physiol Pharmacol. 2007 Mar;58 Suppl 1:77-85
3- Ruiz-Primo E, Jurado JL, Solis H, Maisterrena JA, Fernandez-Guardiola A,
Valverde C. Polysomnographic effects of thyroid hormones primary
myxedema. Electroencephalogr Clin Neurophysiol. 1982 May;53(5):559-64
4- Orr WC, Males JL, Imes NK. Myxedema and obstructive sleep apnea. Am J
Med. 1981 May;70(5):1061-6
Distúrbios do Sono: A Correlação Com Baixos Níveis do Hormônio do
Crescimento
1- Ismailogullari S, Tanriverdi F, Kelestimur F, Aksu M. Sleep architecture in
Sheehan's syndrome before and 6 months after growth hormone replacement
therapy. Psychoneuroendocrinology. 2009 Feb;34(2):212-9
2- Astrom C, Lindholm J. Growth hormone-deficient young adults have
decreased deep sleep. Neuroendocrinology. 1990 Jan;51(1):82-4
Distúrbios do Sono: A Melhora Com a Reposição do Hormônios do
Crescimento
1- Verrillo E, Bruni O, Franco P, Ferri R, Thiriez G, Pavone M, Petrone A,
Paglietti MG, Crinò A, Cutrera R. Analysis of NREM sleep in children with
Prader-Willi syndrome and the effect of growth hormone treatment. Sleep
Med. 2009 Jun;10(6):646-50
2- Ismailogullari S, Tanriverdi F, Kelestimur F, Aksu M. Sleep architecture in
Sheehan's syndrome before and 6 months after growth hormone replacement
therapy. Psychoneuroendocrinology. 2009 Feb;34(2):212-9
3- Miller J, Silverstein J, Shuster J, Driscoll DJ, Wagner M. Short-term effects of
growth hormone on sleep abnormalities in Prader-Willi syndrome. J Clin
Endocrinol Metab. 2006 Feb;91(2):413-7
4- Peker Y, Svensson J, Hedner J, Grote L, Johannsson G. Sleep apnoea and
quality of life in growth hormone (GH)-deficient adults before and after 6
months of GH replacement therapy. Clin Endocrinol (Oxf). 2006 Jul;65(1):98105
5- Astrom C, Pedersen SA, Lindholm J. The influence of growth hormone on
sleep in adults with growth hormone deficiency. Clin Endocrinol (Oxf). 1990
Oct;33(4):495-500
Distúrbios do Sono: A Correlação Com Baixos Níveis de Estradiol
1- Merklinger-Gruchala A, Ellison PT, Lipson SF, Thune I, Jasienska G. Low
estradiol levels in women of reproductive age having low sleep variation. Eur
J Cancer Prev. 2008 Oct;17(5):467-72
2- Hollander LE, Freeman EW, Sammel MD, Berlin JA, Grisso JA, Battistini M.
Sleep quality, estradiol levels, and behavioral factors in late reproductive age
women. Obstet Gynecol. 2001 Sep;98(3):391-7
Distúrbios do Sono: A Melhora Com a Reposição de Estradiol
1- Antonijevic IA, Stalla GK, Steiger A. Modulation of the sleep
electroencephalogram by estrogen replacement in postmenopausal women.
Am J Obstet Gynecol. 2000 Feb;182(2):277-82.
2- Schiff I, Regestein Q, Tulchinsky D, Ryan KJ. Effects of estrogens on sleep
and psychological state of hypogonadal women. JAMA. 1979 Nov
30;242(22):2405-4
Distúrbios do Sono: A Melhora Com a Reposição de Progesterona
1- Montplaisir J, Lorrain J, Denesle R, Petit D. Sleep in menopause: differential
effects of two forms of hormone replacement therapy. Menopause. 2001 JanFeb;8(1):10-6
2- Schüssler P, Kluge M, Yassouridis A, Dresler M, Held K, Zihl J, Steiger A.
Progesterone reduces wakefulness in sleep EEG and has no effect on
cognition in healthy postmenopausal women. Psychoneuroendocrinology.
2008 Sep;33(8):1124-31
Distúrbios do Sono: A Melhora Com a Reposição de Estradiol e Progesterona
1- Hachul H, Bittencourt LR, Andersen ML, Haidar MA, Baracat EC, Tufik S.
Effects of hormone therapy with estrogen and/or progesterone on sleep
pattern in postmenopausal women. Int J Gynaecol Obstet. 2008
Dec;103(3):207-12
2- Soares CN, Arsenio H, Joffe H, Bankier B, Cassano P, Petrillo LF, Cohen LS.
Escitalopram versus ethinyl estradiol and norethindrone acetate for
symptomatic peri- and postmenopausal women: impact on depression,
vasomotor symptoms, sleep, and quality of life. Menopause. 2006 SepOct;13(5):780-6
3- Keefe DL, Watson R, Naftolin F. Hormone replacement therapy may alleviate
sleep apnea in menopausal women: a pilot study. Menopause. 1999
Fall;6(3):196-200.
4- Sarti CD, Chiantera A, Graziottin A, Ognisanti F, Sidoli C, Mincigrucci M,
Parazzini F; Gruppo di Studio IperAOGOI. Hormone therapy and sleep quality
in women around menopause. Menopause. 2005 Sep-Oct;12(5):545-51
104 ESTUDOS PLACEBO-CONTROLADOS DEMONSTRANDO OS BENEFÍCIOS
E CONTROLE EXERCIDOS PELA REPOSIÇÃO DE MELATONINA NOS
MECANISMOS E QUALIDADE DO SONO EM CRIANÇAS E ADULTOS
Crianças
1. Smits MG, Nagtegaal EE, van der Heijden J, Coenen AM, Kerkhof GA.
Melatonin for chronic sleep onset insomnia in children: a randomised
placebo-controlled trial. J Child Neurol. 2001 Feb;16(2):86-92
2. Smits MG, van Stel HF, van der Heijden K, Meijer AM, Coenen AM, Kerkhof
GA. Melatonin improves health status and sleep in children with idiopathic
chronic sleep-onset insomnia: a randomized placebo-controlled trial. J Am
Acad Child Adolesc Psychiatry. 2003 Nov;42(11):1286-93
3. Jan JE, Hamilton D, Seward N, Fast DK, Freeman RD, Laudon M. Clinical
trials of controlled-release melatonin in children with sleep-wake cycle
disorders. J Pineal Res. 2000 Aug;29(1):34-9
4. Jan JE, Espezel H, Appleton RE. The treatment of sleep disorders with
melatonin. Dev Med Child Neurol. 1994 Feb;36(2):97-107
5. Dodge NN, Wilson GA .Melatonin for treatment of sleep disorders in children
with developmental disabilities. J Child Neurol. 2001 Aug;16(8):581-4
6. McArthur AJ, Budden SS.Sleep dysfunction in Rett syndrome: a trial of
exogenous melatonin treatment. Dev Med Child Neurol. 1998 Mar;40(3):18692
7. Coppola G, Iervolino G, Mastrosimone M, La Torre G, Ruiu F, Pascotto A.
Melatonin in wake-sleep disorders in children, adolescents and young adults
with mental retardation with or without epilepsy: a double-blind, cross-over,
placebo-controlled trial. Brain Dev. 2004 Sep;26(6):373-6
8. Niederhofer H, Staffen W, Mair A, Pittschieler K. Brief report: melatonin
facilitates sleep in individuals with mental retardation and insomnia. J Autism
Dev Disord. 2003 Aug;33(4):469-72
Adultos
1- Rahman SA, Kayumov L, Shapiro CM. Antidepressant action of melatonin in
the treatment of Delayed Sleep Phase Syndrome. Sleep Med. 2010
Feb;11(2):131-136
2- Luthringer R, Muzet M, Zisapel N, Staner L. The effect of prolonged-release
melatonin on sleep measures and psychomotor performance in elderly
patients with insomnia. Int Clin Psychopharmacol. 2009 Sep;24(5):239-49
3- Van Den Heuvel CJ, Kennaway DJ, Dawson D. Effects of daytime melatonin
infusion in young adults. Am J Physiol. 1998 Jul;275(1 Pt 1):E19-26
4- Lushington K, Pollard K, Lack L, Kennaway DJ, Dawson D. Daytime
melatonin administration in elderly good and poor sleepers: effects on core
body temperature and sleep latency. Sleep. 1997 Dec;20(12):1135-44
5- Mishima K, Satoh K, Shimizu T, Hishikawa Y. Hypnotic and hypothermic
action of daytime-administered melatonin. Psychopharmacology (Berl). 1997
Sep;133(2):168-71
6- Krauchi K, Cajochen C, Wirz-Justice A. A relationship between heat loss and
sleepiness: effects of postural change and melatonin administration. J Appl
Physiol. 1997 Jul;83(1):134-9
7- Hughes RJ, Badia P. Sleep-promoting and hypothermic effects of daytime
melatonin administration in humans. Sleep. 1997 Feb;20(2):124-31
8- Reid K, Van den Heuvel C, Dawson D. Day-time melatonin administration:
effects on core temperature and sleep onset latency. J Sleep Res. 1996
Sep;5(3):150-4
9- Nave R, Herer P, Haimov I, Shlitner A, Lavie P. Hypnotic and hypothermic
effects of melatonin on daytime sleep in humans: lack of antagonism by
flumazenil. Neurosci Lett. 1996 Aug 23;214(2-3):123-6
10- Cajochen C, Krauchi K, von Arx MA, Mori D, Graw P, Wirz-Justice A. Daytime
melatonin administration enhances sleepiness and theta/alpha activity in the
waking EEG. Neurosci Lett. 1996 Apr 5;207(3):209-13
11- Dijk DJ, Roth C, Landolt HP, Werth E, Aeppli M, Achermann P, Borbely AA.
Melatonin effect on daytime sleep in men: suppression of EEG low frequency
activity and enhancement of spindle frequency activity. Neurosci Lett. 1995
Dec 1;201(1):13-6
12- Deacon S, Arendt J. Melatonin-induced temperature suppression and its
acute phase-shifting effects correlate in a dose-dependent manner in
humans. Brain Res. 1995 Aug 7;688(1-2):77-85
13- Nave R, Iani C, Herer P, Gopher D, Lavie P. Residual effects of daytime
administration of melatonin on performance relevant to flight. Behav Brain
Res. 2002 Apr 1;131(1-2):87-95
14- Matsumoto M. The hypnotic effects of melatonin treatment on diurnal sleep in
humans. Psychiatry Clin Neurosci. 1999 Apr;53(2):243-5
15- Gilbert SS, van den Heuvel CJ, Dawson D. Daytime melatonin and
temazepam in young adult humans: equivalent effects on sleep latency and
body temperatures. J Physiol. 1999 Feb 1;514 ( Pt 3):905-14
16- Rogers NL, Kennaway DJ, Dawson D. Neurobehavioral performance effects
of daytime melatonin and temazepam administration. J Sleep Res. 2003
Sep;12(3):207-12
17- Deacon S, English J, Arendt J. Acute phase-shifting effects of melatonin
associated with suppression of core body temperature in humans. Neurosci
Lett. 1994 Aug 29;178(1):32-4
18- Dollins AB, Zhdanova IV, Wurtman RJ, Lynch HJ, Deng MH. Effect of
inducing nocturnal serum melatonin concentrations in daytime on sleep,
mood, body temperature, and performance. Proc Natl Acad Sci USA. 1994
Mar 1;91(5):1824-8
19- Dollins AB, Lynch HJ, Wurtman RJ, Deng MH, Kischka KU, Gleason RE,
Lieberman HR. Effect of pharmacological daytime doses of melatonin on
human
mood
and
performance.
Psychopharmacology
(Berl).
1993;112(4):490-6
20- Arendt J, Borbely AA, Franey C, Wright J. The effects of chronic, small doses
of melatonin given in the late afternoon on fatigue in man: a preliminary study.
Neurosci Lett. 1984 Apr 6;45(3):317-21
21- Wright J, Aldhous M, Franey C, English J, Arendt J. The effects of exogenous
melatonin on endocrine function in man. Clin Endocrinol (Oxf). 1986
Apr;24(4):375-82
22- Harris AS, Burgess HJ, Dawson D. The effects of day-time exogenous
melatonin administration on cardiac autonomic activity. J Pineal Res. 2001
Oct;31(3):199-205
23- Rajaratnam SM, Middleton B, Stone BM, Arendt J, Dijk DJ. Melatonin
advances the circadian timing of EEG sleep and directly facilitates sleep
without altering its duration in extended sleep opportunities in humans. J
Physiol. 2004 Nov 15;561(Pt 1):339-51
24- Holmes AL, Gilbert SS, Dawson D. Melatonin and zopiclone: the relationship
between sleep propensity and body temperature. Sleep. 2002 May
1;25(3):301-6
25- Paul MA, Gray G, Kenny G, Pigeau RA. Impact of melatonin, zaleplon,
zopiclone, and temazepam on psychomotor performance. Aviat Space
Environ Med. 2003 Dec;74(12):1263-70
26- Paul MA, Gray G, MacLellan M, Pigeau RA. Sleep-inducing pharmaceuticals:
a comparison of melatonin, zaleplon, zopiclone, and temazepam. Aviat Space
Environ Med. 2004 Jun;75(6):512-9
27- Wesensten NJ, Balkin TJ, Reichardt RM, Kautz MA, Saviolakis GA, Belenky
G. Daytime sleep and performance following a zolpidem and melatonin
cocktail. Sleep. 2005 Jan 1;28(1):93-103
28- Rajaratnam SM, Dijk DJ, Middleton B, Stone BM, Arendt J. Melatonin phaseshifts human circadian rhythms with no evidence of changes in the duration of
endogenous melatonin secretion or the 24-hour production of reproductive
hormones. J Clin Endocrinol Metab. 2003 Sep;88(9):4303-9.
29- Nickelsen T, Demisch L, Demisch K, Radermacher B, Schoffling K. Influence
of subchronic intake of melatonin at various times of the day on fatigue and
hormonal levels: a placebo-controlled, double-blind trial. J Pineal Res.
1989;6(4):325-34
30- Tzischinsky O, Lavie P. Melatonin possesses time-dependent hypnotic
effects. Sleep. 1994;17(7):638-45
31- Nave R, Peled R, Lavie P. Melatonin improves evening napping. Eur J
Pharmacol. 1995 Mar 6;275(2):213-6
32- Stone BM, Turner C, Mills SL, Nicholson AN. Hypnotic activity of melatonin.
Sleep. 2000 Aug 1;23(5):66333- Zhdanova IV, Wurtman RJ, Lynch HJ, Ives JR, Dollins AB, Morabito C,
Matheson JK, Schomer DL.Sleep-inducing effects of low doses of melatonin
ingested in the evening. Clin Pharmacol Ther. 1995 May;57(5):552-8
34- Zhdanova IV, Wurtman RJ, Morabito C, Piotrovska VR, Lynch HJ. Effects of
low oral doses of melatonin, given 2-4 hours before habitual bedtime, on
sleep in normal young humans. Sleep. 1996 Jun;19(5):423-31
35- Waldhauser F, Saletu B, Trinchard-Lugan I. Sleep laboratory investigations
on hypnotic properties of melatonin. Psychopharmacology (Berl).
1990;100(2):222-6
36- Seabra ML, Bignotto M, Pinto LR Jr, Tufik S. Randomized, double-blind
clinical trial, controlled with placebo, of the toxicology of chronic melatonin
treatment. J Pineal Res. 2000 Nov;29(4):193-200
37- Pires ML, Benedito-Silva AA, Pinto L, Souza L, Vismari L, Calil HM. Acute
effects of low doses of melatonin on the sleep of young healthy subjects. J
Pineal Res. 2001 Nov;31(4):326-32
38- Pinto LR Jr, Seabra Mde L, Tufik S. Different criteria of sleep latency and the
effect of melatonin on sleep consolidation. Sleep. 2004 Sep 15;27(6):1089-92
39- 123. Attenburrow ME, Cowen PJ, Sharpley AL. Low dose melatonin improves
sleep in healthy middle-aged subjects. Psychopharmacology (Berl). 1996
Jul;126(2):179-81
40- Garfinkel D, Laudon M, Nof D, Zisapel N. Improvement of sleep quality in
elderly people by controlled-release melatonin. Lancet. 1995 Aug
26;346(8974):541-4
41- Garfinkel D, Laudon M, Zisapel N. Improvement of sleep quality by controlledrelease melatonin in benzodiazepine-treated elderly insomniacs. Arch
Gerontol Geriatr. 1997 Mar-Apr;24(2):223-31
42- Haimov I, Lavie P, Laudon M, Herer P, Vigder C, Zisapel N. Melatonin
replacement therapy of elderly insomniacs. Sleep. 1995 Sep;18(7):598-603
43- Zhdanova IV, Wurtman RJ, Regan MM, Taylor JA, Shi JP, Leclair OU.
Melatonin treatment for age-related insomnia. J Clin Endocrinol Metab. 2001
Oct;86(10):4727-30
44- Hughes RJ, Sack RL, Lewy AJ. The role of melatonin and circadian phase in
age-related sleep-maintenance insomnia: assessment in a clinical trial of
melatonin replacement. Sleep. 1998;21(1):52-68
45- MacFarlane JG, Cleghorn JM, Brown GM, Streiner DL. The effects of
exogenous melatonin on the total sleep time and daytime alertness of chronic
insomniacs: a preliminary study. Biol Psychiatry. 1991 Aug 15;30(4):371-6
46- Andrade C, Srihari BS, Reddy KP, Chandramma L. Melatonin in medically ill
patients with insomnia: a double-blind, placebo-controlled study. J Clin
Psychiatry. 2001 Jan;62(1):41-5
47- Garfinkel D, Zisapel N, Wainstein J, Laudon M. Facilitation of benzodiazepine
discontinuation by melatonin: a new clinical approach. Arch Intern Med. 1999
Nov 8;159(20):2456-60
48- Dahlitz M, Alvarez B, Vignau J, English J, Arendt J, Parkes JD. Delayed sleep
phase syndrome response to melatonin.
Lancet. 1991 May
11;337(8750):1121-4
49- Kayumov L, Brown G, Jindal R, Buttoo K, Shapiro CM. A randomized,
double-blind, placebo-controlled crossover study of the effect of exogenous
melatonin on delayed sleep phase syndrome. Psychosom Med. 2001 JanFeb;63(1):40-8
50- Mundey K, Benloucif S, Harsanyi K, Dubocovich ML, Zee PC. Phasedependent treatment of delayed sleep phase syndrome with melatonin.
Sleep. 2005 Oct 1;28(10):1271-8
51- Nagtegaal JE, Kerkhof GA, Smits MG, Swart AC, Van Der Meer YG. Delayed
sleep phase syndrome: A placebo-controlled cross-over study on the effects
of melatonin administered five hours before the individual dim light melatonin
onset. J Sleep Res. 1998 Jun;7(2):135-43
52- Kunz D, Mahlberg R, Muller C, Tilmann A, Bes F. Melatonin in patients with
reduced REM sleep duration: two randomized controlled trials. J Clin
Endocrinol Metab. 2004 Jan;89(1):128-34
53- 148. Suhner A, Schlagenhauf P, Johnson R, Tschopp A, Steffen R.
Comparative study to determine the optimal melatonin dosage form for the
alleviation of jet lag. Chronobiol Int. 1998 Nov;15(6):655-66
54- Petrie K, Dawson AG, Thompson L, Brook R. A double-blind trial of melatonin
as a treatment for jet lag in international cabin crew. Biol Psychiatry. 1993 Apr
1;33(7):526-30
55- Paul MA, Gray G, Sardana TM, Pigeau RA. Melatonin and zopiclone as
facilitators of early circadian sleep in operational air transport crews. Aviat
Space Environ Med. 2004 May;75(5):439-43
56- Revell VL, Burgess HJ, Gazda CJ, Smith MR, Fogg LF, Eastman CI.
Advancing human circadian rhythms with afternoon melatonin and morning
intermittent bright light. J Clin Endocrinol Metab. 2006 Jan;91(1):54-9
57- Jorgensen KM, Witting MD. Does exogenous melatonin improve day sleep or
night alertness in emergency physicians working night shifts? Ann Emerg
Med. 1998 Jun;31(6):699-704
58- Dawson D, Encel N, Lushington K. Improving adaptation to simulated night
shift: timed exposure to bright light versus daytime melatonin administration.
Sleep. 1995 Jan;18(1):11-21
59- Folkard S, Arendt J, Clark M. Can melatonin improve shift workers' tolerance
of the night shift? Some preliminary findings. Chronobiol Int. 1993
Oct;10(5):315-20
60- Sharkey KM, Fogg LF, Eastman CI. Effects of melatonin administration on
daytime sleep after simulated night shift work. J Sleep Res. 2001
Sep;10(3):181-92
61- Yoon IY, Song BG. Role of morning melatonin administration and attenuation
of sunlight exposure in improving adaptation of night-shift workers.
Chronobiol Int. 2002 Sep;19(5):903-13
62- Yang CM, Spielman AJ, D'Ambrosio P, Serizawa S, Nunes J, Birnbaum J. A
single dose of melatonin prevents the phase delay associated with a delayed
weekend sleep pattern. Sleep. 2001 May 1;24(3):272-81
63- Middleton B, Arendt J, Stone BM. Complex effects of melatonin on human
circadian rhythms in constant dim light. J Biol Rhythms. 1997 Oct;12(5):46777
64- Naguib M, Samarkandi AH. Premedication with melatonin: a double-blind,
placebo-controlled comparison with midazolam. Br J Anaesth. 1999
Jun;82(6):875-80
65- Acil M, Basgul E, Celiker V, Karagoz AH, Demir B, Aypar U. Perioperative
effects of melatonin and midazolam premedication on sedation, orientation,
anxiety scores and psychomotor performance. Eur J Anaesthesiol. 2004
Jul;21(7):553-7
66- Dolberg OT, Hirschmann S, Grunhaus L. Melatonin for the treatment of sleep
disturbances in major depressive disorder. Am J Psychiatry. 1998
Aug;155(8):1119-21
67- Leppamaki S, Partonen T, Vakkuri O, Lonnqvist J, Partinen M, Laudon M.
Effect of controlled-release melatonin on sleep quality, mood, and quality of
life in subjects with seasonal or weather-associated changes in mood and
behavior. Eur Neuropsychopharmacol. 2003 May;13(3):137-45
68- Shamir E, Laudon M, Barak Y, Anis Y, Rotenberg V, Elizur A, Zisapel N.
Melatonin improves sleep quality of patients with chronic schizophrenia. J
Clin Psychiatry. 2000 May;61(5):373-7
69- Asayama K, Yamadera H, Ito T, Suzuki H, Kudo Y, Endo S. Double blind
study of melatonin effects on the sleep-wake rhythm, cognitive and noncognitive functions in Alzheimer type dementia. J Nippon Med Sch. 2003
Aug;70(4):334-41
70- O'Callaghan FJ, Clarke AA, Hancock E, Hunt A, Osborne JP.Use of
melatonin to treat sleep disorders in tuberous sclerosis. Dev Med Child
Neurol. 1999 Feb;41(2):123-6
71- Rosenberg SI, Silverstein H, Rowan PT, Olds MJ. Effect of melatonin on
tinnitus. Laryngoscope. 1998 Mar;108(3):305-10
72- Dowling GA, Mastick J, Colling E, Carter JH, Singer CM, Aminoff MJ.
Melatonin for sleep disturbances in Parkinson's disease. Sleep Med. 2005
Sep;6(5):459-66.
73- Sack RL, Brandes RW, Kendall AR, Lewy AJ. Entrainment of free-running
circadian rhythms by melatonin in blind people. N Engl J Med. 2000 Oct
12;343(15):1070-7
74- Sack RL, Lewy AJ, Blood ML, Stevenson J, Keith LD. Melatonin
administration to blind people: phase advances and entrainment. J Biol
Rhythms. 1991 Fall;6(3):249-61
75- Fischer S, Smolnik R, Herms M, Born J, Fehm HL. Melatonin acutely
improves the neuroendocrine architecture of sleep in blind individuals. J Clin
Endocrinol Metab. 2003 Nov;88(11):5315-20
76- Hack LM, Lockley SW, Arendt J, Skene DJ. The effects of low-dose 0.5-mg
melatonin on the free-running circadian rhythms of blind subjects. J Biol
Rhythms. 2003 Oct;18(5):420-9
77- Scheer FA, Van Montfrans GA, van Someren EJ, Mairuhu G, Buijs RM. Daily
night-time melatonin reduces blood pressure in male patients with essential
hypertension. Hypertension. 2004 Feb;43(2):192-7
78- Campos FL, da Silva-Junior FP, de Bruin VM, de Bruin PF. Melatonin
improves sleep in asthma: a randomized, double-blind, placebo-controlled
study. Am J Respir Crit Care Med. 2004 Nov 1;170(9):947-51
79- Shilo L, Dagan Y, Smorjik Y, Weinberg U, Dolev S, Komptel B, Shenkman L.
Effect of melatonin on sleep quality of COPD intensive care patients: a pilot
study. Chronobiol Int. 2000 Jan;17(1):71-6
Distúrbios do Sono: A Correlação Com Baixos Níveis de Testosterona
1- Andersen ML, Tufik S. The effects of testosterone on sleep and sleepdisordered breathing in men: its bidirectional interaction with erectile function.
Sleep Med Rev. 2008 Oct;12(5):365-79
2- Barrett-Connor E, Dam TT, Stone K, Harrison SL, Redline S, Orwoll E;
Osteoporotic Fractures in Men Study Group. The association of testosterone
levels with overall sleep quality, sleep architecture, and sleep-disordered
breathing. Clin Endocrinol Metab. 2008 Jul;93(7):2602-9
3- Penev PD. Association between sleep and morning testosterone levels in
older men. Sleep. 2007 Apr 1;30(4):427-32
Distúrbios do Sono: A Melhora Com a Reposição de Testosterona
1- Davis A, Gilbert K, Misiowiec P, Riegel B. Perceived effects of testosterone
replacement therapy in perimenopausal and postmenopausal women: an
internet pilot study. Health Care Women Int. 2003 Nov;24(9):831-48
-
CONTROLE DA PRESSÃO ARTERIAL
ATRAVÉS DA MODULAÇÃO HORMONAL
6
Hipertensão Arterial: A Associação Com Baixos Níveis de Melatonina
1- Cui HW, Zhang ZX, Gao MT, Liu Y, Su AH, Wang MY. Circadian rhythm of
melatonin and blood pressure changes in patients with essential
hypertension. Zhonghua Xin Xue Guan Bing Za Zhi. 2008 Jan;36(1):20-3
2- Zeman M, Dulková K, Bada V, Herichová I. Plasma melatonin concentrations
in hypertensive patients with the dipping and non-dipping blood pressure
profile. Life Sci. 2005 Mar 4;76(16):1795-803
3- Cagnacci A, Arangino S, Angiolucci M, Melis GB, Tarquini R, Renzi A, Volpe
A. Different circulatory response to melatonin in postmenopausal women
without and with hormone replacement therapy. J Pineal Res. 2000
Oct;29(3):152-8
4- Rapoport SI, Shatalova AM, Malinovskaia NK, Vettenberg L. Melatonin
production in hypertensive patients. Klin Med (Mosk). 2000;78(6):21-4
5- Rapoport SI, Shatalova AM, Oraevskii VN, Malinovskaia NK, Vetterberg L.
Melatonin production in hypertonic patients during magnetic storms. Ter Arkh.
2001;73(12):29-33
6- Tetsuo M, Polinsky RJ, Markey SP, Kopin IJ. Urinary 6-hydroxymelatonin
excretion in patients with orthostatic hypotension. J Clin Endocrinol Metab.
1981 Sep;53(3):607-10
Hipertensão Arterial: A Melhora Com a Reposição de Melatonina
1- Rechciński T, Trzos E, Wierzbowska-Drabik K, Krzemińska-Pakuła M,
Kurpesa M. Melatonin for nondippers with coronary artery disease:
assessment of blood pressure profile and heart rate variability. Hypertens
Res. 2010 Jan;33(1):56-61
2- Reiter RJ, Tan DX, Korkmaz A. The circadian melatonin rhythm and its
modulation: possible impact on hypertension. J Hypertens. 2009 Aug;27
Suppl 6:S17-20.
3- Rechciński T, Kurpesa M, Trzos E, Krzeminska-Pakuła M. The influence of
melatonin supplementation on circadian pattern of blood pressure in patients
with coronary artery disease--preliminary report. Pol Arch Med Wewn. 2006
Jun;115(6):520-8
4- Cagnacci A, Arangino S, Angiolucci M, Maschio E, Melis GB. Influences of
melatonin administration on the circulation of women. Am J Physiol. 1998
Feb;274(2 Pt 2):R335-8
5- Cagnacci A, Arangino S, Angiolucci M, Maschio E, Longu G, Melis GB.
