Portugal - AAP.org

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Portugal - AAP.org

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Protecting Children and
Families from Tobacco:
Leadership Training
Portugal
XVI Congreso Latinoamericano de Pediatría
November 14, 2012
La Asociación Latinoamericana de Pediatría-ALAPE
Table of Contents Click on the links below to access the reports included in this document. WHO Country Profile WHO NCDs WHO TB Tobacco Fact Sheet ‐ Portuguese Treatment Guidelines 2002 – Portuguese Treatment Guidelines 2008 ‐ English Additional Resources WHO Report on the Global Tobacco Epidemic, 2011
Country profile
Portugal
Note: Where no data were available, "…" shows in the table. Where data were not required, "–" shows in the table.
WHO Framework Convention on Tobacco Control (WHO FCTC) status
Date of signature
Date of ratification (or legal equivalent)
9 January 2004
8 November 2005
Socioeconomic context
Population (thousands)
Income group
10 732
High income
Prevalence of tobacco use
Tobacco use data as provided by the country from the latest survey result available to WHO as at
1 November 2010
Adult prevalence, smoking (%)*
Male
Female
Total
Any smoked tobacco
Current
Daily
...
27.6
...
10.6
...
18.7
Adult prevalence, smokeless tobacco use (%)* . . .
Male
Female
Total
Cigarettes
Current
Daily
...
...
...
...
...
...
...
...
...
* Ages 15+, National Health Survey, 2005—2006
"…" Data not reported/not available.
WHO age-standardized estimated prevalence of smoking among those aged 15 years or more:
Year 2009
Adult prevalence, smoking (%)
Male
Female
Total
Any smoked tobacco
Current
Daily
32
28
16
13
24
20
Cigarettes
Current
Daily
32
28
16
13
24
20
Country Profile: Portugal
Tobacco control measures and programmes as at 31 December 2010
Smoke-free environments
2010
Public places with smoke-free legislation:
Health-care facilities
Educational facilities except universities
Universities
Government facilities
Indoor offices
Restaurants
Pubs and bars
Public transport
All other public places
Compliance score §
National law requires fines for smoking
Fines levied on the establishment
Fines levied on the smoker
Dedicated funds for enforcement
Citizen complaints and investigations
Yes
Yes
No
No
No
No
No
Yes
NA
...
Yes
Yes
Yes
No
Yes
§ A score of 0—10, where 0 is low compliance.
Subnational laws on smoke-free environments
Subnational jurisdictions do not have the authority to adopt and implement smoke-free
laws.
2
Treatment of tobacco dependence
2010
Is there a toll-free telephone quit line/help line with a live person available to
discuss cessation with callers in your country?
Yes
Nicotine replacement
therapy (e.g., patch,
gum, lozenge, spray or
inhaler)
Is this product legally sold in the country?
Yes
Where and how can this product be legally
purchased in your country?
In a pharmacy
without a
prescription
No
Bupropion (e.g., Zyban,
Wellbutrin)
Varenicline
Is smoking cessation
support available in the
following places in your
country?
Does the
national/federal health
insurance or the
national health service
cover the cost of this
support?
Does the national/federal health insurance or the
national health service cover the cost of this
product?
Is any NRT on the country's essential drugs list?
No
Is this product legally sold in your country?
Yes
product?
Is this product legally sold in your country?
In a pharmacy with
a prescription
No
product?
Health clinics or other primary care facilities
Hospitals
Office of a health professional
In the community
Other
Health clinics or other primary care facilities
Hospitals
Office of a health professional
In the community
Other
In a pharmacy with
a prescription
No
3
Yes
Yes in some
Yes in some
Yes in some
Yes in some
...
Fully
Fully
No
—
...
Cigarettes
Smokeless
tobacco
2010
Health warnings on tobacco packages
Does the law mandate that health warnings appear on tobacco packages?
What percentage of the principal display areas of the package is legally mandated to be
covered by health warnings? FRONT AND REAR COMBINED
What percentage of the principal display areas of the FRONT of the package is legally
mandated to be covered by health warnings?
What percentage of the principal display areas of the REAR of the package is legally
mandated to be covered by health warnings?
Does the law mandate that the warning be placed at the top of the principle display areas
of the package?
Does the law mandate font style, font size and colour for package warnings?
Are the health warnings rotating on packages?
Are the health warnings on packages written in the principal language(s) of the country?
Does the law require that health warnings on packages are not obscured in any way,
including by required markings such as tax stamps?
Do the health warnings on packages include a photograph or graphic?
Do health warnings appear on each package and any outside packaging and labelling used
in the retail sale?