Potentially beneficial cardiovascular effects of melatonin administration in
women. J Pineal Res. 1997 Jan;22(1):16-9
6- Cagnacci A, Arangino S, Angiolucci M, Melis GB, Facchinetti F, Malmusi S,
Volpe A. Effect of exogenous melatonin on vascular reactivity and nitric oxide
in postmenopausal women: role of hormone replacement therapy. Clin
Endocrinol (Oxf). 2001 Feb;54(2):261-6
7- Arangino S, Cagnacci A, Angiolucci M, Vacca AM, Longu G, Volpe A, Melis
GB. Effects of melatonin on vascular reactivity, catecholamine levels, and
blood pressure in healthy men. Am J Cardiol. 1999 May 1;83(9):1417-9
8- Burgess HJ, Sletten T, Savic N, Gilbert SS, Dawson D. Effects of bright light
and melatonin on sleep propensity, temperature, and cardiac activity at night.
J Appl Physiol. 2001 Sep;91(3):1214-22
9- Nishiyama K, Yasue H, Moriyama Y, Tsunoda R, Ogawa H, Yoshimura M,
Kugiyama K. Acute effects of melatonin administration on cardiovascular
autonomic regulation in healthy men. Am Heart J. 2001 May;141(5):E9
10- Lusardi P, Preti P, Savino S, Piazza E, Zoppi A, Fogari R. Effect of bedtime
melatonin ingestion on blood pressure of normotensive subjects. Blood Press
Monit. 1997 Apr;2(2):99-103
11- Kitajima T, Kanbayashi T, Saitoh Y, Ogawa Y, Sugiyama T, Kaneko Y,
Sasaki Y, Aizawa R, Shimisu T. The effects of oral melatonin on the
autonomic function in healthy subjects. Psychiatry Clin Neurosci. 2001
Jun;55(3):299-300
12- Zaslavskaia RM, Biiasilov NS, Akhmetov Kzh, Teiblium MM. Capozide-50
alone and in combination with melatonin in therapy of hypertension. Klin Med
(Mosk). 2000;78(11):39-41
13- Zaslavskaia RM, Komarov FI, Shakirova AN, Teiblium MM, Akhmetov KZh.
Effect of moxonidine monotherapy and in combination with melatonin on
hemodynamic parameters in patients with arterial hypertension. Klin Med
(Mosk). 2000;78(4):41-4
14- Zaslavskaia RM, Komarov FI, Goncharov LF, Goncharova ZF, Makarova LA.
Comparative study of the effectiveness of Cozaar monotherapy and Cozaar
and melatonin combined therapy in aged patients with hypertension. Klin Med
(Mosk). 1998;76(12):49-51
15- Zaslavskaia RM, Shakirova AN, Komarov FI, Teiblium MM, Akhmetov KZh.
Effects of melatonin alone and in combination with aceten on chronostructure
of diurnal hemodynamic rhythms in patients with hypertension stage II. Ter
Arkh. 1999;71(12):21-4
16- Zaslavskaia RM, Komarov FI, Makarova LA, Shakirova AN, Narmanova OZh,
Biiasilov N. Time-dependent effects of antihypertensive agents and
chronocorrecting action of melatonin in patients with arterial hypertension.
Vestn Ross Akad Med Nauk. 2000;(8):36-41
Hipertensão Arterial: A Associação Com Baixos Níveis de DHEA
1- Herman WA, Seńko A, Korczowska I, Łacka K. Could serum DHEA and
DHEAS levels be good risk predictors of metabolic syndrome and
osteoporosis in the population of ageing men? Pol Merkur Lekarski. 2009
Sep;27(159):197-201
2- Johannes CB, Stellato RK, Feldman HA, Longcope C, McKinlay JB. Relation
of dehydroepiandrosterone and dehydroepiandrosterone sulfate with
cardiovascular disease risk factors in women: longitudinal results from the
Massachusetts Women's Health Study. J Clin Epidemiol. 1999 Feb;52(2):95103
3- Nowaczynski W, Fragachan F, Silah J, Millette B, Genest J. Further evidence
of altered adrenocortical function in hypertension. Dehydroepiandrosterone
excretion rate. Can J Biochem 1968;46(9):1031-8
4- Okamoto K, Yagyu K, Sasaki R. The relationship between serum
dehydroepiandrosterone sulfate levels and factors associated with
cardiovascular diseases: a cross-sectional study in Japan. Nippon Koshu
Eisei Zasshi. 1995;42(2):78-83
5- Legrain S, Berr C, Frenoy N, Gourlet V, Debuire B, Baulieu EE.
Dehydroepiandrosterone sulfate in a long-term care aged population.
Gerontology. 1995;41(6):343-51
6- Suzuki M, Kanazawa A, Hasegawa M, Hattori Y, Harano Y. A close
association between insulin resistance and dehydroepiandrosterone sulfate in
subjects with essential hypertension. Endocr J. 1999;46(4):521-8
7- Maccario M, Mazza E, Ramunni J, Oleandri SE, Savio P, Grottoli S, Rossetto
R, Procopio M, Gauna C, Ghigo E. Relationships between
dehydroepiandrosterone-sulphate and anthropometric, metabolic and
hormonal variables in a large cohort of obese women. Clin Endocrinol (Oxf).
1999;50(5):595-600
8- Barna I, Feher T, de Chatel R. Relationship between blood pressure
variability and serum dehydroepiandrosterone sulfate levels. Am J Hypertens.
1998 May;11(5):532-8
Hipertensão Arterial: A Melhora Com a Reposição de DHEA
1- Dockery F, Bulpitt CJ, Donaldson M, Fernandez S, Rajkumar C. The
relationship between androgens and arterial stiffness in older men. J Am
Geriatr Soc. 2003 Nov;51(11):1627-32
2- Hampl V, Bibova J, Povysilova V, Herget J. Dehydroepiandrosterone
sulphate reduces chronic hypoxic pulmonary hypertension in rats. Eur Respir
J. 2003 May;21(5):862-5
3- Bonnet S, Dumas-de-La-Roque E, Begueret H, Marthan R, Fayon M, Dos
Santos P, Savineau JP, Baulieu EE. Dehydroepiandrosterone (DHEA)
prevents and reverses chronic hypoxic pulmonary hypertension. Proc Natl
Acad Sci USA. 2003 Aug 5;100(16):9488-93
Hipertensão Arterial: A Associação Com Baixos Níveis do Hormônio do
Crescimento
1- Landin-Wilhelmsen K, Wilhelmsen L, Lappas G, Rosen T, Lundstedt G,
Lundberg PA, Bengtssopn BA. Serum insulin-like growth factor 1 in a random
population sample of men and women: relation to age, sex, smoking habits,
coffee consumption and physical activity, blood pressure and concentrations
of plasma lipids, fibrinogen, parathyroid hormone and osteocalcin. Clin
Endocrinol (Oxf). 1994 Sep;41(3):351-7
Hipertensão Arterial: A Melhora Com a Reposição do Hormônio do
Crescimento
1- Holmer H, Svensson J, Rylander L, Johannsson G, Rosén T, Bengtsson BA,
Thorén M, Höybye C, Degerblad M, Bramnert M, Hägg E, Edén Engström B,
Ekman B, Norrving B, Hagmar L, Erfurth EM. Nonfatal stroke, cardiac
disease, and diabetes mellitus in hypopituitary patients on hormone
replacement including growth hormone. J Clin Endocrinol Metab. 2007
Sep;92(9):3560-7
2- Feldt-Rasmussen B, Lange M, Sulowicz W, Gafter U, Lai KN, Wiedemann J,
Christiansen JS, El Nahas M; APCD Study Group. Growth hormone
treatment during hemodialysis in a randomized trial improves nutrition, quality
of life, and cardiovascular risk. J Am Soc Nephrol. 2007 Jul;18(7):2161-71
3- Graham MR, Baker JS, Evans P, Kicman A, Cowan D, Hullin D, Davies B.
Evidence for a decrease in cardiovascular risk factors following recombinant
growth hormone administration in abstinent anabolic-androgenic steroid
users. Growth Horm IGF Res. 2007 Jun;17(3):201-9
4- van Dijk M, Bannink EM, van Pareren YK, Mulder PG, Hokken-Koelega AC.
Risk factors for diabetes mellitus type 2 and metabolic syndrome are
comparable for previously growth hormone-treated young adults born small
for gestational age (sga) and untreated short SGA controls. J Clin Endocrinol
Metab. 2007 Jan;92(1):160-5
5- Caidahl K, Eden S, Bengtsson BA. Cardiovascular and renal effects of growth
hormone. Clin Endocrinol (Oxf). 1994 Mar;40(3):393-400
Hipertensão Arterial: A Associação Com Baixos Níveis de IGF-1
1- Sesti G, Sciacqua A, Scozzafava A, Vatrano M, Angotti E, Ruberto C, Santillo
E, Parlato G, Perticone F. Effects of growth hormone and insulin-like growth
factor-1 on cardiac hypertrophy of hypertensive patients. J Hypertens. 2007
Feb;25(2):471-7
2- Hopkins KD, Lehmann ED, Gosling RG, Parker JR, Sönksen PH.
Biochemical correlates of aortic distensibility in vivo in normal subjects. Clin
Sci (Lond). 1993 Jun;84(6):593-7
3- Lawlor DA, Ebrahim S, Smith GD, Cherry L, Watt P, Sattar N. The
association of insulin-like-growth factor 1 (IGF-1) with incident coronary heart
disease in women: findings from the prospective British Women's Heart and
Health Study. Atherosclerosis. 2008 Nov;201(1):198-204
4- Paolisso G, Tagliamonte MR, Rizzo MR, Rotondi M, Gualdiero P,
Gambardella A, Barbieri M, Carella C, Giugliano D, Varricchio M. Mean
arterial blood pressure and serum levels of the molar ratio of insulin-like
growth factor-1 to its binding protein-3 in healthy centenarians.J Hypertens.
1999 Jan;17(1):67-73.
Hipertensão Arterial: A Associação Com Baixos Níveis dos Hormônios
Tireoidianos
1- Duan Y, Wang X, Peng W, Feng Y, Tang W, Wu X, Mao X, Bo R, Li W, Chen
J, Qin Y, Liu C, Liu C. Gender-specific associations between subclinical
hypothyroidism and blood pressure in Chinese adults. Endocrine. 2010 (2009
Oct 14: Epub ahead of print)
2- Kileĭnikov DV, Makusheva MV, Volkov VS. Pathogenesis of arterial
hypertension in patients with primary hypothyroidism] Klin Med (Mosk).
2009;87(5):30-2
3- Velkoska Nakova V, Krstevska B, Bosevski M, Dimitrovski Ch, Serafimoski V.
Dyslipidaemia and hypertension in patients with subclinical hypothyroidism.
Prilozi. 2009 Dec;30(2):93-102
4- Guasti L, Marino F, Cosentino M, Cimpanelli M, Rasini E, Piantanida E,
Vanoli P, De Palma D, Crespi C, Klersy C, Maroni L, Loraschi A, Colombo C,
Simoni C, Bartalena L, Lecchini S, Grandi AM, Venco A. Pain perception,
blood pressure levels, and peripheral benzodiazepine receptors in patients
followed for differentiated thyroid carcinoma: a longitudinal study in
hypothyroidism and during hormone treatment. Clin J Pain. 2007 JulAug;23(6):518-23
5- Kotsis V, Alevizaki M, Stabouli S, Pitiriga V, Rizos Z, Sion M, Zakopoulos N.
Hypertension and hypothyroidism: results from an ambulatory blood pressure
monitoring study. J Hypertens. 2007 May;25(5):993-9
6- Biondi B, Klein I. Hypothyroidism as a risk factor for cardiovascular disease.
Endocrine. 2004 Jun;24(1):1-13
7- Streeten DH, Anderson GH Jr, Howland T, Chiang R, Smulyan H. Effects of
thyroid function on blood pressure. Recognition of hypothyroid hypertension.
Hypertension. 1988 Jan;11(1):78-83
8- Fommei E, Iervasi G. The role of thyroid hormone in blood pressure
homeostasis: evidence from short-term hypothyroidism in humans. J Clin
Endocrinol Metab. 2002 May;87(5):1996-2000
9- Saito I, Ito K, Saruta T. Hypothyroidism as a cause of hypertension.
Hypertension. 1983 Jan-Feb;5(1):112-5
Hipertensão Arterial: A Melhora Com a Reposição dos Hormônios Tireoidianos
1- Fuller H Jr, Spittell JA Jr, McConahey WM, Schirger A. Myxedema and
hypertension. Postgrad Med. 1966 Oct;40(4):425-8
2- Gasiorowski W, Plazinska MT. Arterial hypertension associated with hyper
and hypothyroidism. Pol Tyg Lek. 1992 Nov 2-9;47(44-45):1009-10
Hipertensão Arterial: A Associação Com Baixos Níveis de Estradiol
1- Harrison-Bernard LM, Schulman IH, Raij L. Postovariectomy hypertension is
linked to increased renal AT1 receptor and salt sensitivity. Hypertension.
2003 Dec;42(6):1157-63
2- Clark JT, Chakraborty-Chatterjee M, Hamblin M, Wyss JM, Fentie IH.
Estrogen depletion differentially affects blood pressure depending on age in
Long-Evans rats. Endocrine. 2004 Nov;25(2):173-86
3- Peng N, Clark JT, Wei CC, Wyss JM. Estrogen depletion increases blood
pressure and hypothalamic norepinephrine in middle-aged spontaneously
hypertensive rats. Hypertension. 2003 May;41(5):1164-7
Hipertensão Arterial: A Melhora Com a Reposição de Estradiol
1- Mercuro G, Zoncu S, Piano D, Pilia I, Lao A, Melis GB, Cherchi A. Estradiol17beta reduces blood pressure and restores the normal amplitude of the
circadian blood pressure rhythm in postmenopausal hypertension. Am J
Hypertens. 1998 Aug;11(8 Pt 1):909-13
2- Del Rio G, Velardo A, Zizzo G, Avogaro A, Cipolli C, Della Casa L, Marrama
P, MacDonald IA. Effect of estradiol on the sympathoadrenal response to
mental stress in normal men. J Clin Endocrinol Metab. 1994 Sep;79(3):83640
3- Pang SC, Greendale GA, Cedars MI, Gambone JC, Lozano K, Eggena P,
Judd HL. Long-term effects of transdermal estradiol with and without
medroxyprogesterone acetate. Fertil Steril. 1993 Jan;59(1):76-82
4- Angerer P, Stork S, von Schacky C. Influence of 17beta-oestradiol on blood
pressure of postmenopausal women at highvascular risk. J Hypertens. 2001
Dec;19(12):2135-42
5- Manhem K, Ahlm H, Dellborg M, Milsom I. Acute effects of transdermal
estrogen in postmenopausal women with coronary artery disease. Using a
clinically relevant estrogen dose and concurrent antianginal therapy.
Cardiology. 2000;94(2):86-90 (“resting diastolic blood pressure was
significantly decreased due to estrogen”)
6- Seely EW, Walsh BW, Gerhard MD, Williams GH. Estradiol with or without
progesterone and ambulatory blood pressure in postmenopausal women.
Hypertension. 1999 May;33(5):1190-4
Hipertensão Arterial: A Melhora Com a Reposição de Estradiol e Progesterona
1- Junge W, El-Samalouti V, Gerlinger C, Schaefers M. Effects of menopausal
hormone therapy on hemostatic parameters, blood pressure, and body
weight: open-label comparison of randomized treatment with estradiol plus
drospirenone versus estradiol plus norethisterone acetate. Eur J Obstet
Gynecol Reprod Biol. 2009 Dec;147(2):195-200
2- Ichikawa A, Sumino H, Ogawa T, Ichikawa S, Nitta K. Effects of long-term
transdermal hormone replacement therapy on the renin-angiotensinaldosterone system, plasma bradykinin levels and blood pressure in
normotensive postmenopausal women. Geriatr Gerontol Int. 2008
Dec;8(4):259-64
3- Kaya C, Cengiz SD, Cengiz B, Akgun G. Long-term effects of low-dose
17beta-estradiol plus dydrogesterone on 24-h ambulatory blood pressure in
healthy postmenopausal women: a 1-year, randomized, prospective study.
Gynecol Endocrinol. 2007 Oct;23 Suppl 1:62-7
4- Preston RA, Norris PM, Alonso AB, Ni P, Hanes V, Karara AH. Randomized,
placebo-controlled trial of the effects of drospirenone-estradiol on blood
pressure and potassium balance in hypertensive postmenopausal women
receiving hydrochlorothiazide. Menopause. 2007 May-Jun;14(3 Pt 1):408-14
5- Gerhard M, Walsh BW, Tawakol A, Haley EA, Creager SJ, Seely EW, Ganz
P, Creager MA. Estradiol therapy combined with progesterone and
endothelium-dependent vasodilation in postmenopausal women. Circulation.
1998 Sep 22;98(12):1158-63
6- Kornhauser C, Malacara JM, Garay ME, Perez-Luque EL. The effect of
hormone replacement therapy on blood pressure and cardiovascular risk
factors in menopausal women with moderate hypertension. J Hum Hypertens.
1997 Jul;11(7):405-11
Hipertensão Arterial: A Associação Com Baixos Níveis de Testosterona
1- Ishikura F, Asanuma T, Beppu S. Low testosterone levels in patients with
mild hypertension recovered after antidepressant therapy in a male
climacterium clinic. Hypertens Res. 2008 Feb;31(2):243-8
2- Hughes GS, Ringer TV, Watts KC, DeLoof MJ, Francom SF, Spillers CR.
Fish oil produces an atherogenic lipid profile in hypertensive men.
Atherosclerosis. 1990 Oct;84(2-3):229-37
3- Tuev AV, Lunegova NV. Several indicators of hormonal homeostasis
(hypophysis - gonads) in patients with hypertension. Ross Med Zh.
1992;(3):10-3
4- Phillips GB, Jing TY, Resnick LM, Barbagallo M, Laragh JH, Sealey JE. Sex
hormones and hemostatic risk factors for coronary heart disease in men with
hypertension. J Hypertens. 1993 Jul;11(7):699-702
Hipertensão Arterial: A Melhora Com a Reposição de Testosterona
1- Shapiro J, Christiana J, Frishman WH. Testosterone and other anabolic
steroids as cardiovascular drugs. Am J Ther. 1999 May;6(3):167-74
-
CONTROLE DA GORDURA CORPORAL E
PROFILAXIA E TRATAMENTO DA OBESIDADE
ATRAVÉS DA MODULAÇÃO HORMONAL
7
Obesidade: A Associação Com Baixos Níveis de Melatonina
1- Blaicher W, Imhof MH, Gruber DM, Schneeberger C, Sator MO, Huber JC.
Endocrinological disorders. Focusing on melatonin's interactions. Gynecol
Obstet Invest. 1999;48(3):179-82
2- Birketvedt GS, Florholmen J, Sundsfjord J, Osterud B, Dinges D, Bilker W,
Stunkard A. Behavioral and neuroendocrine characteristics of the night-eating
syndrome. JAMA. 1999 Aug 18;282(7):657-63
3- Ostrowska Z, Zwirska-Korczala K, Buntner B, Pardela M, Drozdz M.
Association of body mass and body fat distribution with serum melatonin
levels in obese women either non-operated or after jejunoileostomy. Endocr
Regul. 1996 Mar;30(1):33-40
Obesidade: A melhora Com a Reposição de Melatonina
1- Hussein MR, Ahmed OG, Hassan AF, Ahmed MA. Intake of melatonin is
associated with amelioration of physiological changes, both metabolic and
morphological pathologies associated with obesity: an animal model. Int J
Exp Pathol. 2007 Feb;88(1):19-29
2- Rasmussen DD, Boldt BM, Wilkinson CW, Yellon SM, Matsumoto AM. Daily
melatonin administration at middle age suppresses male rat visceral fat,
plasma leptin, and plasma insulin to youthful levels. Endocrinology. 1999
Feb;140(2):1009-12
3- Wolden-Hanson T, Mitton DR, McCants RL, Yellon SM, Wilkinson CW,
Matsumoto AM, Rasmussen DD. Daily melatonin administration to middleaged male rats suppresses body weight, intraabdominal adiposity, and
plasma leptin and insulin independent of food intake and total body fat.
Endocrinology. 2000 Feb;141(2):487-97
4- Rasmussen DD, Mitton DR, Larsen SA, Yellon SM. Aging-dependent
changes in the effect of daily melatonin supplementation on rat metabolic and
behavioral responses. J Pineal Res 2001 Aug;31(1):89-94
5- Bartness TJ, Wade GN. Body weight, food intake and energy regulation in
exercising and melatonin-treated Siberian hamsters. Physiol Behav. 1985
Nov;35(5):805-8
6- Zeman M, Vyboh P, Jurani M, Lamosova D, Kostal L, Bilcik B, Blazicek P,
Juraniova E. Effects of exogenous melatonin on some endocrine, behavioral
and metabolic parameters in Japanese quail Coturnix coturnix japonica.
Comp Biochem Physiol Comp Physiol. 1993 Jun;105(2):323-8
Obesidade: A Associação Com Baixos Níveis dos Hormônios Tideoidianos
1- Rotondi M, Leporati P, La Manna A, Pirali B, Mondello T, Fonte R, Magri F,
Chiovato L. Raised serum TSH levels in patients with morbid obesity: is it
enough to diagnose subclinical hypothyroidism? Eur J Endocrinol. 2009
Mar;160(3):403-8
2- Verma A, Jayaraman M, Kumar HK, Modi KD. Hypothyroidism and obesity.
Cause or effect? Saudi Med J. 2008 Aug;29(8):1135-8
3- Resta O, Pannacciulli N, Di Gioia G, Stefano A, Barbaro MP, De Pergola G.
High prevalence of previously unknown subclinical hypothyroidism in obese
patients referred to a sleep clinic for sleep disordered breathing. Nutr Metab
Cardiovasc Dis. 2004 Oct;14(5):248-53
4- Jung CH, Sung KC, Shin HS, Rhee EJ, Lee WY, Kim BS, Kang JH, Kim H,
Kim SW, Lee MH, Park JR, Kim SW. Thyroid dysfunction and their relation to
cardiovascular risk factors such as lipid profile, hsCRP, and waist hip ratio in
Korea. Korean J Intern Med. 2003 Sep;18(3):146-53
5- Rimm AA, Werner LH, Yserloo BV, Bernstein RA. Relationship of ovesity and
disease in 73,532 weight-conscious women. Public Health Rep. 1975 JanFeb;90(1):44-54
Obesidade: A melhora Com a Reposição dos Hormônios Tideoidianos
1- Moore R, Grant AM, Howard AN, Mills IH. Treatment of obesity with
triiodothyronine and a very-low-calorie liquid formula diet. Lancet. 1980 Feb
2;1(8162):223-6
2- Gelvin EP, Kenigsberg S, Boyd LJ. Results of addition of liothyronine to a
weight-reducing regimen.J Am Med Assoc. 1959 Jul 25;170(13):1507-12
3- Rozen R, Abraham G, Falcou R, Apfelbaum M. Effects of a 'physiological'
dose of triiodothyronine on obese subjects during a protein-sparing diet. Int J
Obes. 1986;10(4):303-12
4- Pasquali R, Baraldi G, Biso P, Piazzi S, Patrono D, Capelli M, Melchionda N.
Effect of 'physiological' doses of triiodothyronine replacement on the
5-
6-
7-
8-
9-
hormonal and metabolic adaptation to short-term semistarvation and to lowcalorie diet in obese patients. Clin Endocrinol (Oxf). 1984 Oct;21(4):357-67
Koppeschaar HP, Meinders AE, Schwarz F. Metabolic responses in grossly
obese subjects treated with a very-low-calorie diet with and without
triiodothyronine treatment. Int J Obes. 1983;7(2):133-41
Koppeschaar HP, Meinders AE, Schwarz F. The effect of a low-calorie diet
alone and in combination with triiodothyronine therapy on weight loss and
hypophyseal thyroid function in obesity. Int J Obes. 1983;7(2):123-31
Wilson JH, Lamberts SW. The effect of triiodothyronine on weight loss and
nitrogen balance of obese patients on a very-low-calorie liquid-formula diet.
Int J Obes. 1981;5(3):279-82
Moore R, Mehrishi JN, Verdoorn C, Mills IH. The role of T3 and its receptor in
efficient metabolisers receiving very-low-calorie diets. Int J Obes.
1981;5(3):283-6
Moore R, Grant AM, Howard AN, Mills IH. Treatment of obesity with
triioidothyronine and a very low caorie liquid formula diet. Lancet 1980 Feb.
2;223-6
Obesidade: A Associação Com Baixos Níveis de DHEA
1- Rabijewski M, Kozakowski J, Zgliczyński W. The relationship between
testosterone and dehydroepiandrosterone sulfate concentrations, insulin
resistance and visceral obesity in elderly men] Endokrynol Pol. 2005 NovDec;56(6):897-903
2- Blanchette S, Marceau P, Biron S, Brochu G, Tchernof A. Circulating
progesterone and obesity in men. Horm Metab Res. 2006 May;38(5):330-5
3- Savastano S, Belfiore A, Guida B, Angrisani L, Orio F Jr, Cascella T, Milone
F, Micanti F, Saldalamacchia G, Lombardi G, Colao A. Role of
dehydroepiandrosterone sulfate levels on body composition after
laparoscopic adjustable gastric banding in pre-menopausal morbidly obese
women. J Endocrinol Invest. 2005 Jun;28(6):509-15
4- Diamond P, Cusan L, Gomez JL, Belanger A, Labrie F. Metabolic effects of
12-month percutaneous dehydroepiandrosterone replacement therapy in
postmenopausal women. J Endocrinol. 1996;150 Suppl:S43-50
5- Herranz L, Megia A, Grande C, Gonzalez-Gancedo P, Pallardo F.
Dehydroepiandrosterone sulphate, body fat distribution and insulin in obese
men. Int J Obes Relat Metab Disord 1995;19(1):57-60
6- De Pergola G, Zamboni M, Sciaraffia M, Turcato E, Pannacciulli N, Armellini
F, Giorgino F, Perrini S, Bosello O, Giorgino R. Body fat accumulation is
possibly responsible for lower dehydroepiandrosterone circulating levels in
premenopausal obese women. Int J Obes Relat Metab Disord. 1996
Dec;20(12):1105-10
7- De Pergola G, Giagulli VA, Garruti G, Cospite MR, Giorgino F, Cignarelli M,
Giorgino R.
Low dehydroepiandrosterone circulating levels in
premenopausal obese women with very high body mass index. Metabolism.
1991 Feb;40(2):187-90
8- De Pergola G. The adipose tissue metabolism: role of testosterone and
dehydroepiandrosterone. Int J Obes Relat Metab Disord. 2000 Jun;24 Suppl
2:S59-63
Obesidade: A melhora Com a Reposição de DHEA
1- Villareal DT, Holloszy JO, Kohrt WM. Effects of DHEA replacement on bone
mineral density and body composition in elderly women and men. Clin
Endocrinol (Oxf). 2000;53(5):561-8
2- Nestler JE, Barlascini CO, Clore JN, Blackard WG. Dehydroepiandrosterone
reduces serum low density lipoprotein levels and body fat but does not alter
insulin sensitivity in normal men. J Clin Endocrinol Metab. 1988;66(1):57-61
3- Abrahamsson L, Hackl H. Catabolic effects and the influence on hormonal
variables under treatment with Gynodian-Depot or dehydroepiandrosterone
(DHEA) oenanthate. Maturitas. 1981;3(3-4):225-34
Obesidade e Adiposidade Visceral: A Associação Com Baixos Níveis do
Hormônio do Crescimento
1- Savastano S, Angrisani L, Di Somma C, Rota F, Savanelli MC, Cascella T,
Orio F, Lombardi G, Colao A. Relationship between growth hormone/insulinlike growth factor-1 axis integrity and voluntary weight loss after gastric
banding surgery for severe obesity. Obes Surg. 2010 Feb;20(2):211-20
2- Irving BA, Weltman JY, Patrie JT, Davis CK, Brock DW, Swift D, Barrett EJ,
Gaesser GA, Weltman A. Effects of exercise training intensity on nocturnal
growth hormone secretion in obese adults with the metabolic syndrome. J
Clin Endocrinol Metab. 2009 Jun;94(6):1979-86
3- Utz AL, Yamamoto A, Hemphill L, Miller KK. Growth hormone deficiency by
growth hormone releasing hormone-arginine testing criteria predicts
increased cardiovascular risk markers in normal young overweight and obese
women. J Clin Endocrinol Metab. 2008 Jul;93(7):2507-14
4- Kelestimur F, Popovic V, Leal A, Van Dam PS, Torres E, Perez Mendez LF,
Greenman Y, Koppeschaar HP, Dieguez C, Casanueva FF. Effect of obesity
and morbid obesity on the growth hormone (GH) secretion elicited by the
combined GHRH + GHRP-6 test. Clin Endocrinol (Oxf). 2006 Jun;64(6):66771
5- Beshyah SA, Freemantle C, Thomas E, Rutherford O, Page B, Murphy M,
Johnston DG. Abnormal body composition and reduced bone mass in growth
hormone deficient hypopituitary adults. Clin Endocrinol (Oxf)
1995
Feb;42(2):179-89
6- Attanasio AF, Bates PC, Ho KK, Webb SM, Ross RJ, Strasburger CJ,
Bouillon R, Crowe B, Selander K, Valle D, Lamberts SW; Hypoptiuitary
Control and Complications Study International Advisory Board. Human
growth hormone replacement in adult hypopituitary patients: long-term effects
on body composition and lipid status--3-year results from the HypoCCS
Database. J Clin Endocrinol Metab. 2002 Apr;87(4):1600-6
7- Stouthart PJ, de Ridder CM, Rekers-Mombarg LT, van der Waal HA.
Changes in body composition during 12 months after discontinuation of
growth hormone therapy in young adults with growth hormone deficiency from
childhood. J Pediatr Endocrinol Metab. 1999 Apr;12 Suppl 1:335-8
8- Biller BM, Sesmilo G, Baum HB, Hayden D, Schoenfeld D, Klibanski A.
Withdrawal of long-term physiological growth hormone (GH) administration:
differential effects on bone density and body composition in men withadultonset GH deficiency. J Clin Endocrinol Metab. 2000 Mar;85(3):970-6
9- Kohno H, Ueyama N, Honda S. Unfavourable impact of growth hormone (GH)
discontinuation on body composition and cholesterol profiles after the
completion of height growth in GH-deficient young adults. Diabetes Obes
Metab. 1999 Sep;1(5):293-6
10- Kuromaru R, Kohno H, Ueyama N, Hassan HM, Honda S, Hara T. Long-term
prospective study of body composition and lipid profiles during and after
growth hormone (GH) treatment in children with GH deficiency: genderspecific metabolic effects. J Clin Endocrinol Metab. 1998 Nov;83(11):3890-6
11- Vahl N, Juul A, Jorgensen JO, Orskov H, Skakkebaek NE, Christiansen JS.
Continuation of growth hormone (GH) replacement in GH-deficient patients
during transition from childhood to adulthood: a two-year placebo-controlled
study. J Clin Endocrinol Metab. 2000 May;85(5):1874-81
12- Norrelund H, Vahl N, Juul A, Moller N, Alberti KG, Skakkebaek NE,
Christiansen JS, Jorgensen JO. Continuation of growth hormone (GH)
therapy in GH-deficient patients during transition from childhood to adulthood:
impact on insulin sensitivity and substrate metabolism. J Clin Endocrinol
Metab. 2000 May;85(5):1912-7
13- Johannsson G. What happens when growth hormone is discontinued at
completion of growth? Metabolic aspects. J Pediatr Endocrinol Metab.
2000;13 Suppl 6:1321-6
Obesidade e Adiposidade Visceral: A melhora Com a Reposição do Hormônio
do Crescimento
1- Mekala KC, Tritos NA. Effects of recombinant human growth hormone
therapy in obesity in adults: a meta analysis. . J Clin Endocrinol Metab. 2009
Jan;94(1):130-7
2- Graham MR, Baker JS, Evans P, Kicman A, Cowan D, Hullin D, Davies B.
Evidence for a decrease in cardiovascular risk factors following recombinant
growth hormone administration in abstinent anabolic-androgenic steroid
users. Growth Horm IGF Res. 2007 Jun;17(3):201-9
3- Beauregard C, Utz AL, Schaub AE, Nachtigall L, Biller BM, Miller KK,
Klibanski A. Growth hormone decreases visceral fat and improves
cardiovascular risk markers in women with hypopituitarism: a randomized,
placebo-controlled study. J Clin Endocrinol Metab. 2008 Jun;93(6):2063-71
4- Lin HY, Lin SP, Tsai LP, Chao MC, Chen MR, Chuang CK, Huang CY, Tsai
FJ, Chou IC, Chiu PC, Huang CH, Yen JL, Lin JL, Kuo PL. Effects of growth
hormone treatment on height, weight, and obesity in Taiwanese patients with
Prader-Willi syndrome. Chin Med Assoc. 2008 Jun;71(6):305-9
5- Follin C, Thilén U, Ahrén B, Erfurth EM. Improvement in cardiac systolic
function and reduced prevalence of metabolic syndrome after two years of
growth hormone (GH) treatment in GH-deficient adult survivors of childhoodonset acute lymphoblastic leukemia. . J Clin Endocrinol Metab. 2006
May;91(5):1872-5
6- Halpern A, Mancini MC, Cercato C, Villares SM, Costa AP. Effects of growth
hormone on anthropometric and metabolic parameters in android. Obesity.
Arq Bras Endocrinol Metabol. 2006 Feb;50(1):68-73
7- Ahn CW, Kim CS, Nam JH, Kim HJ, Nam JS, Park JS, Kang ES, Cha BS, Lim
SK, Kim KR, Lee HC, Huh KB. Effects of growth hormone on insulin
resistance and atherosclerotic risk factors in obese type 2 diabetic patients
with poor glycaemic control. Clin Endocrinol (Oxf). 2006 Apr;64(4):444-9
8- Rudman D, Feller AG, Nagraj HS, Gergans GA, Lalitha PY, Goldberg AF,
Schlenker RA, Cohn L, Rudman IW, Mattson DE. Effects of human growth
hormone in men over 60 years old. N Engl J Med. 1990 Jul 5;323(1):1-6
9- Rudman D, Feller AG, Cohn L, Shetty KR, Rudman IW, Draper MW. Effects
of human growth hormone on body composition in elderly men. Horm Res
1991;36 Suppl 1:73-81
10- Bengtsson BA, Eden S, Lonn L, Kvist H, Stokland A, Lindstedt G, Bosaeus I,
Tolli J, Sjostrom L, Isaksson OG. Treatment of adults with growth hormone
(GH) deficiency with recombinant human GH. J Clin Endocrinol Metab. 1993
Feb;76(2):309-17
11- Munzer T, Harman SM, Hees P, Shapiro E, Christmas C, Bellantoni MF,
Stevens TE, O'Connor KG, Pabst KM, St Clair C, Sorkin JD, Blackman MR.
Effects of GH and/or sex steroid administration on abdominal subcutaneous
and visceral fat in healthy aged women and men. J Clin Endocrinol Metab.
2001 Aug;86(8):3604-10
12- Rodriguez-Arnao J, Jabbar A, Fulcher K, Besser GM, Ross RJ. Effects of
growth hormone replacement on physical performance and body composition
in GH deficient adults. Clin Endocrinol (Oxf). 1999 Jul;51(1):53-60
13- Soares CN, Musolino NR, Cunha Neto M, Caires MA, Rosenthal MC,
Camargo CP, Bronstein MD. Impact of recombinant human growth hormone
(RH-GH) treatment on psychiatric, neuropsychological and clinical profiles of
GH deficient adults. A placebo-controlled trial. Arq Neuropsiquiatr. 1999
Jun;57(2A):182-9
14- Fernholm R, Bramnert M, Hagg E, Hilding A, Baylink DJ, Mohan S, Thoren M.
Growth hormone replacement therapy improves body composition and
increases bone metabolism in elderly patients with pituitary disease. J Clin
Endocrinol Metab. 2000 Nov;85(11):4104-12
15- Attanasio AF, Lamberts SW, Matranga AM, Birkett MA, Bates PC, Valk NK,
Hilsted J, Bengtsson BA, Strasburger CJ. Adult growth hormone (GH)deficient patients demonstrate heterogeneity between childhood onset and
adult onset before and during human GH treatment. Adult Growth Hormone
Deficiency Study Group. J Clin Endocrinol Metab. 1997 Jan;82(1):82-8
16- Beshyah SA, Freemantle C, Shahi M, Anyaoku V, Merson S, Lynch S,
Skinner E, Sharp P, Foale R, Johnston DG. Replacement treatment with
biosynthetic human growth hormone in growth hormone-deficient
hypopituitary adults Clin Endocrinol (Oxf). 1995 Jan;42(1):73-84
17- Moorkens G, Wynants H, Abs R. Effect of growth hormone treatment in
patients with chronic fatigue syndrome: a preliminary study. Growth Horm IGF
Res. 1998 Apr;8 Suppl B:131-3
18- Lo JC, Mulligan K, Noor MA, Schwarz JM, Halvorsen RA, Grunfeld C,
Schambelan M. The effects of recombinant human growth hormone on body
composition and glucose metabolism in HIV-infected patients with fat
accumulation. J Clin Endocrinol Metab. 2001 Aug;86(8):3480-7
19- Christ ER, Cummings MH, Albany E, Umpleby AM, Lumb PJ, Wierzbicki AS,
Naoumova RP, Boroujerdi MA, Sonksen PH, Russell-Jones DL. Effects of
growth hormone (GH) replacement therapy on very low density lipoprotein
apolipoprotein B100 kinetics in patients with adult GH deficiency: a stable
isotope study. J Clin Endocrinol Metab. 1999 Jan;84(1):307-16
20- Florkowski CM, Collier GR, Zimmet PZ, Livesey JH, Espiner EA, Donald RA.
Low-dose growth hormone replacement lowers plasma leptin and fat stores
without affecting body mass index in adults with growth hormone deficiency.
Clin Endocrinol (Oxf). 1996 Dec;45(6):769-73
21- Ezzat S, Fear S, Gaillard RC, Gayle C, Landy H, Marcovitz S, Mattioni T,
Nussey S, Rees A, Svanberg E. Gender-specific responses of lean body
composition and non-gender-specific cardiac function improvement after GH
replacement in GH-deficient adults. J Clin Endocrinol Metab. 2002
Jun;87(6):2725-33
22- Weaver JU, Monson JP, Noonan K, John WG, Edwards A, Evans KA,
Cunningham J. The effect of low dose recombinant human growth hormone
replacement on regional fat distribution, insulin sensitivity, and cardiovascular
risk factors in hypopituitary adults. J Clin Endocrinol Metab. 1995
Jan;80(1):153-9
23- Vahl N, Jorgensen JO, Hansen TB, Klausen IB, Jurik AG, Hagen C,
Christiansen JS. The favourable effects of growth hormone (GH) substitution
on hypercholesterolaemia in GH-deficient adults are not associated with
concomitant reductions in adiposity. A 12 month placebo-controlled study. Int
J Obes Relat Metab Disord. 1998 Jun;22(6):529-36
24- Hansen TB, Gram J, Jensen PB, Kristiansen JH, Ekelund B, Christiansen JS,
Pedersen FB. Influence of growth hormone on whole body and regional soft
tissue composition in adult patients on hemodialysis. A double-blind,
randomized, placebo-controlled study. Clin Nephrol; 2000 Feb;53(2):99-107
25- Fisker S, Vahl N, Hansen TB, Jorgensen JO, Hagen C, Orskov H,
Christiansen JS. Growth hormone (GH) substitution for one year normalizes
elevated GH-binding protein levels in GH-deficient adults secondary to a
reduction in body fat. A placebo-controlled trial. Growth Horm IGF Res. 1998
Apr;8(2):105-12
26- Baum HB, Biller BM, Finkelstein JS, Cannistraro KB, Oppenhein DS,
Schoenfeld DA, Michel TH, Wittink H, Klibanski A. Effects of physiologic
growth hormone therapy on bone density and body composition in patients
with adult-onset growth hormone deficiency. A randomized, placebocontrolled trial. Ann Intern Med. 1996 Dec 1;125(11):883-90
27- Burman P, Johansson AG, Siegbahn A, Vessby B, Karlsson FA. Growth
hormone (GH)-deficient men are more responsive to GH replacement therapy
than women. J Clin Endocrinol Metab. 1997 Feb;82(2):550-5
28- Schambelan M, Mulligan K, Grunfeld C, Daar ES, LaMarca A, Kotler DP,
Wang J, Bozzette SA, Breitmeyer JB. Recombinant human growth hormone
in patients with HIV-associated wasting. A randomized, placebo-controlled
trial. Serostim Study Group. Ann Intern Med. 1996 Dec 1;125(11):873-82
29- Lee PD, Pivarnik JM, Bukar JG, Muurahainen N, Berry PS, Skolnik PR,
Nerad JL, Kudsk KA, Jackson L, Ellis KJ, Gesundheit N. A randomized,
placebo-controlled trial of combined insulin-like growth factor I and low dose
growth hormone therapy for wasting associated with human
immunodeficiency virus infection. J Clin Endocrinol Metab. 1996
Aug;81(8):2968-75
30- Toogood AA, Shalet SM.Growth hormone replacement therapy in the elderly
with hypothalamic-pituitary disease: a dose-finding study. J Clin Endocrinol
Metab. 1999 Jan;84(1):131-6
Obesidade e Elevação do Indice de Massa Corpórea: A Associação Com
Baixos Níveis de IGF-1
1- Rasmussen MH, Frystyk J, Andersen T, Breum L, Christiansen JS, Hilsted J.
The impact of obesity, fat distribution, and energy restriction on insulin-like
growth factor-1 (IGF-1), IGF-binding protein-3, insulin, and growth hormone.
Metabolism. 1994 Mar;43(3):315-9
2- Lawlor DA, Ebrahim S, Smith GD, Cherry L, Watt P, Sattar N. The
association of insulin-like-growth factor 1 (IGF-1) with incident coronary heart
disease in women: findings from the prospective British Women's Heart and
Health Study. Atherosclerosis. 2008 Nov;201(1):198-204
3- Toledo-Corral CM, Roberts CK, Shaibi GQ, Lane CJ, Higgins PB, Davis JN,
Weigensberg MJ, Goran MI. Insulin-like growth factor-I is inversely related to
adiposity in overweight Latino children. J Pediatr Endocrinol Metab. 2008
Sep;21(9):855-64
4- Abdulle AM, Gillett MP, Abouchacra S, Sabri SM, Rukhaimi MA, Obineche
EN, Singh J. Low IGF-1 levels are associated with cardiovascular risk factors
in haemodialysis patients. Mol Cell Biochem. 2007 Aug;302(1-2):195-201
5- Henderson KD, Goran MI, Kolonel LN, Henderson BE, Le Marchand L. Ethnic
disparity in the relationship between obesity and plasma insulin-like growth
factors: the multiethnic cohort. Cancer Epidemiol Biomarkers Prev. 2006
Nov;15(11):2298-302
6- Tong PC, Ho CS, Yeung VT, Ng MC, So WY, Ozaki R, Ko GT, Ma RC, Poon
E, Chan NN, Lam CW, Chan JC. Association of testosterone, insulin-like
growth factor-I, and C-reactive protein with metabolic syndrome in Chinese
middle-aged men with a family history of type 2 diabetes. J Clin Endocrinol
Metab. 2005 Dec;90(12):6418-23
7- De Pergola G, Zamboni M, Pannacciulli N, Turcato E, Giorgino F, Armellini F,
Logoluso F, Sciaraffia M, Bosello O, Giorgino R. Divergent effects of shortterm, very-low-calorie diet on insulin-like growth factor-I and insulin-like
growth factor binding protein-3 serum concentrations inpremenopausal
women with obesity. Obes Res. 1998 Nov;6(6):408-15
8- Mårin P, Kvist H, Lindstedt G, Sjöström L, Björntorp P. Low concentrations of
insulin-like growth factor-I in abdominal obesity. Int J Obes Relat Metab
Disord. 1993 Feb;17(2):83-9
9- Rasmussen MH, Hvidberg A, Juul A, Main KM, Gotfredsen A, Skakkebaek
NE, Hilsted J, Skakkebae NE. Massive weight loss restores 24-hour growth
hormone release profiles and serum insulin-like growth factor-I levels in
obese subjects. J Clin Endocrinol Metab. 1995 Apr;80(4):1407-15
10- Ballerini MG, Ropelato MG, Domené HM, Pennisi P, Heinrich JJ, Jasper HG.
Differential impact of simple childhood obesity on the components of the
growth hormone-insulin-like growth factor (IGF)-IGF binding proteins axis. J
Pediatr Endocrinol Metab. 2004 May;17(5):749-57
11- Reinehr T, Panteliadou A, de Sousa G, Andler W. Insulin-like growth factor-I,
insulin-like growth factor binding protein-3 and growth in obese children
before and after reduction of overweight. J Pediatr Endocrinol Metab. 2009
Mar;22(3):225-33
12- Martha PM, Gorman KM, Blizzard RM, Rogol AD, Veldhuis JD. Endogenous
growth hormone secretion and clearance rates in normal boys, as determined
by deconvolution analysis: relationship to age, pubertal status, and body
mass. J Clin Endocrinol Metab. 1992 Feb;74(2):336-44
Obesidade: A melhora Com a Reposição de IGF-1
1- Thompson JL, Butterfield GE, Gylfadottir UK, Yesavage J, Marcus R, Hintz
RL, Pearman A, Hoffman AR. Effects of human growth hormone, insulin-like
growth factor I, and diet and exercise on body composition of obese
postmenopausal women. : J Clin Endocrinol Metab. 1998 May;83(5):1477-84
2- Laron Z, Anin S, Klipper-Aurbach Y, Klinger B. Effects of insulin-like growth
factor on linear growth, head circumference, and body fat in patients with
Laron-type dwarfism. Lancet. 1992 May 23;339(8804):1258-61
3- Hayes VY, Urban RJ, Jiang J, Marcell TJ, Helgeson K, Mauras N.
Recombinant human growth hormone and recombinant human insulin-like
growth factor I diminish the catabolic effects of hypogonadism in man:
metabolic and molecular effects. J Clin Endocrinol Metab. 2001
May;86(5):2211-9
Obesidade: A Associação Com Baixos Níveis de Testosterona
1.
Knoblovits P, Costanzo PR, Rey Valzacchi GJ, Gueglio MG, Layus AO, Kozak
AE, Balzaretti MI, Litwak LE. Erectile dysfunction, obesity, insulin
resistance, and their relationship with testosterone levels in eugonadal
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
patients in an andrology clinic setting. J Androl. 2010 (2009 Oct 15, Epub
ahead of print)
Martínez Jabaloyas JM, Queipo Zaragoza A, Ferrandis Cortes C, Queipo
Zaragoza JA, Gil Salom M, Chuan Nuez P. Changes in sexual hormones in a
male. Actas Urol Esp. 2008 Jun;32(6):603-10
Chu LW, Tam S, Kung AW, Lo S, Fan S, Wong RL, Morley JE, Lam KS. Serum
total and bioavailable testosterone levels, central obesity, and muscle strength
changes with aging in healthy Chinese men. J Am Geriatr Soc. 2008
Jul;56(7):1286-91
Kapoor D, Aldred H, Clark S, Channer KS, Jones TH. Clinical and biochemical
assessment of hypogonadism in men with type 2 diabetes: correlations with
bioavailable testosterone and visceral adiposity. Diabetes Care. 2007
Apr;30(4):911-7
Kaplan SA, Meehan AG, Shah A. The age related decrease in testosterone is
significantly exacerbated in obese men with the metabolic syndrome. What are
the implications for the relatively high incidence of erectile dysfunction observed
in these men? J Urol. 2006 Oct;176(4 Pt 1):1524-7
Osuna JA, Gómez-Pérez R, Arata-Bellabarba G, Villaroel V. Relationship
between BMI, total testosterone, sex hormone-binding-globulin, leptin, insulin
and insulin resistance in obese men. Arch Androl. 2006 Sep-Oct;52(5):355-61
Rabijewski M, Kozakowski J, Zgliczyński W. The relationship between
testosterone and dehydroepiandrosterone sulfate concentrations, insulin
resistance and visceral obesity in elderly men] Endokrynol Pol. 2005 NovDec;56(6):897-903
Blanchette S, Marceau P, Biron S, Brochu G, Tchernof A. Circulating
progesterone and obesity in men. Horm Metab Res. 2006 May;38(5):330-5
Tibblin G, Adlerberth A, Lindstedt G, Bjorntorp P. The pituitary-gonadal axis
and health in elderly men: a study of men born in 1913. Diabetes. 1996
Nov;45(11):1605-9
Abate N, Haffner SM, Garg A, Peshock RM, Grundy SM. Sex steroid
hormones, upper body obesity, and insulin resistance. J Clin Endocrinol Metab.
2002 Oct;87(10):4522-7
Penotti M, Sironi L, Cannata L, Vigano P, Casini A, Gabrielli L, Vignali M.
Effects of androgen supplementation of hormone replacement therapy on the
vascular reactivity of cerebral arteries. Fertil Steril. 2001 Aug;76(2):235-40
Obesidade: A melhora Com a Reposição de Testosterona
1- Kapoor D, Goodwin E, Channer KS, Jones TH. Testosterone replacement
therapy improves insulin resistance, glycaemic control, visceral adiposity and
hypercholesterolaemia in hypogonadal men with type 2 diabetes. Eur J
Endocrinol. 2006 Jun;154(6):899-906
2- Bhasin S, Parker RA, Sattler F, Haubrich R, Alston B, Umbleja T, Shikuma
CM; AIDS Clinical Trials Group Protocol A5079 Study Team. Effects of
testosterone supplementation on whole body and regional fat mass and
distribution in human immunodeficiency virus-infected men with abdominal
obesity. Clin Endocrinol Metab. 2007 Mar;92(3):1049-57
3- Allan CA, Strauss BJ, Burger HG, Forbes EA, McLachlan RI. Testosterone
therapy prevents gain in visceral adipose tissue and loss of skeletal muscle in
nonobese aging men. Clin Endocrinol Metab. 2008 Jan;93(1):139-46
4- Boyanov MA, Boneva Z, Christov VG. Testosterone supplementation in men
with type 2 diabetes, visceral obesity and partial androgen deficiency. Aging
Male. 2003 Mar;6(1):1-7
5- Marin P. Testosterone and regional fat distribution. Obes Res. 1995 Nov;3
Suppl 4:609S-12S
6- Rebuffe-Scrive M, Marin P, Bjorntorp P. Effect of testosterone on abdominal
adipose tissue in men. Int J Obes. 1991;15(11):791-5
-
MELHORA DA APARÊNCIA FÍSICA, COMPOSIÇÃO
CORPORAL E MASSA MUSCULAR ATRAVÉS DA
MODULAÇÃO HORMONAL
8
Hormônio do Crescimento e Composição Corporal
Sarcopenia: A Associação Com Baixos Níveis de GH/IGF-1
1-
2-
3-
Sartorio A, Narici MV. Growth hormone (GH) treatment in GH-deficient adults:
effects on muscle size,strength and neural activation. Clin Physiol 1994
Sep;14(5):527-37
De Boer H, Blok GJ, Voerman HJ, De Vries PM, van der Veen EA. Body
composition in adult growth hormone-deficient men, assessed by
anthropometry and bioimpedance analysis. J Clin Endocrinol Metab 1992
Sep;75(3):833-7
Cuneo RC, Salomon F, Wiles CM, Hesp R, Sonksen PH. Growth hormone
treatment in growth hormone-deficient adults. I. Effects on muscle mass
and strength. J Appl Physiol 1991 Feb;70(2):688-94
Sarcopenia: A Melhora Com a Reposição de GH
1-
23-
4-
5-
6-
Vahl N, Juul A, Jorgensen JO, Orskov H, Skakkebaek NE, Christiansen JS.
Continuation of growth hormone (GH) replacement in GH-deficient
patients during transition from childhood to adulthood: a two-year placebocontrolled study. J Clin Endocrinol Metab. 2000 May;85(5):1874-81
Butterfield GE, Marcus R, Holloway L, Butterfield G. Clinical use of growth
hormone in elderly people. J Reprod Fertil Suppl. 1993; 46:115-8
Butterfield GE, Thompson J, Rennie MJ, Marcus R, Hintz RL, Hoffman AR.
Effect of rhGH and rhIGF-1 treatment on protein utilization in elderly
women. Am J Physiol. 1997 Jan; 272 (1 Pt 1): E 94-9
Sartorio A, Narici MV. Growth hormone (GH) treatment in GH-deficient adults:
effects on muscle size,strength and neural activation. Clin Physiol. 1994
Sep;14(5):527-37
Janssen YJ, Doornbos J, Roelfsema F. Changes in muscle volume, strength,
and bioenergetics during recombinant human ,growth hormone (GH)
therapy in adults with GH deficiency. J Clin Endocrinol Metab. 1999
Jan;84(1):279-84
Jorgensen JO, Pedersen SA, Thuesen L, Jorgensen J, Ingemann-Hansen T,
Skakkebaek NE, Christiansen JS. Beneficial effects of growth hormone
treatment in GH-deficient adults. Lancet. 1989 Jun 3;1(8649):1221-5
7-
8-
9-
ter Maaten JC, de Boer H, Kamp O, Stuurman L, van der Veen EA. Long-term
effects of growth hormone (GH) replacement in men with childhood-onset
GH deficiency. J Clin Endocrinol Metab. 1999 Jul;84(7):2373-80
Whitehead HM, Boreham C, McIlrath EM, Sheridan B, Kennedy L, Atkinson AB,
Hadden DR. Growth hormone treatment of adults with growth hormone
deficiency: results of a 13-month placebo controlled cross-over study. Clin
Endocrinol (Oxf). 1992 Jan;36(1):45-52
Nam SY, Kim KR, Cha BS, Song YD, Lim SK, Lee HC, Huh KB. Low-dose
growth hormone treatment combined with diet restriction decreases insulin
resistance by reducing visceral fat and increasing muscle mass in obese
type 2 diabetic patients. Int J Obes Relat Metab Disord. 2001
Aug;25(8):1101-7
Massa Muscular: A Associação Com Baixos Níveis de GH/IGF-1
1-
De Boer H, Blok GJ, Voerman HJ, De Vries PM, van der Veen EA. Body
composition in adult growth hormone-deficient men, assessed by
anthropometry and bioimpedance analysis. J Clin Endocrinol Metab. 1992
Sep;75(3):833-7
Massa Muscular: A Melhora Com a Reposição de GH
1-
2-
3-
4-
5-
6-
7-
Feldt-Rasmussen B, Lange M, Sulowicz W, Gafter U, Lai KN, Wiedemann J,
Christiansen JS, El Nahas M; APCD Study Group. Growth hormone
treatment during hemodialysis in a randomized trial improves nutrition,
quality of life, and cardiovascular risk. J Am Soc Nephrol. 2007
Jul;18(7):2161-71
Bengtsson BA, Eden S, Lonn L, Kvist H, Stokland A, Lindstedt G, Bosaeus I,
Tolli J, Sjostrom L, Isaksson OG. Treatment of adults with growth hormone
(GH) deficiency with recombinant human GH. J Clin Endocrinol Metab.
1993 Feb;76(2):309-17
Lombardi G, Luger A, Marek J, Russell-Jones D, Sonksen P, Attanasio AF.
Short-term safety and efficacy of human GH replacement therapy in 595
adults with GH deficiency: a comparison of two dosage algorithms. J Clin
Endocrinol Metab. 2002 May;87(5):1974-9
Vahl N, Juul A, Jorgensen JO, Orskov H, Skakkebaek NE, Christiansen JS.
Continuation of growth hormone (GH) replacement in GH-deficient patients
during transition from childhood to adulthood: a two-year placebo-controlled
study. J Clin Endocrinol Metab. 2000 May;85(5):1874-81
Rudman D, Feller AG, Nagraj HS, Gergans GA, Lalitha PY, Goldberg AF,
Schlenker RA, Cohn L, Rudman IW, Mattson DE. Effects of human growth
hormone in men over 60 years old. N Engl J Med. 1990 Jul 5;323(1):1-6
Davies JS, Obuobie K, Smith J, Rees DA, Furlong A, Davies N, Evans LM,
Scanlon MF. A therapeutic trial of growth hormone in hypopituitary adults
and its influence upon continued prescription by general practitioners. Clin
Endocrinol (Oxf). 2000 Mar;52(3):295-303
Olsovska V, Siprova H, Beranek M, Soska V. The influence of long-term growth
hormone replacement therapy on body composition, bone tissue and some
metabolic parameters in adults with growth hormone deficiency. Vnitr Lek.
2005 Dec;51(12):1356-64
Melhora da Aparência Fìsica e Morfologia Corporal Com a Reposição de GH
12-
3-
4-
Hertoghe T. Growth hormone therapy in aging adults. Anti-aging Med Ther.
1997;1:10-28
Honda M, Yogi A, Ishizuka N, Genka I, Gatanaga H, Teruya K, Tachikawa N,
Kikuchi Y, Oka S. Effectiveness of subcutaneous growth hormone in HIV-1
patients with moderate to severe facial lipoatrophy. Intern Med.
2007;46(7):359-62
Zivicnjak M, Franke D, Ehrich JH, Filler G.Does growth hormone therapy
harmonize distorted morphology and body composition in chronic renal
failure? Pediatr Nephrol. 2000 Dec;15(3-4):229-35
Eiholzer U, Schlumpf M, Nordmann Y, l'Allemand D. Early manifestations of
Prader-Willi syndrome: influence of growth hormone. J Pediatr Endocrinol
Metab 2001;14 Suppl 6:1441-4
Perda de Massa Muscular e Aumento da Massa Gordurosa: A Associação Com
Baixos Níveis de GH/IGF-1
1- Engvall IL, Elkan AC, Tengstrand B, Cederholm T, Brismar K, Hafstrom I.