Does the law on health warnings apply to products whether manufactured domestically,
imported, AND for duty-free sale?
Does the law state that warnings on packages do not remove or diminish the liability of the
tobacco industry?
Do health warnings on packages describe the harmful effects of tobacco use on health?
Does the law mandate specific health warnings on cigarette packages?
How many specific health warnings are approved by the law?
Does the law require or establish fines for violations regarding health warnings on
packages?
Are there any laws requiring that cigarette packaging and labelling do not use misleading
terms which imply the product is less harmful than other similar products, such as “low
tar”, “light”, “ultra-light”, or “mild”?
Are there any laws requiring that cigarette packaging and labelling do not use figurative or
other signs, including colours or numbers, as substitutes for prohibited misleading terms
and descriptors?
Are there any laws requiring that cigarette packaging and labelling do not use descriptors
depicting flavours?
Does the law ban the display of quantitative information on emission yields (such as tar,
nicotine and carbon monoxide) on cigarette packaging, including when used as part of a
brand name or trademark?
Does the law mandate the display of qualitative information on relevant constituents and
emissions of tobacco products on cigarette packaging?
Does the law mandate that this information is displayed on one or more of the principal
display areas (front, rear) of the package?
Does the law prevent the display of expiry dates on cigarette packaging?
Is it mandatory for the quit line number to appear on packaging or labelling?
Does the law mandate plain packaging (ie. prohibit the use of logos, colours, brand images
or promotional information on packaging other than brand names and product names
displayed in a standard colour and font style)?
4
Yes
35
35
30
30
40
40
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
No
Yes
No
Yes
Yes
Yes
No
No
Yes
Yes
16
Yes
Yes
Yes
16
Yes
Yes
Yes
Yes
Yes
No
No
No
No
No
No
—
—
No
No
No
No
No
No
Bans on tobacco advertising, promotion and sponsorship
2010
Direct bans
National TV and radio
International TV and radio
Local magazines and newspapers
International magazines and newspapers
Billboards and outdoor advertising
Point of sale
Internet
Other direct bans
Compliance score of direct bans §
Yes
No
Yes
No
Yes
Yes
Yes
Yes
8
Indirect bans
Free distribution
Promotional discounts
Non-tobacco goods and services identified with tobacco brand names
Brand name of non-tobacco products used for tobacco product
Appearance of tobacco brands in TV and/or films (product
placement)
Appearance of tobacco products in TV and/or films
Sponsored events
Other indirect bans
Compliance score of indirect bans §
Are there subnational laws or regulations banning some or all types
of tobacco advertising, promotion and sponsorship mentioned in the
above questions?
§ A score of 0—10, where 0 is low compliance.
5
Yes
Yes
Yes
No
Yes
Yes
Yes
Yes
7
No
Tobacco taxation policy as at 31 July 2010
Price of lowest-cost brand of cigarettes (Ritz)
A
Tax inclusive retail sales price (TIRSP) for a pack of 20 cigarettes
2008
EUR
3.10
2010
EUR
3.10
2008
EUR
3.55
2010
EUR
3.70
WHO's
comparable
estimate for
2008
WHO's
comparable
estimate for
2010
EUR
3.30
USD
4.59
EUR
3.50
USD
4.56
80
39
23
17
—
0
79
39
23
17
—
0
Price of Marlboro or similar brand of cigarettes (Marlboro)
A
Tax inclusive retail sales price (TIRSP) for a pack of 20 cigarettes
Taxes on the most popular brand of cigarettes (MPPC)
Price of most sold brand, pack of 20 cigarettes
In currency reported by country
In US$ at official exchange rate
Taxes on this brand (% of retail price)
Total taxes
Specific excise
Ad valorem excise
Value added tax (VAT)
Import duty
Other taxes
ᄌ
ᄌ Individual categories of tax may not add to total due to rounding.
National tobacco control programme
Specific national government objectives in tobacco control
National agency or technical unit for tobacco control
Number of full-time equivalent staff
Government expenditure on tobacco control:
In currency reported by country
Year of expenditure
In US$ at official exchange rate
2010
Yes
Yes
2
......
...
US$ . . .