Cachexia in rheumatoid arthritis is associated with inflammatory activity,
physical disability, and low bioavailable insulin-like growth factor. Scand J
Rheumatol. 2008 Sep-Oct;37(5):321-8
2- Gómez JM. Serum leptin, insulin-like growth factor-I components and sexhormone binding globulin. Relationship with sex, age and body composition in
healthy population. Protein Pept Lett. 2007;14(7):708-11
3- Axelsson J, Qureshi AR, Divino-Filho JC, Bárány P, Heimbürger O, Lindholm
B, Stenvinkel P. Are insulin-like growth factor and its binding proteins 1 and 3
clinically useful as markers of malnutrition, sarcopenia and inflammation in
end-stage renal disease? Eur J Clin Nutr. 2006 Jun;60(6):718-26
4- Payette H, Roubenoff R, Jacques PF, Dinarello CA, Wilson PW, Abad LW,
Harris T. Insulin-like growth factor-1 and interleukin 6 predict sarcopenia in
very old community-living men and women: the Framingham Heart Study. J
Am Geriatr Soc. 2003 Sep;51(9):1237-43
5- Waters DL, Yau CL, Montoya GD, Baumgartner RN. Serum Sex Hormones,
IGF-1, and IGFBP3 Exert a Sexually Dimorphic Effect on Lean Body Mass in
Aging. J Gerontol A Biol Sci Med Sci. 2003 Jul;58(7):648-52
6- Gómez JM, Maravall FJ, Gómez N, Navarro MA, Casamitjana R, Soler J.
Interactions between serum leptin, the insulin-like growth factor-I system, and
sex, age, anthropometric and body composition variables in a healthy
population randomly selected. Clin Endocrinol (Oxf). 2003 Feb;58(2):213-9
7- Chang S, Wu X, Yu H, Spitz MR. Plasma concentrations of insulin-like growth
factors among healthy adult men and postmenopausal women: associations
with body composition, lifestyle, and reproductive factors. Cancer Epidemiol
Biomarkers Prev. 2002 Aug;11(8):758-66
8- Figueroa A, Going SB, Milliken LA, Blew R, Sharp S, Lohman TG. Body
composition modulates the effects of hormone replacement therapy on
growth hormone and insulin-like growth factor-I levels in postmenopausal
women. Gynecol Obstet Invest. 2002;54(4):201-6
9- Niebauer J, Pflaum CD, Clark AL, Strasburger CJ, Hooper J, Poole-Wilson
PA, Coats AJ, Anker SD. Deficient insulin-like growth factor I in chronic heart
failure predicts altered body composition, anabolic deficiency, cytokine and
neurohormonal activation. J Am Coll Cardiol. 1998 Aug;32(2):393-7
Deterioração da Composição Corporal: A Melhora Com a Reposição de GH
1- Thompson JL, Butterfield GE, Gylfadottir UK, Yesavage J, Marcus R, Hintz
RL, Pearman A, Hoffman AR. Effects of human growth hormone, insulin-like
growth factor I, and diet and exercise on body composition of obese
postmenopausal women. : J Clin Endocrinol Metab. 1998 May;83(5):1477-84
2- Woods KA, Camacho-Hübner C, Bergman RN, Barter D, Clark AJ, Savage
MO. Effects of insulin-like growth factor I (IGF-I) therapy on body composition
and insulin resistance in IGF-I gene deletion. J Clin Endocrinol Metab. 2000
Apr;85(4):1407-11
3- Ng EH, Rock CS, Lazarus DD, Stiaino-Coico L, Moldawer LL, Lowry SF.
Insulin-like growth factor I preserves host lean tissue mass in cancer
cachexia. Am J Physiol. 1992 Mar;262(3 Pt 2):R426-31
4- Hayes VY, Urban RJ, Jiang J, Marcell TJ, Helgeson K, Mauras N.
Recombinant human growth hormone and recombinant human insulin-like
growth factor I diminish the catabolic effects of hypogonadism in man:
metabolic and molecular effects. J
Clin Endocrinol Metab. 2001
May;86(5):2211-9
5- Herndon DN, Ramzy PI, DebRoy MA, Zheng M, Ferrando AA, Chinkes DL,
Barret JP, Wolfe RR, Wolf SE. Muscle protein catabolism after severe burn:
effects of IGF-1/IGFBP-3 treatment. Ann Surg. 1999 May;229(5):713-20
6- Debroy MA, Wolf SE, Zhang XJ, Chinkes DL, Ferrando AA, Wolfe RR,
Herndon DN. Anabolic effects of insulin-like growth factor in combination with
insulin-like growth factor binding protein-3 in severely burned adults. J
Trauma. 1999 Nov;47(5):904-10
Sarcopenia: A Associação Com Baixos Níveis de Estradiol
1- Iannuzzi-Sucich M, Prestwood KM, Kenny AM. Prevalence of sarcopenia and
predictors of skeletal muscle mass in healthy, older men and women. J
Gerontol A Biol Sci Med Sci. 2002 Dec;57(12):M772-7
Sarcopenia: A Melhora Com A Reposição de Estradiol
1-
Sipila S, Taaffe DR, Cheng S, Puolakka J, Toivanen J, Suominen H.
Effects of hormone replacement therapy and high-impact physical
exercise on skeletal muscle in post-menopausal women: a
randomized placebo-controlled study. Clin Sci (Lond). 2001
Aug;101(2):147-57
Massa Muscular: A Melhora Com a Reposição de Estradiol
1-
2-
3-
Hassager C, Christiansen C. Estrogen/gestagen therapy changes soft
tissue body composition in postmenopausal women. Metabolism.
1989 Jul;38(7):662-5
Sorensen MB, Rosenfalck AM, Hojgaard L, Ottesen B. Obesity and
sarcopenia after menopause are reversed by sex hormone
replacement therapy. Obes Res. 2001 Oct;9(10):622-6
Davis SR, Walker KZ, Strauss BJ. Effects of estradiol with and without
testosterone on body composition and relationships with lipids in
postmenopausal women. Menopause. 2000 Nov-Dec;7(6):395-401
Envelhecimento Cutâneo: A Melhora Com a Reposição de Estradiol
1- Son ED, Lee JY, Lee S, Kim MS, Lee BG, Chang IS, Chung JH. Topical
application of 17beta-estradiol increases extracellular matrix protein synthesis
by stimulating tgf-Beta signaling in aged human skin in vivo. . J Invest
Dermatol. 2005 Jun;124(6):1149-61
Sarcopenia Em Homens: A Melhora Com a Reposição de Testosterona
1-
2-
3-
4-
5-
6-
7-
8-
Allan CA, Strauss BJ, Burger HG, Forbes EA, McLachlan RI. Testosterone
therapy prevents gain in visceral adipose tissue and loss of skeletal muscle
in nonobese aging men. Clin Endocrinol Metab. 2008 Jan;93(1):139-46
Woodhouse LJ, Gupta N, Bhasin M, Singh AB, Ross R, Phillips J, Bhasin S.
Dose-dependent effects of testosterone on regional adipose tissue
distribution in healthy young men. J Clin Endocrinol Metab. 2004
Feb;89(2):718-26
Brodsky IG, Balagopal P, Nair KS. Effects of testosterone replacement on
muscle mass and muscle protein synthesis in hypogonadal men--a clinical
research center study. J Clin Endocrinol Metab. 1996 Oct;81(10):3469-75
Zachwieja JJ, Smith SR, Lovejoy JC, Rood JC, Windhauser MM, Bray GA.
Testosterone administration preserves protein balance but not muscle
strength during 28 days of bed rest. J Clin Endocrinol Metab. 1999
Jan;84(1):207-12
Urban RJ, Bodenburg YH, Gilkison C, Foxworth J, Coggan AR, Wolfe RR,
Ferrando A. Testosterone administration to elderly men increases skeletal
muscle strength and protein synthesis. Am J Physiol. 1995 Nov;269(5 Pt
1):E820-6
Griggs RC, Kingston W, Jozefowicz RF, Herr BE, Forbes G, Halliday D.Effect
of testosterone on muscle mass and muscle protein synthesis. J Appl
Physiol. 1989 Jan;66(1):498-503
Griggs RC, Halliday D, Kingston W, Moxley RT 3rd. Effect of testosterone on
muscle protein synthesis in myotonic dystrophy. Ann Neurol. 1986
Nov;20(5):590-6
Bhasin S, Storer TW, Berman N, Yarasheski KE, Clevenger B, Phillips J, Lee
WP, Bunnell TJ, Casaburi R. Testosterone replacement increases fat-free
mass and muscle size in hypogonadal men. J Clin Endocrinol Metab. 1997
Feb;82(2):407-13.
Massa Muscular em Homens: A Associação Com Baixos Níveis de
Testosterona
1-
2-
Mauras N, Hayes V, Welch S, Rini A, Helgeson K, Dokler M, Veldhuis JD,
Urban RJ. Testosterone deficiency in young men: marked alterations in
whole body protein kinetics, strength, and adiposity. J Clin Endocrinol
Metab. 1998 Jun;83(6):1886-92
Bhasin S, Tenover JS. Age-associated sarcopenia--issues in the use of
testosterone as an anabolic agent in older men. J Clin Endocrinol Metab.
1997 Jun;82(6):1659-60.
Massa Muscular em Homens: A Melhora Com a Reposição de Testosterona
1- Brodsky IG, Balagopal P, Nair KS. Effects of testosterone replacement on
muscle mass and muscle protein synthesis in hypogonadal men - a clinical
research center study. J Clin Endocrinol Metab. 1996 Oct;81(10):3469-75
2- Bhasin S, Woodhouse L, Casaburi R, Singh AB, Bhasin D, Berman N, Chen
X, Yarasheski KE, Magliano L, Dzekov C, Dzekov J, Bross R, Phillips J,
Sinha-Hikim I, Shen R, Storer TW. Testosterone dose-response relationships
in healthy young men.Am J Physiol Endocrinol Metab. 2001
Dec;281(6):E1172-81
3- Wang C, Swerdloff RS, Iranmanesh A, Dobs A, Snyder PJ, Cunningham G,
Matsumoto AM, Weber T, Berman N; Testosterone Gel Study Group.
Transdermal testosterone gel improves sexual function, mood, muscle
strength, and body composition parameters in hypogonadal men. J Clin
Endocrinol Metab. 2000 Aug;85(8):2839-53
4- Wang C, Cunningham G, Dobs A, Iranmanesh A, Matsumoto AM, Snyder PJ,
Weber T, Berman N, Hull L, Swerdloff RS. Long-term testosterone gel
(AndroGel) treatment maintains beneficial effects on sexual function and
mood, lean and fat mass, and bone mineral density in hypogonadal men. J
Clin Endocrinol Metab. 2004 May;89(5):2085-98
5- Bhasin S, Storer TW, Berman N, Yarasheski KE, Clevenger B, Phillips J, Lee
WP, Bunnell TJ, Casaburi R. Testosterone replacement increases fat-free
mass and muscle size in hypogonadal men. J Clin Endocrinol Metab. 1997
Feb;82(2):407-13
6- Bhasin S, Storer TW, Asbel-Sethi N, Kilbourne A, Hays R, Sinha-Hikim I,
Shen R, Arver S, Beall G. Effects of testosterone replacement with a
nongenital, transdermal system, Androderm, in human immunodeficiency
virus-infected men with low testosterone levels. J Clin Endocrinol Metab.
1998 Sep;83(9):3155-62
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Osteoporose: A Associação Com Baixos Níveis do Hormônio do Crescimento
1- Boot AM, van der Sluis IM, Krenning EP, de Muinck Keizer-Schrama SM.
Bone mineral density and body composition in adolescents with childhoodonset growth hormone deficiency. Horm Res. 2009;71(6):364-71
2- Foldes J, Lakatos P, Zsadanyi J, Horvath C. Decreased serum IGF-I and
dehydroepiandrosterone sulphate may be risk factors for the development of
reduced bone mass in postmenopausal women with endogenous subclinical
hyperthyroidism. Eur J Endocrinol. 1997 Mar;136(3):277-81
3- Monson JP, Abs R, Bengtsson BA, Bennmarker H, Feldt-Rasmussen U,
Hernberg-Stahl E, Thoren M, Westberg B, Wilton P, Wuster C. Growth
hormone deficiency and replacement in elderly hypopituitary adults. KIMS
Study Group and the KIMS International Board. Pharmacia and Upjohn
International Metabolic Database. Clin Endocrinol (Oxf). 2000 Sep;53(3):2819
4- Longobardi S, Di Rella F, Pivonello R, Di Somma C, Klain M, Maurelli L,
Scarpa R, Colao A, Merola B, Lombardi G. Effects of two years of growth
hormone (GH) replacement therapy on bone metabolism and mineral density
in childhood and adulthood onset GH deficient patients. J Endocrinol Invest.
1999 May;22(5):333-9
5- Beckers V, Milet J, Legros JJ. Prolonged treatment with recombined growth
hormone improves bone measures: study of body composition in 21 deficient
adults on treatment. Ann Endocrinol (Paris). 2001 Dec;62(6):507-15
6- Gomez JM, Gomez N, Fiter J, Soler J. Effects of long-term treatment with GH
in the bone mineral density of adults with hypopituitarism and GH deficiency
and after discontinuation of GH replacement. Horm Metab Res. 2000
Feb;32(2):66-70
7- Kaufman JM, Taelman P, Vermeulen A, Vandeweghe M. Bone mineral status
in growth hormone-deficient males with isolated and multiple pituitary
deficiencies of childhood onset. J Clin Endocrinol Metab. 1992 Jan;74(1):11823
8- Calo L, Castrignano R, Davis PA, Carraro G, Pagnin E, Giannini S, Semplicini
A, D'Angelo A. Role of insulin-like growth factor-I in primary osteoporosis: a
correlative study. J Endocrinol Invest. 2000 Apr;23(4):223-7
9- Colao A, Di Somma C, Pivonello R, Loche S, Aimaretti G, Cerbone G,
Faggiano A, Corneli G, Ghigo E, Lombardi G. Bone loss is correlated to the
severity of growth hormone deficiency in adult patients with hypopituitarism. J
Clin Endocrinol Metab. 1999 Jun;84(6):1919-24
10- Nakaoka D, Sugimoto T, Kaji H, Kanzawa M, Yano S, Yamauchi M, Sugishita
T, Chihara K. Determinants of bone mineral density and spinal fracture risk in
postmenopausal Japanese women. Osteoporos Int. 2001;12(7):548-54
11- Rico H, Del Rio A, Vila T, Patino R, Carrera F, Espinos D. The role of growth
hormone in the pathogenesis of postmenopausal osteoporosis. Arch Intern
Med. 1979 Nov;139(11):1263-5
12- Ljunghall S, Johansson AG, Burman P, Kampe O, Lindh E, Karlsson FA. Low
plasma levels of insulin-like growth factor 1 (IGF-1) in male patients with
idiopathic osteoporosis. J Intern Med. 1992 Jul;232(1):59-64
Osteoporose: A Melhora Com a Reposição de GH
1- Lopes RF, Coeli CM, Vaisman M, de Farias ML. Additional beneficial effects
of recombinant growth hormone in alendronate-treated patients with
idiopathic osteoporosis. Endocr J. 2009;56(7):851-8
2- Rota F, Savanelli MC, Tauchmanova L, Savastano S, Lombardi G, Colao A,
Di Somma C. Bone density and turnover in young adult patients with growth
hormone deficiency after 2-year growth hormone replacement according with
gender. J Endocrinol Invest. 2008 Feb;31(2):94-102
3- Joseph F, Ahmad AM, Ul-Haq M, Durham BH, Whittingham P, Fraser WD,
Vora JP. Effects of growth hormone administration on bone mineral
metabolism, PTH sensitivity and PTH secretory rhythm in postmenopausal
women with established osteoporosis. J Bone Miner Res. 2008
May;23(5):721-9.
4- Clanget C, Seck T, Hinke V, Wuster C, Ziegler R, Pfeilschifter J. Effects of 6
years of growth hormone (GH) treatment on bone mineral density in GHdeficient adults. Clin Endocrinol (Oxf). 2001 Jul;55(1):93-9
5- Sartorio A, Ortolani S, Galbiati E, Conte G, Vangeli V, Arosio M, Porretti S,
Faglia. Effects of 12-month GH treatment on bone metabolism and bone
mineral density in adults with adult-onset GH deficiency. J Endocrinol Invest.
2001 Apr;24(4):224-30
6- Biller BM, Sesmilo G, Baum HB, Hayden D, Schoenfeld D, Klibanski
A.Withdrawal of long-term physiological growth hormone (GH) administration:
differential effects on bone density and body composition in men with adultonset GH deficiency. J Clin Endocrinol Metab 2000 Mar;85(3):970-6
7- Gomez JM, Gomez N, Fiter J, Soler J. Effects of long-term treatment with GH
in the bone mineral density of adults with hypopituitarism and GH deficiency
and after discontinuation of GH replacement. Horm Metab Res. 2000
Feb;32(2):66-70
8- Benbassat CA, Wass rman M, Laron Z. Changes in bone mineral density
after discontinuation and early reinstitution of growth hormone (GH) in
patients with childhood-onset GH deficiency. Growth Horm IGF Res. 1999
Oct;9(5):290-5
9- ter Maaten JC, de Boer H, Kamp O, Stuurman L, van der Veen EA. Longterm effects of growth hormone (GH) replacement in men with childhoodonset GH deficiency. J Clin Endocrinol Metab. 1999 Jul;84(7):2373-80
10- Valimaki MJ, Salmela PI, Salmi J, Viikari J, Kataja M, Turunen H, Soppi E.
Effects of 42 months of GH treatment on bone mineral density and bone
turnover in GH-deficient adults. Eur J Endocrinol 1999 Jun;140(6):545-54
11- Baum HB, Biller BM, Finkelstein JS, Cannistraro KB, Oppenhein DS,
Schoenfeld DA, Michel TH, Wittink H, Klibanski A. Effects of physiologic
growth hormone therapy on bone density and body composition in patients
with adult-onset growth hormone deficiency. A randomized, placebocontrolled trial. Ann Intern Med. 1996 Dec 1;125(11):883-90
12- Beshyah SA, Thomas E, Kyd P, Sharp P, Fairney A, Johnston DG. The effect
of growth hormone replacement therapy in hypopituitary adults on calcium
and bone metabolism. Clin Endocrinol (Oxf). 1994 Mar;40(3):383-91
13- Vandeweghe M, Taelman P, Kaufman JM.Short and long-term effects of
growth hormone treatment on bone turnover and bone mineral content in
adult growth hormone-deficient males. Clin Endocrinol (Oxf). 1993
Oct;39(4):409-15
14- Finkenstedt G, Gasser RW, Hofle G, Watfah C, Fridrich L. Effects of growth
hormone (GH) replacement on bone metabolism and mineral density in adult
onset of GH deficiency: results of a double-blind placebo- controlled study
with open follow-up. Eur J Endocrinol. 1997 Mar;136(3):282-9
15- Erdtsieck RJ, Pols HA, Valk NK, Van OBM, Lamberts SW, Mulder P,
Birkenhager JC. Treatment of post-menopausal osteoporosis with a
combination of growth hormone and pamidronate:a placebo controlled trial.
Clin Endocrinol (Oxf). 1995;43:557-565
Osteoporose: A Associação Com Baixos Níveis de IGF-1
1- Liu JM, Zhao HY, Ning G, Chen Y, Zhang LZ, Sun LH, Zhao YJ, Xu MY,
Chen JL. IGF-1 as an early marker for low bone mass or osteoporosis in
premenopausal and postmenopausal women. J Bone Miner Metab.
2008;26(2):159-64
2- Reed BY, Zerwekh JE, Sakhaee K, Breslau NA, Gottschalk F, Pak CY.
Serum IGF 1 is low and correlated with osteoblastic surface in idiopathic
osteoporosis. J Bone Miner Res. 1995 Aug;10(8):1218-24
3- Ljunghall S, Johansson AG, Burman P, Kämpe O, Lindh E, Karlsson FA. Low
plasma levels of insulin-like growth factor 1 (IGF-1) in male patients with
idiopathic osteoporosis. J Intern Med. 1992 Jul;232(1):59-64
4- Ali O, Shim M, Fowler E, Cohen P, Oppenheim W. Spinal bone mineral
density, IGF-1 and IGFBP-3 in children with cerebral palsy. Horm Res.
2007;68(6):316-20
Osteoporose: A Melhora Com a Reposição de IGF-1
1- Yakar S, Rosen CJ, Beamer WG, Ackert-Bicknell CL, Wu Y, Liu JL, Ooi GT,
Setser J, Frystyk J, Boisclair YR, LeRoith D. Circulating levels of IGF-1
directly regulate bone growth and density. J Clin Invest. 2002
Sep;110(6):771-81
2- Stabnov L, Kasukawa Y, Guo R, Amaar Y, Wergedal JE, Baylink DJ, Mohan
S. Effect of insulin-like growth factor-1 (IGF-1) plus alendronate on bone
density during puberty in IGF-1-deficient MIDI mice. Bone. 2002
Jun;30(6):909-16
Osteoporose: A Associação Com Baixos Níveis de DHEA
1- Herman WA, Seńko A, Korczowska I, Łacka K. Could serum DHEA and
DHEAS levels be good risk predictors of metabolic syndrome and
osteoporosis in the population of ageing men? Pol Merkur Lekarski. 2009
Sep;27(159):197-201
2- Sambrook P, Birmingham J, Champion D, Kelly P, Kempler S, Freund J,
Eisman J. Postmenopausal bone loss in rheumatoid arthritis: effect of
estrogens and androgens. J Rheumatol. 1992 Mar;19(3):357-61
3- Nordin BE, Robertson A, Seamark RF, Bridges A, Philcox JC, Need AG,
Horowitz M, Morris HA, Deam S. The relation between calcium absorption,
serum dehydroepiandrosterone, and vertebral mineral density in
postmenopausal women. J Clin Endocrinol Metab. 1985;60(4):651-7
4- Wild RA, Buchanan JR, Myers C, Demers LM. Declining adrenal androgens:
an association with bone loss in aging women. Proc Soc Exp Biol Med.
1987;186(3):355-60
5- Audisio M, Fidanza A, Mastroiacovo P, Suraci C, Strollo F, Torella G, Di
Pietro S. Correlations between vitamins A and E and steroid hormones. Boll
Soc Ital Biol Sper. 1987;63(3):281-7
6- Fingerova H, Matlochova J. Reduced serum dehydroepiandrosterone levels
in postmenopausal osteoporosis. Ceska Gynekol. 1998;63(2):110-3
7- Brody S, Carlstrom K, Lagrelius A, Lunell NO, Rosenborg L. Adrenal steroids,
bone mineral content and endometrial pathology in postmenopausal women.
Acta Obstet Gynecol Scand 1981;60(3):325-6
8- Brody S, Carlstrom K, Lagrelius A, Lunell NO, Rosenborg L. Adrenocortical
steroids, bone mineral content and endometrial condition in post-menopausal
women. Maturitas. 1982;4(2):113-2
9- Shono N, Kugino K, Yoshida S, Nakayama M, Ueno H, Nishizumi M. Bone
mineral density by ultrasonic measurement in pre- and postmenopausal
women - relationship with sex hormones and nutritional states. Nippon
Eiseigaku Zasshi. 1997;51(4):755-62
10- Miklos S. Dehydroepiandrosterone sulphate in the diagnosis of osteoporosis.
Acta Biomed Ateneo Parmense. 1995;66(3-4):139-46
11- Devogelaer JP, Crabbe J, Nagant de Deuxchaisnes C. Bone mineral density
in Addison's disease: evidence for an effect of adrenal androgens on bone
mass. Br Med J (Clin Res Ed). 1987;294(6575):798-800
12- Formiga F, Moga I, Nolla JM, Navarro MA, Bonnin R, Roig-Escofet D. The
association of dehydroepiandrosterone sulphate levels with bone mineral
density in systemic lupus erythematosus. Clin Exp Rheumatol.
1997;15(4):387-92
13- Sambrook PN, Eisman JA, Champion GD, Pocock NA. Sex hormone status
and osteoporosis in postmenopausal women with rheumatoid arthritis.
Arthritis Rheum. 1988;31(8):973-8
14- Greendale GA, Edelstein S, Barrett-Connor E. Endogenous sex steroids and
bone mineral density in older women and men: the Rancho Bernardo Study. J
Bone Miner Res. 1997;12(11):1833-43
15- Miller KK, Biller BM, Hier J, Arena E, Klibanski A. Androgens and Bone
Density in Women with Hypopituitarism. J Clin Endocrinol Metab. 2002 Jun
1;87(6):2770-6
16- Ortego-Centeno N, Munoz-Torres M, Jodar E, Hernandez-Quero J, JuradoDuce A, de la Higuera Torres-Puchol J. Effect of tobacco consumption on
bone mineral density in healthy young males. Calcif Tissue Int
1997;60(6):496-500
Osteoporose: A Melhora Com a Reposição de DHEA
1- Jankowski CM, Gozansky WS, Kittelson JM, Van Pelt RE, Schwartz RS,
Kohrt WM. Increases in bone mineral density in response to oral
dehydroepiandrosterone replacement in older adults appear to be mediated
by serum estrogens. J Clin Endocrinol Metab. 2008 Dec;93(12):4767-73
2- von Mühlen D, Laughlin GA, Kritz-Silverstein D, Bergstrom J, Bettencourt R.
Effect of dehydroepiandrosterone supplementation on bone mineral density,
bone markers, and body composition in older adults: the DAWN trial.
Osteoporos Int. 2008 May;19(5):699-707
3- Baulieu EE, Thomas G, Legrain S, Lahlou N, Roger M, Debuire B,
Faucounau V, Girard L, Hervy MP, Latour F, Leaud MC, Mokrane A, PittiFerrandi H, Trivalle C, de Lacharriere O, Nouveau S, Rakoto-Arison B,
Souberbielle JC, Raison J, Le Bouc Y, Raynaud A, Girerd X, Forette F.
Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging: contribution of
the DHEAge Study to a sociobiomedical issue. Proc Natl Acad Sci USA.
2000;97(8):4279-84
4- Sun Y, Mao M, Sun L, Feng Y, Yang J, Shen P Treatment of osteoporosis in
men using dehydroepiandrosterone sulfate. Chin Med J (Engl). 2002
Mar;115(3):402-4
5- Labrie F, Diamond P, Cusan L, Gomez JL, Belanger A, Candas B. Effect of
12-month dehydroepiandrosterone replacement therapy on bone, vagina, and
endometrium in postmenopausal women. J Clin Endocrinol Metab.
1997;82(10):3498-505
6- Mortola JF, Yen SS. The effects of oral dehydroepiandrosterone on
endocrine-metabolic parameters in postmenopausal women. J Clin
Endocrinol Metab. 1990;71(3):696-704
Osteoporose: A Associação Com Baixos Níveis de Estradiol
1- van Geel TA, Geusens PP, Winkens B, Sels JP, Dinant GJ. Measures of
bioavailable serum testosterone and estradiol and their relationships with
muscle mass, muscle strength and bone mineral density in postmenopausal
women: a cross-sectional study. Eur J Endocrinol. 2009 Apr;160(4):681-7
2- Mastaglia SR, Bagur A, Royer M, Yankelevich D, Sayegh F, Oliveri B. Effect
of endogenous estradiol levels on bone resorption and bone mineral density
in healthy postmenopausal women: a prospective study. Climacteric. 2009
Feb;12(1):49-58
3- Richelson LS, Wahner HW, Melton LJ 3rd, Riggs BL. Relative contributions of
aging and estrogen deficiency to postmenopausal bone loss. N Engl J Med.
1984 Nov 15; 311(20): 12273-5
4- Bourdel A, Mahoudeau JA, Guaydier-Souquieres G, Leymarie P, Sabatier JP,
Loyau G. Gonadal function in primary apparent male osteoporosis. 12 cases.
Presse Med. 1989 Oct 21;18(34):1691-4
5- Khosla S, Riggs BL, Robb RA, Camp JJ, Achenbach SJ, Oberg AL, Rouleau
PA, Melton LJ 3rd. Relationship of volumetric bone density and structural
parameters at different skeletal sites to sex steroid levels in women. J Clin
Endocrinol Metab. 2005 Sep;90(9):5096-103
6- Tremollieres FA, Pouilles JM, Ribot C. Withdrawal of hormone replacement
therapy is associated with significant vertebral bone loss in postmenopausal
women Osteoporos Int. 2001;12(5):385-90
7- Huang JS, Wilkie SJ, Sullivan MP, Grinspoon S. Reduced bone density in
androgen-deficient women with acquired immune deficiencysyndrome
wasting. J Clin Endocrinol Metab. 2001 Aug;86(8):3533-9
8- Deutsch S, Benjamin F, Seltzer V, Tafreshi M, Kocheril G, Frank A. The
correlation of serum estrogens and androgens with bone density in the late
postmenopause. Int J Gynaecol Obstet. 1987 Jun;25(3):217-22
9- Garnero P, Sornay-Rendu E, Claustrat B, Delmas PD. Biochemical markers
of bone turnover, endogenous hormones and the risk of fractures in
postmenopausal women: the OFELY study. J Bone Miner Res. 2000
Aug;15(8):1526-36
10- Lau EM, Suriwongpaisal P, Lee JK, Das De S, Festin MR, Saw SM, Khir A,
Torralba T, Sham A, Sambrook P. Risk factors for hip fracture in Asian men
and women: the Asian osteoporosis study. J Bone Miner Res. 2001
Mar;16(3):572-80
11- van den Beld AW, de Jong FH, Grobbee DE, Pols HA, Lamberts SW.
Measures of bioavailable serum testosterone and estradiol and their
relationships with muscle strength, bone density, and body composition in
elderly men. J Clin Endocrinol Metab. 2000 Sep;85(9):3276-82
Osteoporosis: A Melhora Com a Reposição de Estradiol e Progesterona
1- Sorensen MB, Rosenfalck AM, Hojgaard L, Ottesen B. Obesity and
sarcopenia after menopause are reversed by sex hormone replacement
therapy. Obes Res. 2001 Oct;9(10):622-6
2- Christiansen C, Christensen MS, Transbol I. Bone mass in postmenopausal
women after withdrawal of oestrogen/gestagen replacement therapy. Lancet.
1981 Feb 28;1(8218):459-61.
3- Christiansen C, Christensen MS, McNair P, Hagen C, Stocklund KE, Transbol
I. Prevention of early postmenopausal bone loss: controlled 2-year study in
315 normal females. Eur J Clin Invest. 1980 Aug;10(4):273-9.
4- Bagur A, Wittich A, Ghiringhelli G, Vega E, Mautalen C. Hormone
replacement therapy increases trabecular and cortical bone density in
osteoporotic women. Medicina (B Aires). 1996;56(3):247-51
5- Tiras MB, Noyan V, Yildiz A, Biberoglu K. Comparison of different treatment
modalities for postmenopausal patients with osteopenia: hormone
replacement therapy, calcitonin and clodronate. Climacteric. 2000
Jun;3(2):92-101
6- Ringe JD, Meiss F. The avoidance of early postmenopausal bone substance
losses by transdermal estrogen substitution. Dtsch Med Wochenschr. 1993
May 28;118(21):769-74
7- Lufkin EG, Wahner HW, O'Fallon WM, Hodgson SF, Kotowicz MA, Lane AW,
Judd HL, Caplan RH, Riggs BL. Treatment of postmenopausal osteoporosis
with transdermal estrogen. Ann Intern Med. 1992 Jul 1;117(1):1-9
8- Mizunuma H, Taketani Y, Ohta H, Honjo H, GoraiI, Itabashi A, Shiraki M.
Dose effects of oral estradiol on bone mineral density in Japanese women
with osteoporosis. Climacteric. 2009 Jul 7:1-12
9- Riis BJ, Thomsen K, Strom V, Christiansen C. The effect of percutaneous
estradiol and natural progesterone on postmenopausal bone loss. Am J
Obstet Gynecol. 1987 Jan;156(1):61-5
10- Nielsen TF, Ravn P, Bagger YZ, Warming L, Christiansen C. Pulsed estrogen
therapy in prevention of postmenopausal osteoporosis. A 2-year randomized,
double blind, placebo-controlled study. Osteoporos Int. 2004 Feb;15(2):16874
11- Notelovitz M, John VA, Good WR. Effectiveness of Alora estradiol matrix
transdermal delivery system in improving lumbar bone mineral density in
healthy, postmenopausal women. Menopause. 2002 Sep-Oct;9(5):343-53
12- Arrenbrecht S, Boermans AJ.Effects of transdermal estradiol delivered by a
matrix patch on bone density in hysterectomized, postmenopausal women: a
2-year placebo-controlled trial. Osteoporos Int. 2002;13(2):176-83.
13- Castelo-Branco C, Vicente JJ, Figueras F, Sanjuan A, Martinez de Osaba
MJ, Casals E, Pons F, Balasch J, Vanrell JA. Comparative effects of
estrogens plus androgens and tibolone on bone, lipid pattern and sexuality in
postmenopausal women. Maturitas. 2000 Feb
14- Cooper C, Stakkestad JA, Radowicki S, Hardy P, Pilate C, Dain MP, Delmas
PD. Matrix delivery transdermal 17beta-estradiol for the prevention of bone
loss in postmenopausal women. The International Study Group. Osteoporos
Int. 1999;9(4):358-66
15- Evans SF, Davie MW. Low and conventional dose transdermal oestradiol are
equally effective at preventing bone loss in spine and femur at all postmenopausal ages. Clin Endocrinol (Oxf). 1996 Jan;44(1):79-84
16- Ribot C, Tremollieres F, Pouilles JM, Louvet JP, Peyron R. Preventive effects
of transdermal administration of 17 beta-estradiol on postmenopausal bone
loss: a 2-year prospective study. Gynecol Endocrinol. 1989 Dec;3(4):259-67
17- Holland EF, Leather AT, Studd JW. Increase in bone mass of older
postmenopausal women with low mineral bone density after one year of
percutaneous oestradiol implants. Br J Obstet Gynaecol. 1995
Mar;102(3):238-42
18- Liu JH, Muse KN. The effects of progestins on bone density and bone
metabolism in postmenopausal women: a randomized controlled trial. Am J
Obstet Gynecol. 2005 Apr;192(4):1316-23
19- Lydeking-Olsen E, Beck-Jensen JE, Setchell KD, Holm-Jensen T. Soymilk or
progesterone for prevention of bone loss--a 2 year randomized, placebocontrolled trial. Eur J Nutr. 2004 Aug;43(4):246-57
20- Grey A, Cundy T, Evans M, Reid I. Medroxyprogesterone acetate enhances
the spinal bone mineral density response to oestrogen in late postmenopausal women. Clin Endocrinol (Oxf). 1996 Mar;44(3):293-6
21- Lee JR. Osteoporosis reversal with transdermal progesterone. Lancet. 1990
Nov 24;336(8726):1327
22- Lee JR. Is natural progesterone the missing link in osteoporosis prevention
and treatment? Med Hypotheses. 1991 Aug;35(4):316-8
23- Barengolts EI, Gajardo HF, Rosol TJ, D'Anza JJ, Pena M, Botsis J, Kukreja
SC. Effects of progesterone on postovariectomy bone loss in aged rats. J
Bone Miner Res. 1990 Nov;5(11):1143-7
Fraturas do Quadril: A Associação Com Baixos Níveis de Estradiol
1- Chapurlat RD, Garnero P, Breart G, Meunier PJ, Delmas PD. Serum estradiol
and sex hormone-binding globulin and the risk of hip fracture in elderly
women: the EPIDOS study. J Bone Miner Res. 2000 Sep;15(9):1835-41
2- Yates J, Barrett-Connor E, Barlas S, Chen YT, Miller PD, Siris ES. Rapid loss
of hip fracture protection after estrogen cessation: evidence from the National
Osteoporosis Risk Assessment. Obstet Gynecol. 2004 Mar;103(3):440-6(5
years after stopping estrogen use => loss of protection against hip fractures)
Fraturas do Quadril: A Prevenção Com a Reposição de Estradiol e
Progesterona
1- Michaelsson K, Baron JA, Farahmand BY, Persson I, Ljunghall S. Oralcontraceptive use and risk of hip fracture: a case-control study. Lancet. 1999
May 1;353(9163):1481-4 (-50 % less hip fractures)
2- Kiel DP, Felson DT, Anderson JJ, Wilson PW, Moskowitz MA. Hip fracture
and the use of estrogens in postmenopausal women. The Framingham
Study. N Engl J Med. 1987 Nov 5;317(19):1169-74
3- Kiel DP, Baron JA, Anderson JJ, Hannan MT, Felson DT. Smoking eliminates
the protective effect of oral estrogens on the risk for hip fracture among
women. Ann Intern Med. 1992 May 1;116(9):716-21
4- Yates J, Barrett-Connor E, Barlas S, Chen YT, Miller PD, Siris ES. Rapid loss
of hip fracture protection after estrogen cessation: evidence from the National
Osteoporosis Risk Assessment. Obstet Gynecol. 2004 Mar;103(3):440-6
Osteoporose: A Associação Com Baixos Níveis de Testosterona
1- Clapauch R, Mattos TM, Silva P, Marinheiro LP, Buksman S, Schrank Y.
Total estradiol, rather than testosterone levels, predicts osteoporosis in aging
men. Arq Bras Endocrinol Metabol. 2009 Nov;53(8):1020-5
2- Deutsch S, Benjamin F, Seltzer V, Tafreshi M, Kocheril G, Frank A. The
correlation of serum estrogens and androgens with bone density in the late
postmenopause. Int J Gynaecol Obstet. 1987 Jun;25(3):217-22
3- Garnero P, Sornay-Rendu E, Claustrat B, Delmas PD. Biochemical markers
of bone turnover, endogenous hormones and the risk of fractures in
postmenopausal women: the OFELY study. J Bone Miner Res. 2000
Aug;15(8):1526-36
4- Lau EM, Suriwongpaisal P, Lee JK, Das De S, Festin MR, Saw SM, Khir A,
Torralba T, Sham A, Sambrook P. Risk factors for hip fracture in Asian men
and women: the Asian osteoporosis study. J Bone Miner Res. 2001
Mar;16(3):572-80
5- van den Beld AW, de Jong FH, Grobbee DE, Pols HA, Lamberts SW.
Measures of bioavailable serum testosterone and estradiol and their
relationships with muscle strength, bone density, and body composition in
elderly men. J Clin Endocrinol Metab. 2000 Sep;85(9):3276-82
6- Fukui M, Nakamura N. Bone and Men's Health. Association between serum
testosterone and bone mineral density in patients with diabetes. Clin Calcium.
2010 Feb;20(2):206-11
7- Foresta C, Zanatta GP, Busnardo B, Scanelli G, Scandellari C. Testosterone
and calcitonin plasma levels in hypogonadal osteoporotic young men. J
Endocrinol Invest. 1985 Aug;8(4):377-9
8- Jassal SK, Barrett-Connor E, Edelstein SL. Low bioavailable testosterone
levels predict future height loss in postmenopausal women. J Bone Miner
Res. 1995 Apr;10(4):650-4
Osteoporose em Homens: A Melhora Com a Reposição de Testosterona
1- Welch BJ, Denke MA, Kermani A, Adams-Huet B, Gazmen NM, Gruntmanis
U. Comparison of testosterone, alendronate, and a combination of both
therapies in men with low bone mineral density. J Investig Med. 2007
May;55(4):168-73
2- Anderson FH, Francis RM, Faulkner K. Androgen supplementation in
eugonadal men with osteoporosis-effects of 6 months of treatment on bone
mineral density and cardiovascular risk factors. Bone. 1996 Feb;18(2):11-7
3- Katznelson L, Finkelstein JS, Schoenfeld DA, Rosenthal DI, Anderson EJ,
Klibanski A. Increase in bone density and lean body mass during testosterone
administration in men with acquired hypogonadism. J Clin Endocrinol Metab.
1996 Dec;81(12):4358-65
4- Isaia G, Mussetta M, Pecchio F, Sciolla A, di Stefano M, Molinatti GM. Effect
of testosterone on bone in hypogonadal males. Maturitas. 1992 Aug;15(1):4751
5- Salamano G, Isaia GC, Pecchio F, Appendino S, Mussetta M, Molinatti GM.
Effect on phospho-calcium metabolism of testosterone administration in
hypogonadal males. Arch Ital Urol Nefrol Androl. 1990 Mar;62(1):149-53
6- Diamond T, Stiel D, Posen S. Effects of testosterone and venesection on
spinal and peripheral bone mineral in six hypogonadal men with
hemochromatosis. J Bone Miner Res. 1991 Jan;6(1):39-43
7- Kenny AM, Prestwood KM, Gruman CA, Marcello KM, Raisz LG. Effects of
transdermal testosterone on bone and muscle in older men with low
bioavailable testosterone levels. J Gerontol A Biol Sci Med Sci. 2001
May;56(5):M266-72
8- Snyder PJ, Peachey H, Berlin JA, Hannoush P, Haddad G, Dlewati A,
Santanna J, Loh L, Lenrow DA, Holmes JH, Kapoor SC, Atkinson LE, Strom
BL. Effects of testosterone replacement in hypogonadal men. J Clin
Endocrinol Metab. 2000 Aug;85(8):2670-7
9- Snyder PJ, Peachey H, Hannoush P, Berlin JA, Loh L, Holmes JH, Dlewati A,
Staley J, Santanna J, Kapoor SC, Attie MF, Haddad JG Jr, Strom BL. Effect
of testosterone treatment on bone mineral density in men over 65 years of
age. J Clin Endocrinol Metab. 1999 Jun;84(6):1966-72
Fraturas do Quadril: A Associação Com Baixos Níveis de Testosterona
1- Leifke E, Wichers C, Gorenoi V, Lucke P, von zur Muhlen A, Brabant G. Low
serum levels of testosterone in men with minimal traumatic hip fractures. Exp
Clin Endocrinol Diabetes. 2005 Apr;113(4):208-13
-
PREVENÇÃO DO CÂNCER E REDUÇÃO DO
RISCO DE CÂNCER ATRAVÉS DA MODULAÇÃO
HORMONAL
10
Proteção na MENOPAUSA:
o
Raghvendra K et al. Cardiovascular pharmacology of estradiol
metabolites. Journal of Pharmacology and Experimental Therapeutics.
2004; 308-403-409.
 Replace E2 = presence of catecholestradiols and
methoxyestradiols = not activation of the nuclear estrogen
receptors = protection against cancer and other diseases
o
Liu ZJ et al. Selective insensitivity of ZR-75-1 human breast cancer
cells to 2-methoxyestradiol: evidence for type II beta-ydroxisteroid
dehydrogenase as the underlying cause.
Cancer
Res. 2005 Jul 1;65(13):5802-11
 Metabolism of E2 after replacement by P450 produce 2ME2
and confer protection


2ME2 decreases tumor growth, angiogenesis and growth of
cancer cells
2ME2
has strong antiproliferative, apoptotic and
antiangiogenic action
o
Fournier A. et al. Breast cancer risk in relation to different types
of hormone replacement therapy in the E3N-EPIC cohort study.
International Journal of Cancer .2005 Apr 10;114(3):448-54
 Progesterone protects, progestins worsen cancer risk
 The risk was significantly greater ( p < 0.001) with HRT
containing synthetic progestins than with HRT containing
bioidentical Progesterone
 The RR respectively 1.4 and 0.8
 20% decrease in risk with bioidentical progesterone
o
Fournier A. et al. Unequal risks for breast cancer associated with
different hormone replacement thearpies: results of the E3N-EPIC
cohort study.
Breast Cancer Research Treat .2007 Feb
10;104(13):373-91
 80.377 postmenopausal women
 No increase in breast cancer in women on E2 and
Progesterone
 CEE+MPA had RR of 1.69 or 69% increase in risk of breast
cancer
 These findings prove that bioidentical hormones are
undoubtedly safer
o
Campagnoli C. et al. Progesterone and Progestins in relation to
breast cancer risk. Journal of Steroid Biochemistry amd Molecular
Biology.2005 441-450
 Progesterone decreases breast cancer risk
 Synthetic progestins increase BC risk
 Higher P4 during menstrual cycle, 50% reduction risk
 Higher P4 HRT, 78% reduction in risk
Proteção na ANDROPAUSA:
o
Morley, J. et al., “Testosterone replacement and the physiologic
aspects of aging in men”, “ Mayo Clinic Proc 2000; 75(suppl):583-7
 There is absolutelly no clinical evidence that the risk of either
prostate cancer or BPH increases with transdermal
testosterone replacement.
o
Stattin, P. et al., “High levels of circulating testosterone are not
associated with increased prostate cancer risk: a pooled prospective
study”, “ Intl J Cancer 2004 Jan 20; 108(3):418-24.
 Higher T less prostate cancer.
 Higher E2 more prostate câncer
o
Basaria, A. et al., “Anabolic androgenic steroid therapy in the
treatment of chronic diseases”, “ The Journal of Clinical Endocrinology
and Metabolism 2004; Vol 86. No. 11:5108-5117

The increase of prostate cancer is not increased by
Testosterone administration
o
Rhoden, W. et al., “High levels of circulating testosterone are not
associated with increased prostate cancer risk” . New England Journal
of Medicine 2004 Mar; 163(3):824-7
 No compelling evidence at present to suggest that men with
higher testosterone levels are at great risk of prostate cancer
or that treating men who have hipogonadism with exogenous
androgens increases this risk. In fact, it should be recognized
that prostate cancer becomes more prevalent exactly at the
time of a man’s life when testosterone levels decline.
o
o
TESTOSTERONE therapy in men with untreated PCa
Morgentaler et al, J Urol 2011
 All men experienced symptomatic benefit
 No increase in PSA
 No increase in prostate volume
 No definite cancer progression
 54% of biopsies- no cancer seen!
o
Muller M, van der Schouw YT, Thijssen JH, Grobbee DE. Endogenous
sex hormones and cardiovascular disease in men. J Clin Endocrinol
Metab. 2003; 88 (11): 5076-86.
 A report in The Journal of Clinical Endocrinology and
Metabolism (November 2003) sheds more light on the
beneficial effects of testosterone supplementation in
andropausal men. The study authors conducted a rigorous
database search of testosterone’s effect on heart disease in
men, and identified multiple studies showing that men with low
testosterone levels had higher blood pressure, LDL cholesterol
levels, triglyceride levels, and body mass index compared to
men with optimal testosterone levels. Discussing the potential
side effects of testosterone supplementation in elderly men,
the authors noted, “the scientific basis for these concerns is
scarce.”*
HORMÔNIO DO CRESCIMENTO E CÂNCER:
o
Vance M, CJ. et al., “GH Therapy in Adults and Children. The New
England Journal of Medicine. October 14, 2000
 “No evidence that GH replacement therapy affects the risk of
cancer”
o
Molitch ME. et al., “Diagnosis of GH deficiency in adults – how good
the criteria need to be ? J Clin Endocrinol Metab 2002 Feb;
87(2):473-6
 Although there has been concerns about an increased risk of
cancer, reviews of existing well-maintained databases of
treated patients have shown this theoretical risk to be
nonexistent.
o
Fiebig HH et al. No evidence of tumor growth stimulation in human
tumors in vitro following treatment with recombinant human growth
hormone. Anticancer Drugs J 2000 Sep; 11(8):659-64
 GH improves cancer cachexia
 No evidence of tumor growth stimulation
o
Growth Hormone Research Society. J Clin Endo Metab, May 2001.
 There is no data to suggest that IGF-1 and IGFBP 3 modulate
cancer risk in GH treated patients.
 There is no data to support that active malignancy is a
contraindication for GH supplementation.
 No evidence that GH increases cancer recurrence or de novo
cancer or leukemia.
o
Swerdlow A. et al. Growth Hormone Treatment of Children with Brain
Tumors and Risk of Tumor Recurrence. The Journal of Clinical
Endocrinology and Metabolism Vol 85, No. 12, December 2000.
 Children with brain tumors  180 treated with GH
 891 not treated with GH
 In treated patients
 Decreased risk of recurrence: 60%
 Decreased risk of mortality: 50%
o
Murray R.D. et al. GH-Deficient Survivors of Chidlhood Cancer: GH
Replacement During Adult Life. The Journal of Clinical Endocrinology
and Metabolism 2002 Jan;87(1):129-35
 GH Replacement and Cancer
 Improved QOL
 “Importantly, during the 12-24 months of GH replacement
therapy, there was absolutely no clinical suggestion of tumor
reccurence.
o
Hong J et al. IGFBP 3 mutants that do not bind IGFs stimulate
apoptosis in human cancer cells. Journal of Bio Chem 2002 Jan 9.
 IGFBP 3 Independent Anti-Cancer Actions
 IGFBP 3 triggers cell cycle and stimulates apoptosis.
 IGFBP 3 independent mechanisms are major contributors to
IGFBP 3 induced apoptosis in cancer cells.
 IGFBP 3 plays a wider hole in the anti-proliferative and antitumorgenic actions.
 IGFBP 3 may be considered “The Guardian of the Genome”.
o
Kurek R et al. The significance of serum levels of insulin-like growth
factor 1 in patients with prostate cancer. J Clin Endoc Metab, 2000
Jan;85(1):125-9.
 No association between IGF-1, GH and prostate cancer risk.
 Androgen decline or withdrawal did not change IGF-1.
o
Baffa R et al. Low serum insulin-like growth factor 1 : a significant
association with prostate cancer. J Urology, 2000 Sep;6(3):236-239.
 Low IGF-1 Associated with Prostate Cancer
 IGF-1 considerably lower in Prostate CA patients than control.



o
No association of IGF-1, GH levels and PSA increase.
IGF-1 decresed with age
Prostate cancer risk increased with age
.
Finne P et Al IGf-1 Tumor Marker for cancer prostate ? . Can
Research 2004 15;63(14)3991-496 Mar 28;334(13): 800-14
 Declínio IGF-1 diretamente correlacionado com aumento do
risco de câncer de próstata
 Queda 55% de IGF-1, representa aumento de 48% no
risco de ca próstata
Câncer: Efeito Protetor da Reposição de Melatonina
177. Mills E, Wu P, Seely D, Guyatt G. Melatonin in the treatment of cancer: a
systematic review of randomized controlled trials and meta-analysis. J Pineal
Res. 2005 Nov;39(4):360-6
178. Lissoni P, Barni S, Ardizzoia A, Paolorossi F, Crispino S, Tancini G, Tisi E,
Archili C, De Toma D, Pipino G, et al. Randomized study with the pineal
hormone melatonin versus supportive care alone in advanced nonsmall cell
lung cancer resistant to a first-line chemotherapy containing cisplatin.
Oncology. 1992;49(5):336-9
179. Lissoni P, Brivio O, Brivio F, Barni S, Tancini G, Crippa D, Meregalli S.
Adjuvant therapy with the pineal hormone melatonin in patients with lymph
node relapse due to malignant melanoma. J Pineal Res. 1996 Nov;21(4):23942
180. Lissoni P. Is there a role for melatonin in supportive care? Support Care
Cancer. 2002 Mar;10(2):110-6
181. Lissoni P, Rovelli F, Malugani F, Bucovec R, Conti A, Maestroni GJ. Antiangiogenic activity of melatonin in advanced cancer patients. Neuroendocrinol
Lett. 2001;22(1):45-7
182. Neri B, de Leonardis V, Gemelli MT, di Loro F, Mottola A, Ponchietti R, Raugei
A, Cini G. Melatonin as biological response modifier in cancer patients.
Anticancer Res. 1998 Mar-Apr;18(2B):1329-32
183. Lissoni P, Paolorossi F, Tancini G, Barni S, Ardizzoia A, Brivio F, Zubelewicz B,
Chatikhine V. Is there a role for melatonin in the treatment of neoplastic
cachexia? Eur J Cancer. 1996 Jul;32A(8):1340-3
184. Gonzalez R, Sanchez A, Ferguson JA, Balmer C, Daniel C, Cohn A, Robinson
WA. Melatonin therapy of advanced human malignant melanoma. Melanoma
Res. 1991 Nov-Dec;1(4):237-43
185. Bartsch C, Bartsch H. Melatonin in cancer patients and in tumor-bearing
animals. Adv Exp Med Biol. 1999;467:247-64
186. Cos S, Fernandez R, Guezmes A, Sanchez-Barcelo EJ. Influence of melatonin
on invasive and metastatic properties of MCF-7 human breast cancer cells.
Cancer Res. 1998 Oct 1;58(19):4383-90
187. Kossoy G, Ben-Hur H, Popovich I, Zabezhinski M, Anisimov V, Zusman I.
Melatonin and colon carcinogenesis. IV. Effect of melatonin on proliferative
activity and expression of apoptosis-related proteins in the spleen of rats
exposed to 1,2-dimethylhydrazine. Oncol Rep. 2000 Nov-Dec;7(6):1401-5
188. Kumar CA, Das UN. Effect of melatonin on two stage skin carcinogenesis in
Swiss mice. Med Sci Monit. 2000 May-Jun;6(3):471-5
189. Lissoni P, Paolorossi F, Ardizzoia A, Barni S, Chilelli M, Mancuso M, Tancini G,
Conti A, Maestroni GJ. A randomized study of chemotherapy with cisplatin plus
etoposide versus chemoendocrine therapy with cisplatin, etoposide and the
pineal hormone melatonin as a first-line treatment of advanced non-small cell
lung cancer patients in a poor clinical state. J Pineal Res. 1997 Aug;23(1):15-9
190. Lissoni P, Rovelli F, Frassineti A, Fumagalli L, Malysheva O, Conti A, Maestroni
G. Oncostatic activity of pineal neuroendocrine treatment with the pineal
indoles melatonin and 5-methoxytryptamine in untreatable metastatic cancer
patients progressing on melatonin alone. Neuroendocrinol Lett. 2000;21(4):31923
Câncer: A Associação Com Baixos Niveis do Hormônio do Crescimento
1- Woodson K, Tangrea JA, Pollak M, Copeland TD, Taylor PR, Virtamo J,
Albanes D. Serum IGF-1: tumor marker or etiologic factor? A prospective
study of prostate cancer among Finnish men. Cancer Res. 2003 Jul
15;63(14):3991-4
2- Chokkalingam AP, Pollak M, Fillmore CM, Gao YT, Stanczyk FZ, Deng J,
Sesterhenn IA, Mostofi FK, Fears TR, Madigan MP, Ziegler RG, Fraumeni JF
Jr, Hsing AW. Insulin-like growth factors and prostate cancer: a populationbased case-control study in China. Cancer Epidemiol Biomarkers Prev. 2001
May;10(5):421-7
3- Baffa R, Reiss K, El-Gabry EA, Sedor J, Moy ML, Shupp-Byrne D, Strup SE,
Hauck WW, Baserga R, Gomella LG. Low serum insulin-like growth factor 1
(IGF-1): a significant association with prostate cancer. Tech Urol. 2000
Sep;6(3):236-9
4- Finne P, Auvinen A, Koistinen H, Zhang WM, Maattanen L, Rannikko S,
Tammela T, Seppala M, Hakama M, Stenman UH. Insulin-like growth factor I
is not a useful marker of prostate cancer in men with elevated levels of
prostate-specific antigen. J Clin Endocrinol Metab. 2000 Aug;85(8):2744-7
5- Colombo F, Iannotta F, Fachinetti A, Giuliani F, Cornaggia M, Finzi G,
Mantero G, Fraschini F, Malesci A, .Bersani M, et al. Changes in hormonal
and biochemical parameters in gastric adenocarcinoma. Minerva Endocrinol.
1991 Jul-Sep;16(3):127-39
Estudos em Humanos Relacionando Baixos Níveis de GH/IGF-1 em Pacientes
Com Câncer
Baixos Níveis de IGF-1 no Glioma
1.
Lönn S, Inskip PD, Pollak MN, Weinstein SJ, Virtamo J, Albanes D. Glioma risk
in relation to serum levels of insulin-like growth factors. Cancer Epidemiol
Biomarkers Prev. 2007 Apr;16(4):844-6
Baixos Níveis de IGF-1 no Câncer de Próstata
1- Agurs-Collins T, Adams-Campbell LL, Kim KS, Cullen KJ.Ins ulin-like growth
factor-1 and breast cancer risk in postmenopausal African-American women.
Cancer Detect Prev. 2000;24(3):199-206
2- Fuhrman B, Barba M, Schünemann HJ, Hurd T, Quattrin T, Cartagena R,
Carruba G, Muti P. Basal growth hormone concentrations in blood and the
risk for prostate cancer: a case-control study. Prostate. 2005 Jul 1;64(2):10915
3- Woodson K, Tangrea JA, Pollak M, Copeland TD, Taylor PR, Virtamo J,
Albanes D. Serum insulin-like growth factor I: tumor marker or etiologic
factor? A prospective study of prostate cancer among Finnish men. Cancer
Res. 2003 Jul 15;63(14):3991-4
4- Chen C, Lewis SK, Voigt L, Fitzpatrick A, Plymate SR, Weiss NS. Prostate
carcinoma incidence in relation to prediagnostic circulating levels of insulinlike growth factor I, insulin-like growth factor binding protein 3, and insulin.
Cancer. 2005 Jan 1;103(1):76-84
Baixos Níveis de IGF-1 no Câncer Colorretal
1- Palmqvist R, Hallmans G, Rinaldi S, Biessy C, Stenling R, Riboli E, Kaaks R.