*****
6
Portugal
2010 total population: 10 675 572
Income group: High
NCD mortality
Proportional mortality (% of total deaths, all ages)
males females
45.4
43.4
2008 estimates
Total NCD deaths (000s)
NCD deaths under age 60
(percent of all NCD deaths)
Age-standardized death rate per 100 000
All NCDs
Cancers
Chronic respiratory diseases
Cardiovascular diseases and diabetes
15.7
8.1
483.4
182.1
34.8
184.5
276.4
89.3
15.1
125.3
Communicable,
maternal,
perinatal and
nutritional
conditions
9%
Injuries
4%
CVD
37%
Other NCDs
13%
Behavioural risk factors
2008 estimated prevalence (%)
Current daily tobacco smoking
Physical inactivity
males females
27.0
10.7
50.0
57.5
total
18.5
53.9
males females
50.4
45.7
8.3
7.5
61.8
56.6
21.6
26.3
58.0
58.2
total
47.9
7.9
59.1
24.0
58.1
Diabetes
5%
Metabolic risk factors
2008 estimated prevalence (%)
Raised blood pressure
Raised blood glucose
Overweight
Obesity
Raised cholesterol
Respiratory
diseases
6%
Cancers
26%
NCDs are estimated to account for 86% of all deaths.
Metabolic risk factor trends
Mean systolic blood pressure
141
28
kg/m2
mmHg
139
137
135
26
133
24
131
22
129
20
1980
1984
1988
1992
1996
2000
2004
2008
1980
Mean fasting blood glucose
5.8
1984
5.6
5.4
5.2
1988
1992
1996
2000
2004
2008
2004
2008
Mean total cholesterol
6.0
mmol/l
mmol/l
Mean body mass index
30
5.8
5.6
5.4
5.2
5.0
5.0
4.8
1980
1984
1988
1992
1996
2000
2004
2008
Males
1980
1984
1988
1992
1996
2000
Females
Country capacity to address and respond to NCDs
Has a Unit / Branch / Dept in MOH with responsibility for NCDs
NR
There is funding available for:
NCD treatment and control
NCD prevention and health promotion
NCD surveillance, monitoring and evaluation
Yes
Yes
Yes
National health reporting system includes:
NCD cause-specific mortality
NCD morbidity
NCD risk factors
Yes
NR
NR
Has a national, population-based cancer registry
NR
NR = Country replied to survey but did not give a response to specific question
World Health Organization - NCD Country Profiles , 2011.
Has an integrated or topic-specific policy / programme / action
plan which is currently operational for:
Cardiovascular diseases
Yes
Cancer
Yes
Chronic respiratory diseases
NR
Diabetes
NR
Alcohol
NR
Unhealthy diet / Overweight / Obesity
Yes
Physical inactivity
NR
Tobacco
NR
Number of tobacco (m)POWER measures
implemented at the highest level of achievement
1/5
TUBERCULOSE
& TABAGISMO
Organização
Mundial
da Saúde
www.who.int/tb
www.who.int/tobacco
UMA FORTE ASSOCIAÇÃO
•
•
•
•
Fumar aumenta significativamente o risco de adoecimento e morte por tuberculose
Mais de 20% da incidência global por tuberculose pode ser atribuida ao tabagismo
Controlar a epidemia de tabaco vai ajudar a controlar a epidemia da tuberculose
Fumar é um fator de risco para a tuberculose independente do uso de álcool e de
outros fatores sócio-econômicos
•
•
Fumar aumenta em mais do que duas vezes e meia o risco de adoecer por tuberculose
A monografia WHO monograph on TB and tobacco oferece informações adicionais
Correlação do alto impacto da TB e do uso de produtos do tabaco em países selecionados
•
•
•
40%
35%
5 países são líderes mundiais na proporção de casos de tuberculose e de fumantes
40% da carga de doença na India por tuberculose pode ser atribuida ao tabagismo
Uma dramática redução do tabagismo e da exposição ao tabagismo passivo na China poderia reduzir a incidência
da tuberculose em 14-52% até 2033
30%
25%
Turquia
Alemanha
Japão
Brasil
EUA
Rússia
Etiópia
Mianmar
Proporção de fumantes no mundo(2005)
Filipinas
Bangladesh
Paquistão
Indonésia
5%
China
10%
India
15%
Africa do Sul
Proporções de casos de tuberculose no mundo(2007)
20%
0%
A epidemia da tuberculose:
¾
¾
¾
¾
¾
2 bilhões de pessoas estão infectadas pelo
bacilo da TB
TB é uma doença da pobreza com a maioria das
mortes ocorrendo em países de baixo a médio
poder aquisitivo com mais da metade de todas
as mortes ocorrendo na Ásia
9.27 milhões de novos casos de TB ocorreram
em 2007
1.75 milhões de pessoas morreram por TB em
2007
5% dos casos de TB são multiresistentes às
drogas
A epidemia de tabaco:
¾
¾
¾
Mais do que 1 bilhão de pessoas fumam e
aproximadamente 70% vivem em países de
baixa a média renda
O uso do tabaco é a maior causa evitável de
morte
Mais do que 5 milhões de pessoas morrem por
ano por usarem tabaco. Sem controle, a
epidemia vai matar mais de 8 milhões por ano
em 2030
Políticas recomendadas pela OMS para combater o tabagismo e a tuberculose
•
Controle o tabagismo em qualquer lugar especialmente onde pessoas estejam em risco de contrair infecção por
tuberculose
•
•
•
•
•
Coordene os programas de tabagismo e tuberculose e treine profissionais de saúde nas duas áreas
Investigue e registre o uso do tabaco pelo paciente com TB e ofereça aconselhamento e tratamento
Promova e apoie ambientes livres de fumo particularmente onde os serviços de TB são oferecidos
Integre intervenções mínimas (5 'A's e 5 'R's) nas atividades de controle da TB
Implemente procedimentos de cessação de fumar através da estratégia PAL (Abordagem prática à saúde
pulmonar)
Ações de saúde pública
Programas de controle da tuberculose podem apoiar
programas de controle do tabagismo:
¾ Promovendo o aumento de impostos e preços
¾ Oferecendo proteção da exposição à fumaça
ambiental do tabaco
¾ Proibindo a publicidade, promoção e patrocínio de
produtos de tabaco
¾ Regulando o empacotamento e etiquetagem de
produtos do tabaco
¾ Aumentando a conscientização do público sobre os
malefícios do tabaco
¾ Tratando a dependência à nicotina
A cessação de fumar pode ser abordada através da