Plasma insulin-like growth factor 1, insulin-like growth factor binding protein 3,
and risk of colorectal cancer: a prospective study in northern Sweden. Gut.
2002 May;50(5):642-6
Baixos Níveis de IGF-1 no Câncer Pancreático
1- Stolzenberg-Solomon RZ, Limburg P, Pollak M, Taylor PR, Virtamo J,
Albanes D. Insulin-like growth factor (IGF)-1, IGF-binding protein-3, and
pancreatic cancer in male smokers. Cancer Epidemiol Biomarkers Prev.
2004 Mar;13(3):438-44
Baixos Níveis de IGF-1 no Câncer Cervical
1- Schaffer A, Koushik A, Trottier H, Duarte-Franco E, Mansour N, Arseneau J,
Provencher D, Gilbert L, Gotlieb W, Ferenczy A, Coutlée F, Pollak MN,
Franco EL; Biomarkers of Cervical Cancer Risk Study Team . Insulin-like
growth factor-I and risk of high-grade cervical intraepithelial neoplasia.
Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):716-22
2- Serrano ML, Romero A, Cendales R, Sánchez-Gómez M, Bravo MM.
Serum levels of insulin-like growth factor-I and -II and insulin-like growth
factor binding protein 3 in women with squamous intraepithelial lesions and
cervical cancer. Biomedica. 2006 Jun;26(2):258-68
Estudos em Humanos Reportando Ausência de Correlação ou Associação dos
Níveis de IGF-1 e Câncer
Câncer de Próstata
1- Weiss JM, Huang WY, Rinaldi S, Fears TR, Chatterjee N, Chia D, Crawford
ED, Kaaks R, Hayes RB. IGF-1 and IGFBP-3: Risk of prostate cancer among
men in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Int
J Cancer. 2007 Nov 15;121(10):2267-73
Câncer Colorrectal
1- Probst-Hensch NM, Yuan JM, Stanczyk FZ, Gao YT, Ross RK, Yu MC. IGF-1,
IGF-2 and IGFBP-3 in prediagnostic serum: association with colorectal
cancer in a cohort of Chinese men in Shanghai. Br J Cancer. 2001 Nov
30;85(11):1695-9
Câncer Mama
1- Del Giudice ME, Fantus IG, Ezzat S, McKeown-Eyssen G, Page D, Goodwin
PJ. Insulin and related factors in premenopausal breast cancer risk. Breast
Cancer Res Treat
1998 Jan;47(2):111-20 (No statistically significant
differences between breast cancer patients and controls for IGF-I and IGFBP1 levels in premenopausal women)
2- Kajdaniuk D, Marek B. Influence of adjuvant chemotherapy with
cyclophosphamide methotrexate and 5-fluorouracil on plasma insulin-like
growth factor-I and chosen hormones in breast cancer pre-menopausal
patients. J Clin Pharm Ther
2000 Feb;25(1):67-72 (Plasma IGF-I
concentration in breast cancer patients prior to treatment did not differ
significantly from that of healthy women)
Câncer: Possível Melhora da Evolução Com Reposição do Hormônio do
Crescimento
12-
3-
Torosian MH. Growth hormone and prostate cancer growth and metastasis in
tumor-bearing animals. J Pediatr Endocrinol. 1993 Jan-Mar;6(1):93-7
Ng EH, Rock CS, Lazarus DD, Stiaino-Coico L, Moldawer LL, Lowry SF.
Insulin-like growth factor I preserves host lean tissue mass in cancer
cachexia. Am J Physiol. 1992 Mar;262(3 Pt 2):R426-31
Bartlett DL, Charland S, Torosian MH. Growth hormone, insulin, and
somatostatin therapy of cancer cachexia. Cancer. 1994 Mar 1;73(5):1499504
Câncer: A Associação Com Baixos de DHEA
1- Herman WA, Seńko A, Korczowska I, Łacka K. Could serum DHEA and
DHEAS levels be good risk predictors of metabolic syndrome and
osteoporosis in the population of ageing men? Pol Merkur Lekarski. 2009
Sep;27(159):197-201
2- Alberg AJ, Gordon GB, Hoffman SC, Comstock GW, Helzlsouer KJ. Serum
dehydroepiandrosterone and dehydroepiandrosterone sulfate and the
subsequent risk of developing colon cancer. Cancer Epidemiol Biomarkers
Prev. 2000 May;9(5):517-21
3- Alberg AJ, Gordon GB, Genkinger JM, Hoffman SC, Selvin E, Comstock GW,
Helzlsouer KJ. Serum dehydroepiandrosterone and dehydroepiandrosterone
sulfate and risk of melanoma or squamous cell carcinoma of the skin.
Anticancer Res. 2001 Nov-Dec;21(6A):4051-4
4- Karasek M, Pawlikowski M. Pineal gland, melatonin and cancer.
Neuroendocrinol Lett. 1999;20(3-4):139-44
5- Lissoni P, Rovelli F, Giani L, Mandala M, Meregalli S, Barni S, Confalonieri G,
Bonfanti A. Dehydroepiandrosterone sulfate (DHEAS) secretion in early and
advanced solid neoplasms: selective deficiency in metastatic disease. Int J
Biol Markers. 1998 Jul-Sep;13(3):154-7
Câncer: Possível Melhora da Evolução Com Reposição de DHEA
1- Luo S, Sourla A, Labrie C, Belanger A, Labrie F. Combined effects of
dehydroepiandrosterone and EM-800 on bone mass, serum lipids, and the
development of dimethylbenz(A)anthracene-induced mammary carcinoma in
the rat. Endocrinology. 1997;138(10):4435-44
2- Mcikova-Kalicka K, Bojkova B, Adamekova E, Mnichova-Chamilova M,
Kubatka P, Ahlersova E, Ahlers I. Preventive effect of indomethacin and
melatonin
on
7,
12-dimethybenz/a/anthracene-induced
mammary
carcinogenesis in female Sprague-Dawley rats. A preliminary report. Folia
Biol (Praha). 2001;47(2):75-9
3- Melvin WS, Boros LG, Muscarella P, Brandes JL, Johnson JA, Fisher
WE,Schirmer WJ, Ellison EC.. Dehydroepiandrosterone-sulfate inhibits
pancreatic carcinoma cell proliferation in vitro and in vivo. Surgery.
1997;121(4):392-7
4- Nyce JW, Magee PN, Hard GC, Schwartz AG. Inhibition of 1,2dimethylhydrazine-induced colon tumorigenesis in Balb/c mice by
dehydroepiandrosterone. Carcinogenesis. 1984;5(1):57-62
5- Orner GA, Hendricks JD, Arbogast D, Williams DE. Modulation of aflatoxin-B1
hepatocarcinogenesis in trout by dehydroepiandrosterone: initiation/postinitiation and latency effects. Carcinogenesis. 1998;19(1):161-7
6- Rao KV, Johnson WD, Bosland MC, Lubet RA, Steele VE, Kelloff GJ,
McCormick DL. Chemoprevention of rat prostate carcinogenesis by early and
delayed administration of dehydroepiandrosterone. Cancer Res. 1999 Jul
1;59(13):3084-9
7- McCormick DL, Rao KV, Johnson WD, Bowman-Gram TA, Steele VE, Lubet
RA, Kellof GJ. Exceptional chemopreventive activity of low-dose
dehydroepiandrosterone in the rat mammary gland. Cancer Res. 1996 Apr
15;56(8):1724-6
8- McCormick DL, Rao KV. Chemoprevention of hormone-dependent prostate
cancer in the Wistar-Unilever rat. Eur Urol. 1999;35(5-6):464-7
Câncer de Mama: Melhora Com a Reposição de DHEA
1- Boccuzzi G, Aragno M, Brignardello E, Tamagno E, Conti G, Di Monaco M,
Racca S, Danni O, Di Carlo F. Opposite effects of dehydroepiandrosterone
on the growth of 7,12-dimethylbenz(a)anthracene-induced rat mammary
carcinomas. Anticancer Res. 1992 Sep-Oct;12(5):1479-83
2- Boccuzzi G, Brignardello E, di Monaco M, Forte C, Leonardi L, Pizzini A.
Influence of dehydroepiandrosterone and 5-en-androstene-3 beta, 17 betadiol on the growth of MCF-7 human breast cancer cells induced by 17 betaestradiol. Anticancer Res. 1992 May-Jun;12(3):799-803
ESTUDOS EM HUMANOS
Estudos Demonstrando Associação Entre Baixos Níveis de DHEA e Aumento
do Risco de Câncer de Mama
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
Rose DP, Stauber P, Thiel A, Crowley JJ, Milbrath JR. Plasma DHEAs,
Androstenedione and cortisol, and urinary free cortisol excretion in breast
cancer. Europ J Cancer. 1977; 13: 43-7
Gomes P, Cassanas G, Halberg F, Hermida R, Robel P, Baulieu EE, Lakatua
D, Haus E. Taux sanguin de la DHEA-S et risque de cancer du sein. C R Acad
Sci III. 1988;306(7):261-4
Brownsey B, Cameron EH, Griffiths K, Gleave EN, Forrest AP, Campbell H..
Plasma dehydroepiandrosterone sulphate levels in patients with benign and
malignant breast disease., Eur J Cancer. 1972;8(1):131-7
Wang DY, Bulbrook RD, Herian M, Hayward JL. Studies on the sulphate esters
of dehydroepiandrosterone and androsterone in the blood of women with breast
cancer. Eur J Cancer. 1974;10(8):477-82
Cameron EH, Griffiths K, Gleave E, Stewart HJ, Forrest AP, Campbell H.,
Benign and malignant breast disease in South Wales: a study of urinary
steroids., Br Med J. 1970;4(738):768-71
Bulbrook RD, Hayward JL, Spicer CC, Thomas BS. Abnormal excretion of
urinary steroids by women with early breast cancer. Lancet. 1962; 1238-40
Tominaga T, Tei N, Kitamura M, Taguchi T, Kudo Y. Urinary excretion of
steroids by Japanese women with breast cancer. Gann 1975 Jun;66(3):305-10
Hindy I, Prajda N, Tapolcsanyi L, Sellei C, Eckhardt S. Investigation of 17ketosteriod excretion in mastopathia and premenopausal breast cancer. Arch
Geschwulstforsch 1975;45(5):453-6
Tominaga T, Tei N, Kitamura M, Taguchi T, Kudo Y. Urinary excretion of
steroids by Japanese women with breast cancer. Gann 1975 Jun;66(3):305-10
Hindy I, Prajda N, Tapolcsanyi L, Sellei C, Eckhardt S. Investigation of 17ketosteriod excretion in mastopathia and premenopausal breast cancer. Arch
Geschwulstforsch 1975;45(5):453-6
Thijssen JH, van Landeghem AA, Poortman J. Uptake and concentration of
steroid hormones in mammary tissues. Ann N Y Acad Sci. 1986;464:106-16.
Lissoni P, Rovelli F, Giani L, Mandala M, Meregalli S, Barni S, Confalonieri G,
Bonfanti A. Dehydroepiandrosterone sulfate (DHEAS) secretion in early and
advanced solid neoplasms: selective deficiency in metastatic disease. Int J Biol
Markers. 1998;13(3):154-7
Labrie F, Luu-The V, Belanger A, Lin SX, Simard J, Pelletier G, Labrie C. Is
dehydroepiandrosterone a hormone? J Endocrinol. 2005 Nov;187(2):169-96
Cutler SY, Young JL. Third National Cancer Survey: incidence data.
Washington DC: National Cancer Institute Monograph; 1975; vol. 41
Baixos Níveis de DHEA Tem Sido Observados em Outros Tipos de Câncer:
Leucemia, Metástases e Câncer do Ovário
1- Cuzick J, Bulstrode JC, Stratton I, Thomas BS, Bulbrook RD, Hayward JL. A
prospective study of urinary androgen levels and ovarian cancer. Int J Cancer
1983 Dec 15;32(6):723-6
2- Heinonen PK, Koivula T, Pystynen P. Decreased serum level of
dehydroepiandrosterone sulfate in postmenopausal women with ovarian
cancer. Gynecol Obstet Invest 1987;23(4):271-4
3- Blaakaer J, Hogdall CK, Hording U, Bennett P, Toftager-Larsen K, Daugaard
S,Bock J. Hormonal factors and prognosis in epithelial ovarian cancer: a
multivariate analysis. Eur J Obstet Gynecol Reprod Biol 1993 Sep;51(1):21-7
4- Uozumi K, Uematsu T, Otsuka M, Nakano S, Takatsuka Y, Iwahashi M,
Hanada S, Arima T. Serum dehydroepiandrosterone and DHEA-sulfate in
patients with adult T-cell leukemia and human T-lymphotropic virus type I
carriers.Am J Hematol 1996;53(3):165-8
5- Lissoni P, Rovelli F, Giani L, Mandala M, Meregalli S, Barni S, Confalonieri G,
Bonfanti A. Dehydroepiandrosterone sulfate (DHEAS) secretion in early and
advanced solid neoplasms: selective deficiency in metastatic disease. Int J
Biol Markers. 1998;13(3):154-7
Câncer: A Associação Com Baixos Níveis de Estradiol
1- Holmberg L, Norden T, Lindgren A, Wide L, Degerman M, Adami HO. Preoperative oestradiol levels - relation to survival in breast cancer. Eur J Surg
Oncol 2001 Mar;27(2):152-6
2- MacMahon B, Cole P, Brown JB, Aoki K, Lin TM, Morgan RW, Woo NC.
Urine oestrogen profiles of Asian and North American women. Int J Cancer.
1974 Aug 15;14(2):161-7
3- MacMahon B, Cole P, Brown JB, Aoki K, Lin TM, Morgan RW, Woo N.
Oestrogen profiles of Asian and North American women. Lancet. 1971 Oct
23;2(7730):900-2
4- Ursin G, Wilson M, Henderson BE, Kolonel LN, Monroe K, Lee HP, Seow A,
YuMC, Stanczyk FZ, Gentzschein E Do urinary estrogen metabolites reflect
the differences in breast cancer risk between Singapore Chinese and United
States African-American and white women? Cancer Res. 2001 Apr
15;61(8):3326-9
5- Ursin G, London S, Stanczyk FZ, Gentzschein E, Paganini-Hill A, Ross RK,
Pike MC. Urinary 2-hydroxyestrone/16alpha-hydroxyestrone ratio and risk of
breast cancer in postmenopausal women. J Natl Cancer Inst 1999 Jun
16;91(12):1067-72
6- Lemon HM. Pathophysiologic considerations in the treatment of menopausal
patients withoestrogens; the role of oestriol in the prevention of mammary
carcinoma. Acta Endocrinol Suppl (Copenh) 1980;233:17-27
7- Vorherr H, Messer RH. Breast cancer: potentially predisposing and protecting
factors. Role of pregnancy, lactation, and endocrine status. Am J Obstet
Gynecol 1978 Feb 1;130(3):335-58
Câncer: A Associação Com Baixos Níveis de Progesterona
1- Cowan LD, Gordis L, Tonascia JA, Jones GS. Breast cancer incidence in
women with a history of progesterone deficiency. Am J Epidemiol 1981
Aug;114(2):209-17
2- Adami HO, Bergstrom R, Holmberg L, Klareskog L, Persson I, Ponten J.The
effect of female sex hormones on cancer survival. A register-based study in
patients younger than 20 years at diagnosis. JAMA. 1990 Apr
25;263(16):2189-93
3- Adami HO, Holmberg L, Persson I. Survival and age at diagnosis in breast
cancer. N Engl J Med. 1987 ; 316(12): 750-2
4- Mohr PE, Wang DY, Gregory WM, Richards MA, Fentiman IS. Serum
progesterone and prognosis in operable breast cancer. Br J Cancer. 1996
Jun;73(12):1552-5
5- Badwe RA, Wang DY, Gregory WM, Fentiman IS, Chaudary MA, Smith P,
Richards MA, Rubens RD. Serum progesterone at the time of surgery and
survival in women with premenopausal operable breast cancer.Eur J Cancer.
1994;30A(4):445-8
Câncer: Possível Proteção Com a Reposição de Estradiol
1- . Henderson BE, Paganini-Hill,A, Ross RK. Decreased mortality in users of
estrogen replacement therapy. Arch Intern Med 1991; 151:75
Estudos Demonstrando A Redução do Risco do Câncer de Mamam Coma
Reposição de Estradiol
1-
2-
3-
45-
6-
7-
Plu-Bureau G, Le MG, Thalabard JC, Sitruk-Ware R, Mauvais-Jarvis
P. Percutaneous progesterone use and risk of breast cancer: results
from a French cohort study of premenopausal women with benign
breast disease. Cancer Detect Prev 1999;23(4):290-6
Lauritzen C et al. Risks of endometrial and mammary cancer
morbidity and mortality in long-term estrogen treatment. In The
Climacteric -An Update, ed by van Herendael H & B, Riphagen FE,
Goessens L, van der Pars H Lancaster, England, MTP Press Ltd
1984; 207
Peters GN, Fodera T, Sabol J, Jones S, Euhus D. Estrogen
replacement therapy after breast cancer: a 12-year follow-up. Ann
Surg Oncol 2001 Dec;8(10):828-32
Gambrell RD Jr. Hormones in the etiology and prevention of breast and
endometrial cancer. South Med J.1984 Dec: 77(12): 1509-15.
Gambrell RD Jr, Maier RC, Sanders BI. Decreased incidence of
breast cancer in postmenopausal estrogen progestogen users..
Obstet Gynecol 1983 Oct;62(4):435-43
Wingo PA, Layde PM, Lee NC, Rubin G, Ory HW. The risk of breast
cancer in postmenopausal women who have used estrogen
replacement therapy. JAMA. 1987 Jan 9; 257(2): 209-15
Nachtigall LE, Nachtigall RH, Nachtigall RD, Beckman EM. Estrogen
replacement Il: A prospective study in the relationship to carcinoma
and cardiovascular and metabolic problems. Obstet Gynecol. 1979;
54: 74-9
8-
9-
10-
11-
12-
Davelaar EM, Gerretsen G, Relyveld J.. No increase in the incidence
of breast carcinoma with subcutaneous administration of estradiol Ned
Tijdsch Geneeskd. 1991 Apr 6 ; 135(14): 613-5
Rosenberg L, Miller DR, Kaufman DW, Helmrich SP, Stolley PD,
Schottenfeld. D; Shapiro S. Breast cancer and oral contraceptive use.
Am J Epidemiol 1984 Feb;119(2):167-76
Kaufman DW, Miller DR, Rosenberg, Miller DR, Rosenberg L,
Helmrich SP, Stolley P, Schottenfeld D, Shapiro S. Noncontraceptive
estrogen use and the risk of breast JAMA 1984 Jul 6;252(1):63-7
Hammond CB, Jelovsek FR, Lee KI, WT, Parker. Effects of long term
estrogen replacement therapy. II - Neoplasia. Am J Obstet Gynecol.
1979; 133: 537 (Reduced aggressivity of breast cancer if HRT before)
Sellers, TA, Mink, PJ, Cerhan, JR, g W, Anderson KE, Kushi LH,
Folson AR. The role of hormone replacement therapy in the risk for
breast cancer and total mortality in women with a family history of
breast cancer. Ann Intern Med 1997; 127:973
Estudos Demonstrando o Aumento da Longevidade e a Redução de
Recorrência em Mulheres Com História Prévia de Câncer de Mama Submetidas
a Reposição de Estradiol
1- Wile AG, Opfell RW, Margileth DA. Hormone replacement therapy in
previously treated breast cancer patients. Am J Surg. 1993 Mar;165(3):372-5
2- O'Meara ES, Rossing MA, Daling JR, Elmore JG, Barlow WE, Weiss NS.
Hormone replacement therapy after a diagnosis of breast cancer in relation to
recurrence & mortality. J Natl Cancer Inst. 2001;93(10):754-62
3- Dew JE, Wren BG, Eden JA. Tamoxifen, hormone receptors & hormone
replacement therapy in women previously treated for breast cancer: a cohort
study. Climacteric. 2002;5(2):151-5
4- Dew J, Eden J, Beller E, Magarey C, Schwartz P, Crea P, Wren B. A cohort
study of hormone replacement therapy given to women previously treated for
breast cancer. Climacteric.1998;1(2):137-42
5- Durna EM, Wren BG, Heller GZ, Leader LR, Sjoblom P, Eden JA. Hormone
replacement therapy after a diagnosis of breast cancer: cancer recurrence
and mortality. Med J Aust. 2002 Oct 7;177(7):347-51
6- Steinberg KK, Thacker SB, Smith SJ, Stroup DF, Zack MM, Flanders WD,
Berkelman RL. A meta-analysis of the effect of estrogen replacement therapy
on the risk of breast cancer. JAMA. 1991 Apr 17;265(15):1985-90
7- Grodstein F, Stampfer MJ, Colditz GA, Willett WC, Manson JE, Joffe M,
Rosner B, Fuchs C, Hankinson SE, Hunter DJ, Hennekens CH, Speizer FE.
Postmenopausal hormone therapy and mortality. N Engl J Med. 1997;
336:1769-75
8- Mohammed SN, Smith P, Hodgson SV, Fentiman IS, Miles DW, Barnes DM,
Millis RR, Rubens RD Family history and survival in premenopausal breast
cancer. Br J Cancer. 1998 Jun;77(12):2252-6
9- Gajdos C, Tartter PI, Babinszki A. Breast cancer diagnosed during hormone
replacement therapy. Obstet Gynecol. 2000 Apr;95(4):513-8
10- Holli K, Isola J, Cuzick J. Low biologic aggressiveness in breast cancer in
women using hormone replacement therapy. J Clin Oncol. 1998
Sep;16(9):3115-20
11- Magnusson C, Holmberg L, Norden T, Lindgren A, Persson I. Prognostic
characteristics in breast cancers after hormone replacement therapy. Breast
Cancer Res Treat. 1996;38(3):325-34
12- Meurer LN, Lena S. Cancer recurrence and mortality in women using
hormone replacement therapy: meta-analysis.J Fam Pract. 2002
Dec;51(12):1056-62
13- Ursin G, Tseng CC, Paganini-Hill A, Enger S, Wan PC, Formenti S, Pike MC,
Ross RK. Does menopausal hormone replacement therapy interact with
known factors to increase risk of breast cancer? Arch 1: J Clin Oncol 2002
Feb 1;20(3):699-706
14- Nanda K, Bastian LA, Schulz K. Hormone replacement therapy and the risk of
death from breast cancer: a systematic review. Am J Obstet Gynecol. 2002
Feb; 186 (2):325-34
15- Willis DB, Calle EE, Miracle-McMahill HL, Heath CW Jr. Estrogen
replacement therapy and risk of fatal breast cancer in a prospective cohort of
postmenopausal women in the United States. Cancer Causes Control. 1996
Jul;7(4):449-57
16- Schairer C, Gail M, Byrne C, Rosenberg PS, Sturgeon SR, Brinton LA,
Hoover RN.Estrogen replacement therapy and breast cancer survival in a
large screening study. J Natl Cancer Inst. 1999 Feb 3;91(3):264-70
17- Ettinger B, Friedman, GD, Bush, T, Quesenberry CP Jr. Reduced mortality
associated with long-term postmenopausal estrogen therapy. Obstet
Gynecol. 1996 Jan;87(1):6-12 1140 Jernstrom H, Frenander J, Ferno M,
Olsson H. Hormone replacement therapy before breast cancer diagnosis
significantly reduces the overall death rate compared with never-use among 984
breast cancer patients. Br J Cancer. 1999 Jul;80(9):1453-8
18- Hunt K, Vessey M, McPherson K. Long-term surveillance of mortality and
cancer incidence in women recieving hormone replacement therapy. Br J
Obstet Gynaecol. 1987; 94: 620-35
19- Plu-Bureau G, Le MG, Sitruk-Ware R, Thalabard JC, Mauvais-Jarvis P.
Progestogen use and decreased risk of breast cancer in a cohort study of
premenopausal women with benign breast disease. Br J Cancer. 1994
Aug;70(2):270-7
20- Lundgren S, Lonning PE. Influence of progestins on serum hormone levels in
postmenopausal women with advanced breast cancer -II. A differential effect
of megestrol acetate and medroxyprogesterone acetate on serum estrone
sulfate and sex hormone binding globulin. J Steroid Biochem. 1990 Jun ;
36(1-2): 105-9
´
Câncer: A Associação Com Baixos Níveis de Testosterona
17.
18.
19.
20.
21.
Imamoto T, Suzuki H, Fukasawa S, Shimbo M, Inahara M, Komiya A, Ueda T,
Shiraishi T, Ichikawa T. Pretreatment serum testosterone level as a predictive
factor of pathological stage in localized prostate cancer patients treated with
radical prostatectomy. Eur Urol. 2005 Mar;47(3):308-12
Meikle AW, Stanish WM. Familial prostatic cancer risk and low testosterone. J Clin
Endocrinol Metab 1982 Jun;54(6):1104-8
Turkes AO, Turkes A, Read GF, Fahmy DR. A sensitive fluorometric enzyme
immunoassay for testosterone in plasma and saliva [proceedings] J Endocrinol.
1979 Oct;83(1):31P.
Vestsi Akademii Medicina Navuk USSR 1980; 3: 72-7 (mentioned in The
natural prostate cure (Proger Mason 2000 ISBN 1-884820-61-1)°
Kumar VL, Wadhwa SN, Kumar V, Farooq A.
Androgen, estrogen, and
progesterone receptor contents and serum hormone profiles in patients with
benign hypertrophy and carcinoma of the prostate. J Surg Oncol. 1990
Jun;44(2):122-8
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
Progress in Clinical Biological Research 1975; 6: 143-58 (mentioned in The
natural prostate cure, Proger Mason 2000 ISBN 1-884820-61-1)
Zhonghua Yixue Zazhi 1993; 73: 489-90 (mentioned in The natural prostate
cure (Proger Mason 2000 ISBN 1-884820-61-1)
Hulka BS, Hammond JE, DiFerdinando G, Mickey DD, Fried FA, Checkoway H,
Stumpf WE, Beckman WC Jr, Clark TD. Serum hormone levels among patients
with prostatic carcinoma or benign prostatic hyperplasia and clinic controls.
Prostate 1987;11(2):171-82
Ortega E, Ruiz E, Mendoza MC, Martin-Andres A, Osorio C. Plasma steroid
and protein hormone concentrations in patients with benign prostatic
hypertrophy and in normal men. Experientia. 1979 Jun 15;35(6):844-5
Wright F, Poizat, Bongini M,Bozzolan F Doukani A, Mauvais-Jarvis P.
Decreased urinary 5-alpha-androstanediol glucuronide excretion in patients
with benign prostatic hyperplasia. J Clin Endocrinol Metab. 1985; 60 (2) 294-8
Wu AH, Whittemore AS, Kolonel LN, John EM, Gallagher RP, West DW, Hankin
J, Teh CZ, Dreon DM, Paffenbarger RS Jr. Serum androgens and sex hormonebinding globulins in relation to lifestyle factors in older African-American, white,
and Asian men in the United States and Canada. Cancer Epidemiol Biomarkers
Prev. 1995 Oct-Nov;4(7):735-41
Zumoff B, Levin J, Strain GW, Rosenfeld RS, O'Connor J, Freed SZ, Kream J,
Whitmore WS, Fukushima DK, Hellman L. Abnormal levels of plasma
hormones in men with prostate cancer: evidence toward a " two-disease"
theory. Prostate 1982;3(6):579-88
Signorello LB, Tzonou A, Mantzoros CS, Lipworth L, Lagiou P, Hsieh C,
Stampfer M, Trichopoulos D. Serum steroids in relation to prostate cancer risk
in a case-control study (Greece). Cancer Causes Control 1997 Jul;8(4):632-6
Gustafsson O, Norming U, Gustafsson S, Eneroth P, Astrom G, Nyman CR.
Dihydrotestosterone and testosterone levels in men screened for prostate
cancer:a study of a randomized population. Br J Urol. 1996 Mar;77(3):433-40
Nomura A, Heilbrun LK, Stemmermann GN, Judd HL. Prediagnostic serum
hormones and the risk of prostate cancer. Cancer Res 1988 Jun
15;48(12):3515-7
Hoffman MA, DeWolf WC, Morgentaler A.Is low serum free testosterone a
marker for high grade prostate cancer? J Urol 2000 Mar;163(3):824-7
Wynder EL, Laakso K, Sotarauta M, Rose DP. Metabolic epidemiology of
prostatic cancer. Prostate 1984;5(1):47-53
Mortalidade Aumentada em Homens Com Câncer de Próstata e Baixos Níveis
de Testosterona
1-
2-
3-
4-
Carrero JJ, Qureshi AR, Parini P, Arver S, Lindholm B, Bárány P, Heimbürger
O, Stenvinkel P. Low serum testosterone increases mortality risk among
male dialysis patients. J Am Soc Nephrol. 2009 Mar;20(3):613-20
Tivesten A, Vandenput L, Labrie F, Karlsson MK, Ljunggren O, Mellström D,
Ohlsson C. Low serum testosterone and estradiol predict mortality in elderly
men. . J Clin Endocrinol Metab. 2009 Jul;94(7):2482-8
Khaw KT, Dowsett M, Folkerd E, Bingham S, Wareham N, Luben R, Welch A,
Day N. Endogenous testosterone and mortality due to all causes,
cardiovascular disease, and cancer in men: European prospective
investigation into cancer in Norfolk (EPIC-Norfolk) Prospective Population
Study. Circulation. 2007 Dec 4;116(23):2694-701
Laughlin GA, Barrett-Connor E, Bergstrom J. Low serum testosterone and
mortality in older men. . J Clin Endocrinol Metab. 2008 Jan;93(1):68-75
5-
6-
7-
8-
Shores MM, Matsumoto AM, Sloan KL, Kivlahan DR. Low serum testosterone
and mortality in male veterans. Arch Intern Med. 2006 Aug 1428;166(15):1660-5
Ribeiro M, Ruff P, Falkson G. Low serum testosterone and a younger age
predict for a poor outcome in metastatic prostate cancer. Am J Clin Oncol.
1997 Dec;20(6):605-8
Iversen P, Rasmussen F, Christensen IJ. Serum testosterone as a prognostic
factor in patients with advanced prostatic carcinoma. Scand J Urol Nephrol
Suppl. 1994; 157: 41-7
Haapiainen R, Rannikko S, Alfthan O, Adlercreutz H. Pretreatment plasma
levels of testosterone and sex hormone binding globulin binding capacity in
relation to clinical staging and survival in prostatic cancer patients. Prostate.
1988;12(4):325-32
Câncer em Homens: Possível Proteção Com a Reposição de Testosterona
1- Dimitrakakis C, Jones RA, Liu A, Bondy CA. Breast cancer incidence in
postmenopausal women using testosterone in addition to usual hormone
therapy. Menopause. 2004 Sep-Oct;11(5):531-535
2- Morales A, Connolly JG, Bruce AW. Androgen therapy in advanced
carcinoma of the prostate. Can Med Assoc J. 1971;105(1):71-2
3- Prout GR Jr, Brewer WR. Response of men with advanced prostatic
carcinoma to exogenous administration of testosterone. Cancer. 1967
Nov;20(11):1871-8
4- Joly-Pharaboz MO, Soave MC, Nicolas B, Mebarki F, Renaud M, Foury O,
Morel Y, Andre JG. Androgens inhibit the proliferation of a variant of the
human prostate cancer cell line LNCaP. J Steroid Biochem Mol Biol 1995
Oct;55(1):67-76
5- Wolf DA, Schulz P, Fittler F. Synthetic androgens suppress the trans- formed
phenotype in human prostate carcinoma cell line LNCaP. Br J Cancer. 1991
Jul; 64 (1): 47-53
6- Andrews P, Krygier S, Djakiew D. Dihydrotestosterone (DHT) modulates the
ability of NSAIDs to induce apoptosis of prostate cancer cells. Cancer
Chemother Pharmacol 2002 Mar;49(3):179-86
Estudos Aonde a Reposição Com Testosterona Parece Conferir Proteção
Contra o Câncer de Próstata
1.
2.
Morales A, Connolly JG, Bruce AW. Androgen therapy in advanced carcinoma
of the prostate. Can Med Assoc J. 1971;105(1):71-2
Prout GR Jr, Brewer WR. Response of men with advanced prostatic carcinoma
to exogenous administration of testosterone. Cancer. 1967 Nov;20(11):1871-8
Estudos Aonde a Reposição Com Testosterona Promove Inibição da
Proliferação do Câncer de Próstata ou Induz a Sua Apoptose
1-
Joly-Pharaboz MO, Soave MC, Nicolas B, Mebarki F, Renaud M, Foury O,
Morel Y, Andre JG. Androgens inhibit the proliferation of a variant of the
2-
3-
human prostate cancer cell line LNCaP. J Steroid Biochem Mol Biol 1995
Oct;55(1):67-76
Wolf DA, Schulz P, Fittler F. Synthetic androgens suppress the transformed
phenotype in human prostate carcinoma cell line LNCaP. Br J Cancer. 1991
Jul; 64 (1): 47-53
Andrews P, Krygier S, Djakiew D. Dihydrotestosterone (DHT) modulates the
ability of NSAIDs to induce apoptosis of prostate cancer cells. Cancer
Chemother Pharmacol. 2002 Mar;49(3):179-86
Estudos Onde a Reposição de Testosterona Reduz Queixas Prostáticas Como
Disúria e Nictúria
1-
2-
34567-
8-
Flamm J, Kiesswetter H, Englisch M. An urodynamic study of patients with
benign prostatic hypertrophy treated conservatively with phytotherapy or
testosterone. Wien Klin Wochenschr 1979 Sep 28;91(18):622-7
Kearns WM. Testosterone in the treatment of testicular deficiency and prostatic
enlargement. Wisconsin Med J. 1941; 40:927 (testosterone proprionate
therapy did not reduce the size of the prostate, but reduced the dysuria)
Meltzer M. Male hormone therapy of prostatic hypertrophy. Lancet. 1939; 59:
279
Trasoff A. The treatment of benign prostatic hypertrophy with testosterone
propionate. J Lab Clin Med. 1940; 25: 377
Markham MJ. The clinical use of peroral methyltestosterone in benign prostatic
hypertrophy. Urol Cutan Rev. 1942; 46: 225
Markham MJ. The clinical use of testosterone propionate in benign prostatic
hypertrophy. Urol Cutan Rev. 1941; 45: 35
Laqueur E. Behandlung der Prostathypertropie mit männlichen Hormone
(Hombreol) une experimentell Begründung dieser Therapie. Schweiz Med
Wochenschr. 1934; 64: 1116
South Med J, 1939, 32: 154
Estudos Onde a Reposição de Testosterona Reduziu o Volume da Próstata e
as Queixas Prostáticas
123-
4-
South Med J, 1939, 32: 154
de Lignieres B. Transdermal dihydrotestosterone treatment of 'andropause.
Ann Med 1993 Jun;25(3):235-41
Swerdloff RS, Wang C. Dihydrotestosterone: a rationale for its use as a nonaromatizable androgen replacement therapeutic agent. Baillieres Clin
Endocrinol Metab. 1998 Oct;12(3):501-6
Sitruk-Ware R. Contraception, 1989, 39: 1-191
Estudos de Revisão Onde os Autores Não Acharam Associação Entre Os
Níveis de Testosterona e o Risco de Câncer de Próstata e Demonstram
Claramente Que Não Existem Dados ou Evidências Que Dêem Suporte a Visão
de Que a Reposição de Testosterona Esteja Correlacionada Com o Risco de
Câncer
1-
2-
3-
4-
567-
Rhoden NEJM 2004 (“No compelling evidence at present to suggest that men
with higher testosterone levels are at greater risk of prostate cancer or that
treating men who have hypogonadism with exogenous androgens
increases this risk. In fact, it should be recognized that prostate cancer
becomes more prevalent exactly at the time of a man's life when
testosterone levels decline.“)
Morales A. Androgen replacement therapy and prostate safety. Eur Urol 2002
Feb;41(2):113-20 (“To date there is no evidence that exogenous androgens
promote development of prostate cancer”)
Basaria S, Wahlstrom JT, Dobs AS. Anabolic-Androgenic Steroid Therapy in
the Treatment of Chronic Diseases. J Clin Endocrinol Metab. 2001
Nov;86(11):5108-17(“..recent reviews suggest that the incidence of prostate
cancer is not increased by testosterone administration”)
Morley JE. Testosterone replacement and the physiologic aspects of aging in
men. Mayo Clin Proc. 2000 Jan;75 Suppl:S83-7 (“There is no clinical
evidence that the risk of either prostate cancer or benign prostate
hypertrophy increases with testosterone treatment”)
Wirth MP, Hakenberg OW Testosterone and the prostate. Urologe A 2000
Sep;39(5):418-20
Rolf C, Nieschlag E. Potential adverse effects of long-term testosterone
therapy. Baillieres Clin Endocrinol Metab. 1998 Oct;12(3):521-34.
Prehn RT. On the prevention and therapy of prostate cancer by androgen
administration. Cancer Res. 1999 Sep 1;59(17):4161-4 (“… contrary to
prevalent opinion, declining rather than high levels of androgens probably
contribute more to human prostate carcinogenesis and ;.. androgen
supplementation would probably lower the incidence of the disease. …
consider the possibility that the growth of androgen-independent prostate
cancers might be reduced by the administration of androgens”)
Estudos Onde a Reposição de Testosterona em Homens Com Câncer de
Próstata Não Exerce Qualquer Efeito Adverso na Progressão ou Recorrência
do Câncer e, Ao Mesmo Tempo, Melhora a Qualidade de Vida e Os Parâmetros
Gerais de Saúde
1- Morales A, Black AM, Emerson LE. Testosterone administration to men with
testosterone deficiency syndrome after external beam radiotherapy for
localized prostate cancer: preliminary observations. BJU Int. 2009
Jan;103(1):62-4 (n = 5; “Men with testosterone deficiency syndrome after
external beam radiotherapy for localised prostate cancer are candidates for
testosterone
therapy
..no
adverse
effects
from
testosterone
supplementation”)
2- Sarosdy MF. Testosterone replacement for hypogonadism after treatment of
early prostate cancer with brachytherapy. Cancer. 2007 Feb 1;109(3):536-41
( (n = 31; For patients with low serum testosterone levels and symptoms of
hypogonadism, testosterone therapy may be used with caution and close
follow-up after prostate brachytherapy)
3- Agarwal PK, Oefelein MG. Testosterone replacement therapy after primary
treatment for prostate cancer. J Urol. 2005 Feb;173(2):533-6 (n = 10
hypogonadal men treated with radical retropubic prostatectomy for organ
confined prostate cancer; testosterone replacement therapy can be
administered carefully and with benefit to hypogonadal patients with prostate
cancer)
Estudos Onde a Reposição de Testosterona Não Demonstra Efeitos Adversos
No Risco de Câncer de Próstata
1- Prout GRJ, Brewer WR. Response of men with advanced prostatic carcinoma
to exogenous administration of testosterone. Cancer (Phila.). 1967;20:1871-8
2- Trunnell JD, Duffy BJ Jr. The influence of certain steroids on the behavior of
human prostate cancer. Trans. NY Acad Sci. 1950;II:12:238-41
3- Brendler H, Lowry O, Brock M. Further investigation of hormonal
relationships. Arch Surg. 1950,61:433-40
4- Pearson OH. Discussion of Dr. Huggins’ paper: “Control of cancers of man by
endocrinological methods." Cancer Res. 1957:17:473-9
5- Morales A, Connolly J, Burr R, Bruce A. The use of radioactive phosphorus to
treat bone pain in metastatic carcinoma of the prostate. Can Med Assoc J.
1970;103: 372-3
Estudos Onde a Reposição de Testosterona Não Demonstra Quaisquer Efeitos
Nos Níveis de PSA ou do Volume da Próstata
3.
4.
5.
6.
7.
8.
9.
10.
11.
Rhoden EL, Morgentaler A. Influence of demographic factors and biochemical
characteristics on the prostate-specific antigen (PSA) response to testosterone
replacement therapy. Int J Impot Res. 2005 Sep 22 (No statistical increase:
average = 0.31 ng/ml after 1 year of treatment of hypogonadal men)
Shibasaki T, Sasagawa I, Suzuki Y, Yazawa H, Ichiyanagi O, Matsuki S, Miura
M, Nakada T. Effect of testosterone replacement therapy on serum PSA in
patients with Klinefelter syndrome. Arch Androl. 2001 Nov-Dec;47(3):173-6
Cooper CS, Perry PJ, Sparks AE, MacIndoe JH, Yates WR, Williams RD. Effect
of exogenous testosterone on prostate volume, serum and semen prostate
specific antigen levels in healthy young men. J Urol. 1998 Feb;159(2):441-3
Cooper CS, MacIndoe JH, Perry PJ, Yates WR, Williams RD. The effect of
exogenous testosterone on total and free prostate specific antigen levels in
healthy young men. J Urol. 1996 Aug;156(2 Pt 1):438-41
Behre HM, Bohmeyer J, Nieschlag E. Prostate volume in testosterone-treated
and untreated hypogonadal men in comparison to age-matched normal
controls. Clin Endocrinol (Oxf). 1994 Mar;40(3):341-9
Douglas TH, Connelly RR, McLeod DG, Erickson SJ, Barren R 3rd, Murphy
GP. Effect of exogenous testosterone replacement on prostate-specific antigen
and prostate-specific membrane antigen levels in hypogonadal men. J Surg
Oncol. 1995 Aug;59(4):246-50
Sih R, Morley JE, Kaiser FE, Perry HM 3rd, Patrick P, Ross C. Testosterone
replacement in older hypogonadal men: a 12-month randomized controlled trial.
J Clin Endocrinol Metab. 1997 Jun;82(6):1661-7
Hajjar RR, Kaiser FE, Morley JE. Outcomes of long-term testosterone
replacement in older hypogonadal males: a retrospective analysis. J Clin
Endocrinol Metab. 1997 Nov;82(11):3793-6
Monath JR, McCullough DL, Hart LJ, Jarow JP. Physiologic variations of serum
testosterone within the normal range do not affect serum prostate-specific
antigen. Urology. 1995 Jul;46(1):58-61
-
EXPANSÃO DA LONGEVIDE E MELHORA DA
QUALIDADE DE VIDA ATRAVÉS DA MODULAÇÃO
HORMONAL
11
Longevidade em Homens: A Associação Com Baixos Níveis de Testosterona
1-
2-
3-
4-
56-
Khaw KT, Dowsett M, Folkerd E, Bingham S, Wareham N, Luben R, Welch A,
Day N. Endogenous testosterone and mortality due to all causes,
cardiovascular disease, and cancer in men: European prospective
investigation into cancer in Norfolk (EPIC-Norfolk) Prospective Population
Study. Circulation. 2007 Dec 4;116(23):2694-701
Jankowska EA, Biel B, Majda J, Szklarska A, Lopuszanska M, Medras M,
Anker SD, Banasiak W, Poole-Wilson PA, Ponikowski P. Anabolic
deficiency in men with chronic heart failure: prevalence and detrimental
impact on survival. Circulation. 2006 Oct 24;114(17):1829-37
Shores MM, Matsumoto AM, Sloan KL, Kivlahan DR. Low serum testosterone
and mortality in male veterans. Arch Intern Med. 2006 Aug 1428;166(15):1660-5
Shores MM, Moceri VM, Gruenewald DA, Brodkin KI, Matsumoto AM, Kivlahan
DR. Low testosterone is associated with decreased function and increased
mortality risk: a preliminary study of men in a geriatric rehabilitation unit. J
Am Geriatr Soc. 2004 Dec;52(12):2077-81
Suzuki M. Centenarians in Japan. Nakayamshoten Tokyo (Japan), 1995: 64-78
Haapiainen R, Rannikko S, Alfthan O, Adlercreutz H. Pretreatment plasma
levels of testosterone and sex hormone binding globulin binding capacity in
relation to clinical staging and survival in prostatic cancer patients. Prostate.
1988;12(4):325-32
Longevidade em Homens: A Melhora da Sobrevida Com A Reposição de
Testosterona
1- Morales A, Connolly JG, Bruce AW. Androgen therapy in advanced
carcinoma of the prostate. Can Med Assoc J. 1971;105(1):71-2
2- Prout GR Jr, Brewer WR. Response of men with advanced prostatic
carcinoma to exogenous administration of testosterone. Cancer. 1967
Nov;20(11):1871-8
Longevidade em Homens: A Associação Com Baixos Níveis de GH
12-
Stochholm K, Christiansen J, Laursen T, Gravholt CH. Mortality and reduced
growth hormone secretion. Horm Res. 2007;68 Suppl 5:173-6
Rosen T, Bengtsson BA. Premature mortality due to cardiovascular disease in
hypopituitarism. Lancet. 1990 Aug 4;336(8710):285-8
3-
4-
Besson A, Salemi S, Gallati S, Jenal A, Horn R, Mullis PS, Mullis PE..
Reduced longevity in untreated patients with isolated growth hormone
deficiency. J Clin Endocrinol Metab. 2003 Aug;88(8):3664-7
Bates AS, Van't Hoff W, Jones PJ , Clayton RN. The effect of hypopituitarism
on life expectancy. J Clin Endocrinol Metab. 1996;81(3):1169-72
Longevidade: A Melhora Com a Reposição de GH
1-
2-
3-
4-
Li N, Zhou L, Zhang B, Dong P, Lin W, Wang H, Xu R, Ding H. Recombinant
human growth hormone increases albumin and prolongs survival in patients
with chronic liver failure: a pilot open, randomized, and controlled clinical
trial. Dig Liver Dis. 2008 Jul;40(7):554-9
Sonntag WE, Carter CS, Ikeno Y, Ekenstedt K, Carlson CS, Loeser RF,
Chakrabarty S, Lee S, Bennett C, Ingram R, Moore T, Ramsey M. Adultonset growth hormone and insulin-like growth factor I deficiency reduces
neoplastic disease, modifies age-related pathology, and increases life span.
Endocrinology. 2005;146(7):2920-32
Khansari DN, Gustad T. Effects of long-term, low-dose growth hormone therapy
on immune function and life expectancy of mice. Mech Ageing Dev. 1991
Jan;57(1):87-100
Bengtsson BA, Koppeschaar HP, Abs R, Bennmarker H, Hernberg-Stahl E,
Westberg B, Wilton P, Monson JP, Feldt-Rasmussen U, Wuster C. Growth
hormone replacement therapy is not associated with any increase in
mortality. KIMS Study Group. J Clin Endocrinol Metab. 1999;84(11):4291-2
Longevidade: A Associação Com Baixos Níveis de IGF-1
1- Guimarães SM, Lima EQ, Cipullo JP, Lobo SM, Burdmann EA. Low insulinlike growth factor-1 and hypocholesterolemia as mortality predictors in acute
kidney injury in the intensive care unit. Crit Care Med. 2008 Dec;36(12):316570
2- Arai Y, Takayama M, Gondo Y, Inagaki H, Yamamura K, Nakazawa S,
Kojima T, Ebihara Y, Shimizu K, Masui Y, Kitagawa K, Takebayashi T, Hirose
N. Adipose endocrine function, insulin-like growth factor-1 axis, and
exceptional survival beyond 100 years of age. J Gerontol A Biol Sci Med Sci.
2008 Nov;63(11):1209-18
3- Brugts MP, van den Beld AW, Hofland LJ, van der Wansem K, van Koetsveld
PM, Frystyk J, Lamberts SW, Janssen JA. Low circulating insulin-like growth
factor I bioactivity in elderly men is associated with increased mortality. J Clin
Endocrinol Metab. 2008 Jul;93(7):2515-22
4- Petretta M, Colao A, Sardu C, Scopacasa F, Marzullo P, Pivonello R,
Fontanella L, de Caterina M, de Simone A, Bonaduce D. NT-proBNP, IGF-I
and survival in patients with chronic heart failure. Growth Horm IGF Res.
2007 Aug;17(4):288-96
5- Jankowska EA, Biel B, Majda J, Szklarska A, Lopuszanska M, Medras M,
Anker SD, Banasiak W, Poole-Wilson PA, Ponikowski P. Anabolic deficiency
in men with chronic heart failure: prevalence and detrimental impact on
survival. Circulation. 2006 Oct 24;114(17):1829-37
6- Rasmuson T, Grankvist K, Jacobsen J, Olsson T, Ljungberg B. Serum
insulin-like growth factor-1 is an independent predictor of prognosis in
patients with renal cell carcinoma. Acta Oncol. 2004;43(8):744-8
7- Denti L, Annoni V, Cattadori E, Salvagnini MA, Visioli S, Merli MF, Corradi F,
Ceresini G, Valenti G, Hoffman AR, Ceda GP. Insulin-like growth factor 1 as a
predictor of ischemic stroke outcome in the elderly. Am J Med. 2004 Sep
1;117(5):312-7
8- Onenli-Mungan N, Yildizdas D, Yapicioglu H, Topaloglu AK, Yüksel B, Ozer
G. Growth hormone and insulin-like growth factor 1 levels and their relation to
survival in children with bacterial sepsis and septic shock. J Paediatr Child
Health. 2004 Apr;40(4):221-6
9- Laughlin GA, Barrett-Connor E, Criqui MH, Kritz-Silverstein D. The
prospective association of serum insulin-like growth factor I (IGF-I) and IGFbinding protein-1 levels with all cause and cardiovascular disease mortality in
older adults: the Rancho Bernardo Study. J Clin Endocrinol Metab. 2004
Jan;89(1):114-20
10- Vasan RS, Sullivan LM, D'Agostino RB, Roubenoff R, Harris T, Sawyer DB,
Levy D, Wilson PW. Serum insulin-like growth factor I and risk for heart failure
in elderly individuals without a previous myocardial infarction: the
Framingham Heart Study. Ann Intern Med. 2003 Oct 21;139(8):642-8
11- Roubenoff R, Parise H, Payette HA, Abad LW, D'Agostino R, Jacques PF,
Wilson PW, Dinarello CA, Harris TB. Cytokines, insulin-like growth factor 1,
sarcopenia, and mortality in very old community-dwelling men and women:
the Framingham Heart Study. Am J Med. 2003 Oct 15;115(6):429-35
12- Roubenoff R, Parise H, Payette HA, Abad LW, D'Agostino R, Jacques PF,
Wilson PW, Dinarello CA, Harris TB. Cytokines, insulin-like growth factor 1,
sarcopenia, and mortality in very old community-dwelling men and women:
the Framingham Heart Study. Am J Med. 2003 Oct 15;115(6):429-35
13- Ruiz-Torres A, Soares de Melo Kirzner M. Ageing and longevity are related to
growth hormone/insulin-like growth factor-1 secretion. Gerontology. 2002
Nov-Dec;48(6):401-7
14- Fernández-Reyes MJ, Alvarez-Ude F, Sánchez R, Mon C, Iglesias P, Díez
JJ, Vázquez A. Inflammation and malnutrition as predictors of mortality in
patients on hemodialysis. J Nephrol. 2002 Mar-Apr;15(2):136-43
15- Caregaro L, Alberino F, Amodio P, Merkel C, Angeli P, Plebani M, Bolognesi
M, Gatta A. Nutritional and prognostic significance of insulin-like growth factor
1 in patients with liver cirrhosis. Nutrition. 1997 Mar;13(3):185-90.
Longevidade: A Melhora Com a Reposição de IGF-1
1- Serose A, Salmon A, Fiszman MY, Fromes Y. Short-term treatment using
insulin-like growth factor-1 (IGF-1) improves life expectancy of the deltasarcoglycan deficient hamster. J Gene Med. 2006 Aug;8(8):1048-55
Longevidade: A Associação Com Baixos Níveis de DHEA
1-
Cappola AR, O'Meara ES, Guo W, Bartz TM, Fried LP, Newman AB.
Trajectories of dehydroepiandrosterone sulfate predict mortality in older adults:
the cardiovascular health study. J Gerontol A Biol Sci Med Sci. 2009
Dec;64(12):1268-74
2-
34-
5-
6-
Enomoto M, Adachi H, Fukami A, Furuki K, Satoh A, Otsuka M, Kumagae S,
Nanjo Y, Shigetoh Y, Imaizumi T. Serum dehydroepiandrosterone sulfate levels
predict longevity in men: 27-year follow-up study in a community-based cohort
(Tanushimaru study). J Am Geriatr Soc. 2008 Jun;56(6):994-8
Glei DA, Goldman N. Dehydroepiandrosterone sulfate (DHEAS) and risk for
mortality among older Taiwanese. Ann Epidemiol. 2006 Jul;16(7):510-5
Jankowska EA, Biel B, Majda J, Szklarska A, Lopuszanska M, Medras M, Anker
SD, Banasiak W, Poole-Wilson PA, Ponikowski P. Anabolic deficiency in men
with chronic heart failure: prevalence and detrimental impact on survival.
Circulation. 2006 Oct 24;114(17):1829-37
Mazat L, Lafont S, Berr C, Debuire B, Tessier JF, Dartigues JF, Baulieu EE.
Prospective measurements of dehydroepiandrosterone sulfate in a cohort of
elderly subjects: relationship to gender, subjective health, smoking habits, and
10-year mortality. Proc Natl Acad Sci USA. 2001;98(14):8145-50
Feldman HA, Johannes CB, Araujo AB, Mohr BA, Longcope C, McKinlay JB.
Low dehydroepiandrosterone and ischemic heart disease in middle-aged men:
prospective results from the Massachusetts Male Aging Study. Am J Epidemiol.
2001 Jan 1;153(1):79-89
Longevidade: A Associação Com os Níveis de Progesterona
1-
Mohr PE, Wang DY, Gregory WM, Richards MA, Fentiman IS. Serum
progesterone and prognosis in operable breast cancer. Br J Cancer.
1996 Jun;73(12):1552-5
Longevidade: A Melhora Com a Reposição de Estradiol
1-
2-
3-
4-
Petitti DB, Perlman JA, Sidney S. Noncontraceptive estrogens and
mortality: long-term follow-up of women in the Walnut Creek Study.
Obstet Gynecol. 1987 Sep;70(3 Pt 1):289-93
Natrajan PK, Soumakis K, Gambrell RD Jr. Estrogen replacement
therapy in women with previous breast cancer. Am J Obstet Gynecol.
1999;181(2):288-95
DiSaia PJ, Brewster WR, Ziogas A, Anton-Culver H. Breast cancer
survival and hormone replacement therapy: a cohort analysis. Am J
Clin Oncol. 2000 Dec;23(6):541-5
Jernstrom H, Frenander J, Ferno M, Olsson H. Hormone replacement
therapy before breast cancer diagnosis significantly reduces the
overall death rate compared with never-use among 984 breast cancer
patients. Br J Cancer. 1999;80(9):1453-8
Longevidade: A Melhora Com a Reposição de Progesterona
1-
Wright DW, Kellermann AL, Hertzberg VS, Clark PL, Frankel M,
Goldstein FC, Salomone JP, Dent LL, Harris OA, Ander DS, Lowery
DW, Patel MM, Denson DD, Gordon AB, Wald MM, Gupta S, Hoffman
SW, Stein DG. ProTECT: A Randomized Clinical Trial of
Progesterone for Acute Traumatic Brain Injury. Ann Emerg Med. 2007
Apr;49(4):391-402, 402.e1-2
Longevidade: A Possível Associação Com a Persistência do Ritmo Cirdadiano
da Melatonina em Idosos
1- Cugini P, Touitou Y, Bogdan A, Auzeby A, Pellegrino AM, Fontana S, Vacca K,
Siena GD, Di Rosa R, Zannella FP, Zannella P, Zannella A, Sepe FA, Sepe L. Is
melatonin circadian rhythm a physiological feature associated with healthy
longevity? A study of long-living subjects and their progeny. Chronobiol Int. 2001
Jan;18(1):99-107
Longevidade: A Melhora Com a Reposição de Melatonina
1- Rodríguez MI, Escames G, López LC, López A, García JA, Ortiz F, Sánchez V,
Romeu M, Acuña-Castroviejo D. Improved mitochondrial function and increased
life span after chronic melatonin treatment in senescent prone mice. Exp
Gerontol. 2008 Aug;43(8):749-56
2- Vinogradova IA, Bukalev AV, Zabezhinskiĭ MA, Semenchenko AV, Anisimov VN.