estratégia PAL – Abordagem prática à saúde pulmonar,
que:
¾ É uma abordagem centrada no paciente para
diagnóstico e tratamento de doenças respiratórias
comuns nas unidades básicas de saúde
¾ Promove gerenciamento integrado e baseado em
sintomas
¾ Procura padronizar a prestação de serviços através
do desenvolvimento e implementação de
abordagens clínicas
A estratégia PAL e outras recomendações podem ser
encontradas na Estratégia Stop TB da OMS
Estas e outras recomendações se encontram na
Convenção Quadro para o Controle do Tabaco da
OMS
Ações voltadas aos pacientes
Use 5 ‘A's
¾ ABORDE pacientes de tuberculose para
saber se eles fumam
¾ ACONSELHE a que eles parem de
fumar
¾ AVALIE a possibilidade real de que eles
parem
¾ AJUDE na sua tentativa de parar
¾ AGENDE uma consulta de seguimento
Os 5 'R's
¾ RELEVÂNCIA – garanta que o paciente de TB
saiba que seu tratamento será mais efetivo se
parar de fumar
¾ RISCOS – mostre todos os riscos de continuar
fumando, inclusive os riscos de recaída
¾ RECOMPENSAS – eduque seu paciente de TB
sobre os outros benefícios de deixar de fumar
¾ RESISTÊNCIAS – ajude seu paciente de TB a
identificar obstáculos para deixar de fumar
¾ REPETIÇÕES – continue encorajando seu
paciente com tuberculose a parar de fumar
Projetos piloto e próximos passos
•
•
•
Egito, Indonésia, e Nepal – ações de cessação de fumar foram introduzidas nos serviços de saúde em áreas
piloto através da estratégia PAL
Quirguistão – serviços de cessação de fumar foram inseridos como parte da estratégia PAL na maioria das
unidades básicas de saúde do país
Brasil – estratégias para cessação de fumar foram testadas nos serviços de atenção ao paciente de tuberculose
no município do Rio de Janeiro
Próximos passos
•
•
•
•
Monitorar, avaliar e documentar abordagens para cessação de fumar através da estratégia PAL e dos
serviços de atenção à tuberculose
Expandir projetos piloto que tenham obtido sucesso para outras populações
Aumentar a concientização política dos efeitos da associação entre a tuberculose e o tabagismo
Aumentar a concientização entre os diversos departamentos ministeriais dos benefícios sociais, econômicos e
da saúde da ação conjunta no controle da tuberculose e do tabagismo
© WHO Nov 2009
NOC de cessação de tabagismo - IQS
Instituto da Qualidade em Saúde
- Ministério da Saúde -
Norma de Orientação Clínica
TRATAMENTO DO USO E
DEPENDÊNCIA DO
TABACO
2002
1
INDICE
INDICE ...................................................................................................................................................................... 2
SECÇÕES QUE CONSTITUEM ESTA NORMA DE ORIENTAÇÃO CLÍNICA ............................................ 4
TÍTULO..................................................................................................................................................................... 6
INTRODUÇÃO ........................................................................................................................................................ 6
NATUREZA DA DEPENDÊNCIA DE TABACO ............................................................................................................. 7
REFERÊNCIAS ......................................................................................................................................................... 7
ADAPTAÇÃO........................................................................................................................................................... 8
FONTES DE FINANCIAMENTO ......................................................................................................................... 8
COMITÉS E GRUPO RESPONSÁVEL ............................................................................................................... 9
OBJECTIVOS .......................................................................................................................................................... 9
TÓPICO/DOENÇA.................................................................................................................................................. 9
CATEGORIA............................................................................................................................................................ 9
UTILIZADORES POTENCIAIS ........................................................................................................................... 9
POPULAÇÃO – ALVO ........................................................................................................................................... 9
INTERVENÇÕES PRÁTICAS .............................................................................................................................. 9
RESULTADOS ....................................................................................................................................................... 10
MÉTODOS DE SELECÇÃO DA EVIDÊNCIA CIENTÍFICA ....................................................................... 10
FONTES DE EVIDÊNCIA CIENTÍFICA .......................................................................................................... 10
ARTIGOS PUBLICADOS EM REVISTAS OU BASES DE DADOS ELECTRÓNICAS .............................. 10
REVISTAS .......................................................................................................................................................... 12
LIVROS ............................................................................................................................................................... 12