[Effect of light regimens and melatonin on homeostasis, life span and
spontaneous tumorigenesis in male rats] Vopr Onkol. 2008;54(1):70-7
3- Ayer RE, Sugawara T, Chen W, Tong W, Zhang JH. Melatonin decreases
mortality following severe subarachnoid hemorrhage. J Pineal Res. 2008
Mar;44(2):197-204
4- Xu J, Sun S, Wei W, Fu J, Qi W, Manchester LC, Tan DX, Reiter RJ. Melatonin
reduces mortality and oxidatively mediated hepatic and renal damage due to
diquat treatment. J Pineal Res. 2007 Mar;42(2):166-71
5- Pierpaoli W, Regelson W. Pineal control of aging: effect of melatonin and pineal
grafting on aging mice. Proc Natl Acad Sci USA. 1994 Jan 18;91(2):787-91
6- Gitto E, Karbownik M, Reiter RJ, Tan DX, Cuzzocrea S, Chiurazzi P, Cordaro S,
Corona G, Trimarchi G, Barberi I. Effects of melatonin treatment in septic
newborns. Pediatr Res. 2001 Dec;50(6):756-60
7- Barni S, Lissoni P, Cazzaniga M, Ardizzoia A, Meregalli S, Fossati V, Fumagalli
L, Brivio F, Tancini G. A randomized study of low-dose subcutaneous interleukin2 plus melatonin versus supportive care alone in metastatic colorectal cancer
patients progressing under 5-fluorouracil and folates. Oncology. 1995 MayJun;52(3):243-5
Longevidade: A Associação Com Baixos Níveis dos Hormônios Tireoidianos
1-
2-
3-
Razvi S, Weaver JU, Vanderpump MP, Pearce SH. The incidence of ischemic
heart disease and mortality in people with subclinical hypothyroidism:
Reanalysis of the Whickham Survey Cohort. J Clin Endocrinol Metab. 2010
Apr;95(4):1734-40
Rodondi N, Newman AB, Vittinghoff E, de Rekeneire N, Satterfield S, Harris
TB, Bauer DC. Subclinical hypothyroidism and the risk of heart failure, other
cardiovascular events, and death. Arch Intern Med. 2005 Nov
28;165(21):2460-6
Cerillo AG, Bevilacqua S, Storti S, Mariani M, Kallushi E, Ripoli A, Clerico A,
Glauber M. Free triiodothyronine: a novel predictor of postoperative atrial
fibrillation. Eur J Cardiothorac Surg. 2003 Oct;24(4):487-92
4-
5-
6-
Iervasi G, G, Pingitore A, Landi P, Raciti M, Ripoli A, Scarlattini M, L'Abbate A,
Donato L. Low T3 syndrome: a strong predictor of death in patients with heart
disease. Circulation. 2003;107(5):708-13
Kozdag G, Ural D, Vural A, Agacdiken A, Kahraman G, Sahin T, Ural E,
Komsuoglu B. Relation between free triiodothyronine/free thyroxine ratio,
echocardiographic parameters and mortality in dilated cardiomyopathy. Eur J
Heart Fail. 2005 Jan;7(1):113-8
Pingitore A, Landi P, Taddei MC, Ripoli A, L'Abbate A, Iervasi G.
Triiodothyronine levels for risk stratification of patients with chronic heart
failure. Am J Med. 2005 Feb;118(2):132-6
Longevidade: A Melhora Com a Reposição dos Hormônios Tireoidianos
1-
Razvi S, Weaver JU, Vanderpump MP, Pearce SH. The Incidence of Ischemic
Heart Disease and Mortality in People with Subclinical Hypothyroidism:
Reanalysis of the Whickham Survey Cohort. J Clin Endocrinol Metab. 2010
Apr;95(4):1734-40
12PROFILAXIA E TRATAMENTO DA
DEPRESSÃO
ATRAVÉS
DA
MODULAÇÃO HORMONAL:
Depressão: A Associação Com Baixos Níveis de Melatonina
1- Rahman SA, Marcu S, Kayumov L, Shapiro CM. Altered sleep architecture
and higher incidence of subsyndromal depression in low endogenous
melatonin secretors. Eur Arch Psychiatry Clin Neurosci. 2010 (2009, Dec 18
Epub ahead of print)
2- Parry BL, Meliska CJ, Sorenson DL, Lopez AM, Martinez LF, Nowakowski S,
Elliott JA, Hauger RL, Kripke DF. Plasma melatonin circadian rhythm
disturbances during pregnancy and postpartum in depressed women and
women with personal or family histories of depression. Am J Psychiatry. 2008
Dec;165(12):1551-8
3- Fountoulakis KN, Karamouzis M, Iacovides A, Nimatoudis J, Diakogiannis J,
Kaprinis G, Demitriadou A, Bech P. Morning and evening plasma melatonin
and dexamethasone suppression test in patients with nonseasonal major
depressive disorder from northern Greece (latitude 40-41.5 degrees ).
Neuropsychobiology. 2001;44(3):113-7
4- Frazer A, Brown R, Kocsis J, Caroff S, Amsterdam J, Winokur A, Sweeney J,
Stokes P.Patterns of melatonin rhythms in depression. J Neural Transm
Suppl. 1986;21:269-90
5- McIntyre IM, Judd FK, Norman TR, Burrows GD. Plasma melatonin
concentrations in depression. Aust N Z J Psychiatry. 1986 Sep;20(3):381-3
6- Steiner M, Brown GM, Goldman S. Nocturnal melatonin and cortisol secretion
in newly admitted psychiatric inpatients. Implications for affective disorders.
Eur Arch Psychiatry Clin Neurosci 1990;240(1):21-7
7- Bozhko GKh, Tsaritsinskii VI, Kostiukovskaia LS, Kulabukhov VM. The effect
of an increased intensity of light on changes in the serotonin and melatonin
content in patients with depression. Lik Sprava 1994 Jul-Aug;(7-8):88-90
8- Brown R, Kocsis JH, Caroff S, Amsterdam J, Winokur A, Stokes PE, Frazer
A. Differences in nocturnal melatonin secretion between melancholic
depressed patients and control subjects. Am J Psychiatry. 1985
Jul;142(7):811-6
9- Chazot G, Claustrat B, Brun J, Borson F, Dalery J. Melatonin. Chronobiologic
peripheral endocrine index in depressive states. Encephale. 1985 MayJun;11(3):113-6
10- Nair NP, Hariharasubramanian N, Pilapil C. Circadian rhythm of plasma
melatonin in endogenous depression. Prog Neuropsychopharmacol Biol
Psychiatry. 1984;8(4-6):715-8
11- Claustrat B, hazot G, Brun J, Jordan D, Sassolas G. A chronobiological study
of melatonin and cortisol secretion in depressed subjects: plasma melatonin,
a biochemical marker in major depression. Biol Psychiatry. 1984
Aug;19(8):1215-28
12- Souetre E, Salvati E, Belugou JL, Pringuey D, Candito M, Krebs B, Ardisson
JL, Darcourt G. Circadian rhythms in depression and recovery: evidence for
blunted amplitude as the main chronobiological abnormality. Psychiatry Res
1989 Jun;28(3):263-78
13- Brown RP, Kocsis JH, Caroff S, Amsterdam J, Winokur A, Stokes P, Frazer
A. Depressed mood and reality disturbance correlate with decreased
nocturnal melatonin in depressed patients. Acta Psychiatr Scand. 1987
Sep;76(3):272-5
14- Hariharasubramanian N, Nair NP, Pilapil C, Isaac I, Quirion R. Effect of
imipramine on the circadian rhythm of plasma melatonin in unipolar
depression. Chronobiol Int. 1986; 3 (1): 65-9
15- Beck-Friis J, Kjellman BF, Aperia B, Unden F, von Rosen D, Ljunggren JG,
Wetterberg L. Serum melatonin in relation to clinical variables in patients with
major depressive disorder and a hypothesis of a low melatonin syndrome.
Acta Psychiatr Scand 1985 Apr;71(4):319-30
16- Beck-Friis J, von Rosen D, Kjellman BF, Ljunggren JG, Wetterberg L.
Melatonin in relation to body measures, sex, age, season and the use of
drugs in patients with major affective disorders and healthy subjects.
Psychoneuroendocrinology. 1984;9(3):261-77
Depressão: A Melhora Com a Reposição de Melatonina
1- Rahman SA, Kayumov L, Shapiro CM. Antidepressant action of melatonin in
the treatment of Delayed Sleep Phase Syndrome. Sleep Med. 2010
Feb;11(2):131-6
2- Zisapel N. Controlled release melatonin (Circadin) in the treatment of
insomnia in older patients: efficacy and safety in patients with history of use
and non-use of hypnotic drugs Harefuah. 2009 May;148(5):337-41, 348
3- Jean-Louis G, von Gizycki H, Zizi F. Melatonin effects on sleep, mood, and
cognition in elderly with mild cognitive impairment. J Pineal Res 1998
Oct;25(3):177-83
4- Raghavendra V, Kaur G, Kulkarni SK. Anti-depressant action of melatonin in
chronic forced swimming-induced behavioral despair in mice, role of
peripheral benzodiazepine receptor modulation. Eur Neuropsychopharmacol.
2000 Dec;10(6):473-81
5- Bellipanni G, Bianchi P, Pierpaoli W, Bulian D, Ilyia E. Effects of melatonin in
perimenopausal and menopausal women: a randomized and placebo
controlled study. Exp Gerontol 2001 Feb;36(2):297-310
6- Lewy AJ, Bauer VK, Cutler NL, Sack RL. Melatonin treatment of winter
depression: a pilot study. Psychiatry Res. 1998 Jan 16;77(1):57-61
7- Ishizaki A, Sugama M, Takeuchi N. Usefulness of melatonin for
developmental sleep and emotional/behavior disorders--studies of melatonin
trial on 50 patients with developmental disorders. No To Hattatsu; 1999
Sep;31(5):428-37
Depressão: A Associação Com Baixos Níveis do Hormônio do Crescimento
1- Jarrett DB, Miewald JM, Kupfer DJ. Recurrent depression is associated with a
persistent reduction in sleep-related growth hormone secretion. Arch Gen
Psychiatry. 1990 Feb;47(2):113-8
2- Jarrett DB, Kupfer DJ, Miewald JM, Grochocinski VJ, Franz B. Sleep-related
growth hormone secretion is persistently suppressed in women with recurrent
depression: a preliminary longitudinal analysis. J Psychiatr Res. 1994 MayJun;28(3):211-23)
3- Rubin RT, Poland RE, Lesser IM. Neuroendocrine aspects of primary
endogenous depression. X: Serum growth hormone measures in patients and
matched control subjects. Biol Psychiatry. 1990 May 15;27(10):1065-82
4- Schilkrut R, Chandra O, Osswald M, Ruther E, Baafusser B, Matussek.
Growth hormone release during sleep and with thermal stimulation in
depressed patients. Neuropsychobiology. 1975;1(2):70-9
5- Barry S, Dinan TG. Neuroendocrine challenge tests in depression: a study of
growth hormone, TRH and cortisol release. J Affect Disord. 1990
Apr;18(4):229-34
6- Dinan TG, Barry S. Responses of growth hormone to desipramine in
endogenous and non-endogenous depression. Br J Psychiatry. 1990
May;156:680-4
7- Voderholzer U, Laakmann G, Wittmann R, Daffner-Bujia C, Hinz A, Haag C,
Baghai T. Profiles of spontaneous 24-hour and stimulated growth hormone
secretion in male patients with endogenous depression. Psychiatry Res. 1993
Jun;47(3):215-27
8- Harro J, Rimm H, Harro M, Grauberg M, Karelson K, Viru AM. Association of
depressiveness with blunted growth hormone response to maximal physical
exercise in young healthy men. Psychoneuroendocrinology. 1999
Jul;24(5):505-17
9- Greden JF. Biological markers of melancholia and reclassification of
depressive disorders. Encephale. 1982;8(2):193-202
10- McMillan CV, Bradley C, Gibney J, Healy ML, Russell-Jones DL, Sonksen
PH. Psychological effects of withdrawal of growth hormone therapy from
adults with growth hormone deficiency. Clin Endocrinol. (Oxf). 2003
Oct;59(4):467-75
Depressão: A Melhora Com a Reposição do Hormônio do Crescimento
1- Arwert LI, Deijen JB, Müller M, Drent ML. Long-term growth hormone
treatment preserves GH-induced memory and mood improvements: a 10-
year follow-up study in GH-deficient adult men. Horm Behav. 2005
Mar;47(3):343-9
2- Mahajan T, Crown A, Checkley S, Farmer A, Lightman S. Atypical depression
in growth hormone deficient adults, and the beneficial effects of growth
hormone treatment on depression and quality of life. Eur J Endocrinol. 2004
Sep;151(3):325-32
3- Johansson JO, Larson G, Andersson M, Elmgren A, Hynsjo L, Lindahl A,
Lundberg PA, Isaksson OG, Lindstedt S, Bengtsson BA. Treatment of growth
hormone-deficient adults with recombinant human growth hormone increases
the concentration of growth hormone in the cerebrospinal fluid and affects
neurotransmitters. Neuroendocrinology. 1995 Jan;61(1):57-66 (GH increases
endorphins, reduces dopamine)
Depressão: A Associação Com Baixos Níveis dos Hormônios Tireoidianos
1- Constant EL, Adam S, Seron X, Bruyer R, Seghers A, Daumerie C. Anxiety
and depression, attention, and executive functions in hypothyroidism. J Int
Neuropsychol Soc. 2005 Sep;11(5):535-44
2- Pop VJ, Maartens LH, Leusink G, van Son MJ, Knottnerus AA, Ward AM,
Metcalfe R, Weetman AP. Are autoimmune thyroid dysfunction and
depression related? J Clin Endocrinol Metab. 1998 Sep;83(9):3194-7
3- Haggerty JJ Jr, Stern RA, Mason GA, Beckwith J, Morey CE, Prange AJ Jr.
Subclinical hypothyroidism: a modifiable risk factor for depression? Am J
Psychiatry. 1993 Mar;150(3):508-10
4- Gold MS, Pottash AL, Extein I. "Symptomless" autoimmune thyroiditis in
depression. Psychiatry Res. 1982 Jun;6(3):261-9
5- O'Shanick GJ, Ellinwood EH Jr. Persistent elevation of thyroid-stimulating
hormone in women with bipolar affective disorder. Am J Psychiatry. 1982
Apr;139(4):513-4
6- Howland RH. Thyroid dysfunction in refractory depression: implications for
pathophysiology and treatment. J Clin Psychiatry. 1993 Feb;54(2):47-54
7- Kirkegaard C, Norlem N, Lauridsen UB, Bjorum N, Christiansen C. Protirelin
stimulation test and thyroid function during treatment of depression. Arch Gen
Psychiatry. 1975 Sep;32(9):1115-8
8- Bauer MS, Whybrow PC, Winokur A. Rapid cycling bipolar affective disorder.
I. Association with grade I hypothyroidism. Arch Gen Psychiatry. 1990
May;47(5):427-32
9- Haggerty JJ Jr, Evans DL, Golden RN, Pedersen CA, Simon JS, Nemeroff
CB. The presence of antithyroid antibodies in patients with affective and
nonaffective psychiatric disorders. Biol Psychiatry. 1990 Jan 1;27(1):51-60
10- Cole DP, Thase ME, Mallinger AG, Soares JC, Luther JF, Kupfer DJ, Frank
E. Slower treatment response in bipolar depression predicted by lower pretreatment thyroid function. Am J Psychiatry. 2002 Jan;159(1):116-21
11- Joffe RT, Marriott M. Thyroid hormone levels and recurrence of major
depression. Am J Psychiatry. 2000 Oct;157(10):1689-91 (“the time to
recurrence of major depression was inversely related to T3 levels but not to
T4 levels”)
Depressão: A Melhora Com a Reposição dos Hormônios Tireoidianos
1- Bauer MS, Whybrow PC. Rapid cycling bipolar affective disorder. II.
Treatment of refractory rapid cycling with high-dose levothyroxine: a
preliminary study. Arch Gen Psychiatry. 1990 May;47(5):435-40
2- Afflelou S, Auriacombe M, Cazenave M, Chartres JP, Tignol J. Administration
of high dose levothyroxine in treatment of rapid cycling bipolar disorders.
Review of the literature and initial therapeutic application apropos of 6 cases.
Encephale. 1997 May-Jun;23(3):209-17
3- Bauer M, Baur H, Berghofer A, Strohle A, Hellweg R, Muller-Oerlinghausen
B, Baumgartner A. Effects of supraphysiological thyroxine administration in
healthy controls and patients with depressive disorders. J Affect Disord. 2002
Apr;68(2-3):285-94
4- Schwarcz G, Halaris A, Baxter L, Escobar J, Thompson M, Young M. Normal
thyroid function in desipramine nonresponders converted to responders by
the addition of L-triiodothyronine. Am J Psychiatry. 1984 Dec;141(12):1614-6
5- Prange AJ Jr. Novel uses of thyroid hormones in patients with affective
disorders. Thyroid. 1996 Oct;6(5):537-43
6- Birkenhager TK, Vegt M, Nolen WA. An open study of triiodothyronine
augmentation of tricyclic antidepressants in inpatients with refractory
depression. Pharmacopsychiatry. 1997 Jan;30(1):23-6
7- Joffe RT, Singer W, Levitt AJ, MacDonald C. A placebo-controlled
comparison of lithium and triiodothyronine augmentation of tricyclic
antidepressants in unipolar refractory depression. Arch Gen Psychiatry. 1993
May;50(5):387-93
8- Altshuler LL, Bauer M, Frye MA, Gitlin MJ, Mintz J, Szuba MP, Leight KL,
Whybrow PC. Does thyroid supplementation accelerate tricyclic
antidepressant response? A review and meta-analysis of the literature. Am J
Psychiatry. 2001 Oct;158(10):1617-22
Depressão: A Associação Com Baixos Níveis de Cortisol
1-
Rocco A, Martocchia A, Frugoni P, Baldini R, Sani G, Di Simone Di
Giuseppe B, Vairano A, Girardi P, Monaco E, Tatarelli R, Falaschi P. Inverse
correlation between morning plasma cortisol levels and MMPI psychasthenia
and depression scale scores in victims of mobbing with adjustment disorders.
Neuro Endocrinol Lett. 2007 Oct;28(5):610-3
2- Mutsuura H, Kanbara K, Fukunaga M, Yamamoto K, Ban I, Kitamura K, Nakai
Y. Depression and anxiety correlate differently with salivary free cortisol in the
morning in patients with functional somatic syndrome. Appl Psychophysiol
Biofeedback. 2009 Dec;34(4):291-8 (“depressive scores showed a significant
negative correlation with salivary free cortisol in the morning in patients”)
3- Stetler C, Miller GE. Blunted cortisol response to awakening in mild to
moderate depression: regulatory influences of sleep patterns and social
contacts. J Abnorm Psychol. 2005 Nov;114(4):697-705 (“Blunted cortisol
response to awakening in women with mild to moderate depression”)
Depressão: A Associação Com Baixos Níveis de DHEA
1- Arlt W, Callies F, van Vlijmen JC, Koehler I, Reincke M, Bidlingmaier M, Huebler
D, Oettel M, Ernst M, Schulte HM, Allolio B. Dehydroepiandrosterone
replacement in women with adrenal insufficiency. N Engl J Med.
1999;341(14):1013-20
2- Johannsson G, Burman P, Wiren L, Engstrom BE, Nilsson AG, Ottosson M,
Jonsson B, Bengtsson BA, Karlsson FA Low dose dehydroepiandrosterone
affects behavior in hypopituitary androgen-deficient women: a placebocontrolled trial. J Clin Endocrinol Metab. 2002 May;87(5):2046-52
3- Nagata C, Shimizu H, Takami R, Hayashi M, Takeda N, Yasuda K. Serum
concentrations of estradiol and dehydroepiandrosterone sulfate and soy
product intake in relation to psychologic well-being in peri- and
postmenopausal Japanese women. Metabolism. 2000;49(12):1561-4
4- Yaffe K, Ettinger B, Pressman A, Seeley D, Whooley M, Schaefer C,
Cummings S. Neuropsychiatric function and dehydroepiandrosterone sulfate
in elderly women: a prospective study. Biol Psychiatry. 1998;43(9):694-700
5- Goodyer IM, Herbert J, Altham PM, Pearson J, Secher SM, Shiers HM.
Adrenal secretion during major depression in 8- to 16-year-olds. I. Altered
diurnal rhythms in salivary cortisol and dehydroepiandrosterone (DHEA) at
presentation. Psychol Med. 1996;26(2):245-56
6- Buckwalter JG, Stanczyk FZ, McCleary CA, Bluestein BW, Buckwalter DK,
Rankin KP, Chang L, Goodwin TM. Pregnancy, the postpartum, and steroid
hormones: effects on cognition and mood. Psychoneuroendocrinology.
1999;24(1):69-84
7- Heinz A, Weingartner H, George D, Hommer D, Wolkowitz OM, Linnoila M.
Severity of depression in abstinent alcoholics is associated with monoamine
metabolites and dehydroepiandrosterone-sulfate concentrations. Psychiatry
Res. 199920;89(2):97-106
8- Berr C, Lafont S, Debuire B, Dartigues JF, Baulieu EE.
Dehydroepiandrosterone sulfate in the elderly with functional, psychological,
and mental status, and short-term mortality: a French community-based
study. Proc Natl Acad Sci USA. 1996;93(23):13410-5
9- Barrett-Connor E, von Muhlen D, Laughlin GA, Kripke A. Endogenous levels
of dehydroepiandrosterone sulfate, but not other sex hormones, are
associated with depressed mood in older women: the Rancho Bernardo
Study. J Am Geriatr Soc. 1999;47(6):685-91
10- Goodyer IM, Herbert J, Altham PM. Adrenal steroid secretion and major
depression in 8- to 16-year-olds, III. Influence of cortisol/DHEA ratio at
presentation on subsequent rates of disappointing life events and persistent
major depression. Psychol Med. 1998;28(2):265-73
11- Herbert J. Neurosteroids, brain damage, and mental illness. Exp Gerontol.
1998;33(7-8):713-27
12- Fava M, Littman A, Lamon-Fava S, Milani R, Shera D, MacLaughlin R,
Cassem E,Leaf A, Marchio B, Bolognesi E, et al. Psychological, behavioral
and biochemical risk factors for coronary artery disease among American and
Italian male corporate managers. Am J Cardiol. 1992 Dec 1;70(18):1412-6
Depressão: A Melhora Com a Reposição de DHEA
1- Alhaj HA, Massey AE, McAllister-Williams RH. Effects of DHEA administration
on episodic memory, cortisol and mood in healthy young men: a double-blind,
placebo-controlled study. Psychopharmacology (Berl). 2006 Nov;188(4):54151
2- Stomati M, Rubino S, Spinetti A, Parrini D, luisi S, Casarosa E, Petraglia F,
Gennazzani AR. E Endocrine, neuroendocrine and behavioral effects of oral
dehydroepiandrosterone sulfate supplementation in postmenopausal women.
Gynecol Endocrinol. 1999;13(1):15-25
Depressão: A Melhora Com a Reposição de Estradiol
1- Soares CN, Arsenio H, Joffe H, Bankier B, Cassano P, Petrillo LF, Cohen LS.
Escitalopram versus ethinyl estradiol and norethindrone acetate for
symptomatic peri- and postmenopausal women: impact on depression,
vasomotor symptoms, sleep, and quality of life. Menopause. 2006 SepOct;13(5):780-6
2- Carranza-Lira S, Valentino-Figueroa ML. Estrogen therapy for depression in
postmenopausal women. Int J Gynaecol Obstet. 1999 Apr;65(1):35-8
3- Ditkoff EC, Crary WG, Cristo M, Lobo RA. Estrogen improves psychological
function in asymptomatic postmenopausal women. Obstet Gynecol. 1991
Dec;78(6):991-5
4- Lawrie TA, Herxheimer A, Dalton K. Oestrogens and progestogens for
preventing and treating postnatal depression. Cochrane Database Syst Rev.
2000;(2):CD001690
5- Rudolph I, Palombo-Kinne E, Kirsch B, Mellinger U, Breitbarth H, Graser T.
Influence of a continuous combined HRT (2 mg estradiol valerate and 2 mg
dienogest) on postmenopausal depression. Climacteric. 2004 Sep;7(3):30111
6- Rasgon NL, Altshuler LL, Fairbanks LA, Dunkin JJ, Davtyan C, Elman S,
Rapkin AJ. Estrogen replacement therapy in the treatment of major
depressive disorder in perimenopausal women. J Clin Psychiatry. 2002;63
Suppl 7:45-8
7- de Lignieres B, Vincens M. Differential effects of exogenous oestradiol and
progesterone on mood in post-menopausal women: individual dose/effect
relationship. Maturitas. 1982 Apr;4(1):67-72
8- Best NR, Rees MP, Barlow DH, Cowen PJ. Effect of estradiol implant on
noradrenergic
function
and
mood
in
menopausal
subjects.
Psychoneuroendocrinology. 1992;17(1):87-93
9- Brincat M, Magos A, Studd JW, Cardozo LD, O'Dowd T, Wardle PJ, Cooper
D. Subcutaneous hormone implants for the control of climacteric symptoms.
A prospective study. Lancet. 1984 Jan 7;1(8367):16-8
10- Sherwin BB, Gelfand MM. Sex steroids and affect in the surgical menopause:
a
double-blind,
cross-over
study.
Psychoneuroendocrinology.
1985;10(3):325-35
11- Gregoire AJ, Kumar R, Everitt B, Henderson AF, Studd JW. Transdermal
oestrogen for treatment of severe postnatal depression. Lancet. 1996 Apr
6;347(9006):930-3
12- Ahokas A, Kaukoranta J, Wahlbeck K, Aito M. Estrogen deficiency in severe
postpartum depression: successful treatment with sublingual physiologic
17beta-estradiol: a preliminary study. J Clin Psychiatry. 2001 May;62(5):3326
13- Nathorst-Boos J, von Schoultz B, Carlstrom K. Elective ovarian removal and
estrogen replacement therapy--effects on sexual life, psychological well-being
and androgen status. J Psychosom Obstet Gynaecol. 1993 Dec;14(4):283-93
14- Soares CN, Almeida OP, Joffe H, Cohen LS. Arch Gen Psychiatry. 2001
Jun;58(6):529-34. Efficacy of estradiol for the treatment of depressive
disorders in perimenopausal women: a double-blind, randomized, placebocontrolled trial. Arch Gen Psychiatry. 2001 Jun;58(6):537-8.
Depressão: A Associação Com Baixos Níveis de Testosterona
1- Barrett-Connor E, Von Muhlen DG, Kritz-Silverstein D. Bioavailable
testosterone and depressed mood in older men: the Rancho Bernardo Study.
J Clin Endocrinol Metab. 1999 Feb;84(2):573-7
2- Werner AA. The male climateric JAMA. 1946; 132 (4):188-94
3- Steiger A, von Bardeleben U, Wiedemann K, Holsboer F. Sleep EEG and
nocturnal secretion of testosterone and cortisol in patients with major
endogenous depression during acute phase and after remission. J Psychiatr
Res. 1991;25(4):169-77
4- 3Unden F, Ljunggren JG, Beck-Friis J, Kjellman BF, Wetterberg L.
Hypothalamic-pituitary-gonadal axis in major depressive disorders. Acta
Psychiatr Scand 1988 Aug;78(2):138-46
5- Shores MM, MD; Sloan KL, Matsumoto AM, Moceri VM, Felker B, Kivlahan D.
Increased incidence of diagnosed depressive illness in hypogonadal older
men. Arch Gen Psychiatry. 2004;61:162-7
6- Grinspoon S, Corcoran C, Stanley T, Baaj A, Basgoz N, Klibanski A. Effects
of hypogonadism and testosterone administration on depression indices in
HIV-infected men. J Clin Endocrinol Metab. 2000 Jan;85(1):60-5
Depressão: A Melhora Com a Reposição de Testosterona
1- Pope HG Jr, Cohane GH, Kanayama G, Siegel AJ, Hudson JI. Testosterone
gel supplementation for men with refractory depression: a randomized,
placebo-controlled trial. Am J Psychiatry. 2003 Jan;160(1):105-11
2- Wagner GJ, Rabkin R. A double-blind, placebo-controlled trial of testosterone
therapy for HIV-positive men with hypogonadal symptoms. Arch Gen
Psychiatry. 2000 Feb;57(2):141-7
3- Grinspoon S, Corcoran C, Stanley T, Baaj A, Basgoz N, Klibanski A. Effects
of hypogonadism and testosterone administration on depression indices in
HIV-infected men. J Clin Endocrinol Metab. 2000 Jan;85(1):60-5
4- Schmitz G. Erfahrungen mit dem neuen synthetischen testes-hormonpreparat "Perandren." Deutsche Medizinische Wochenschrift. 1937; 63:230–1
5- Davidoff E, Goodstone GL. Use of testosterone propionate in treatment of
involutional psychosis in the male. Arch Neurol Psychiatry. 1942; 48:811–7
6- Altschule MD, Tillotson KJ. The use of testosterone in the treatment of
depression. N Engl J Med. 1948; 239:1036–8
7- Lamar CP. Clinical endrocrinology of the male: with special reference to the
male climacteric. J Fla Med Assoc. 1940; 26:398–404
8- O'Carroll R, Shapiro C, Bancroft J. Androgens, behavior and nocturnal
erection in hypogonadal men: the effects of varying the replacement dose.
Clin Endocrinol. 1985; 23:527–538
9- Skakkebaek NE, Bancroft J, Davidson DW, Warner P. Androgen replacement
with oral testosterone undeconoate in hypogonadal men: a double-blind
controlled study. Clin Endocrinol. 1981; 14:49–61
10- Rabkin JG, Rabkin R, Wagner G: Testosterone replacement therapy in HIV
illness. Gen Hosp Psychiatry 1995;17:37–47
11- Malkin CJ, Pugh PJ, Morris PD, Kerry KE, Jones RD, Jones TH, Channer KS.
Testosterone replacement in hypogonadal men with angina improves
ischaemic threshold and quality of life. Heart. 2004 Aug;90(8):871-6.

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