CDROMS ............................................................................................................................................................. 12
INTERNET .......................................................................................................................................................... 12
METODOLOGIA DE AVALIAÇÃO CRITICA DA EVIDÊNCIA CIENTÍFICA....................................... 13
ESQUEMA DA HIERARQUIZAÇÃO DA EVIDÊNCIA CIENTÍFICA ....................................................... 14
APOIANTES E SUBSCRITORES....................................................................................................................... 17
ESTRATÉGIA DE IMPLEMENTAÇÃO........................................................................................................... 17
RECOMENDAÇÕES PRINCIPAIS.................................................................................................................... 17
AVALIAÇÃO DO USO DE TABACO .............................................................................................................. 17
INTERVENÇÕES CLÍNICAS BREVES ........................................................................................................... 19
INTERVENÇÕES CLÍNICAS INTENSIVAS................................................................................................... 26
RASTREIO E AVALIAÇÃO.............................................................................................................................. 28
ESTRUTURA E INTENSIDADE DO TRATAMENTO ................................................................................... 28
ELEMENTOS DE TRATAMENTO................................................................................................................... 29
POPULAÇÕES ESPECIAIS............................................................................................................................... 30
GRAVIDEZ...................................................................................................................................................... 30
MINORIAS RACIAIS E ÉTNICAS.................................................................................................................. 30
FUMADORES HOSPITALIZADOS ............................................................................................................... 30
CRIANÇAS E ADOLESCENTES.................................................................................................................... 31
DOENTES IDOSOS........................................................................................................................................ 31
TÓPICOS ESPECIAIS ........................................................................................................................................ 31
AUMENTO DE PESO APÓS A CESSAÇÃO DO TABAGISMO................................................................... 31
OUTROS PRODUTOS DO TABACO ............................................................................................................ 31
FORMAÇÃO DOS CLÍNICOS ....................................................................................................................... 32
2
ALGORITMO CLÍNICO...................................................................................................................................... 32
RESERVAS QUALITATIVAS............................................................................................................................. 33
ANÁLISE DE CUSTOS......................................................................................................................................... 33
BENEFÍCIOS POTENCIAIS GERAIS DE SUB-GRUPOS............................................................................. 33
RISCOS POTENCIAIS E DE SUB-GRUPOS.................................................................................................... 33
DISPONIBILIDADE.............................................................................................................................................. 33
DOCUMENTAÇÃO ANEXA ............................................................................................................................... 33
RECURSOS DE DOENTES ................................................................................................................................. 33
DATA DE PUBLICAÇÃO .................................................................................................................................... 34
DATA DE REVISÃO PREVISTA ....................................................................................................................... 34
3
SECÇÕES QUE CONSTITUEM ESTA NORMA DE ORIENTAÇÃO CLÍNICA
Secção
Descrição
•
identifica o título completo
•
esclarece se a NOC foi adaptada de outra e, no caso afirmativo,
identifica-a
•
identifica a organização responsável pela elaboração da NOC
•
indica as eventuais fontes de financiamento para elaboração da NOC
e, no caso afirmativo, pormenoriza as condições contratualizadas
•
identifica formalmente os comités e sub-comités dentro do grupo
responsável e descreve a composição individual deste, incluindo
graus profissionais, académicos e afiliações existentes
•
descreve os objectivos gerais da NOC
•
identifica as áreas major de medicina clínica ou de cuidados de
saúde sobre as quais incidirão as recomendações
•
classifica a NOC em termos de tipo (ver atrás)
•
identifica as categorias profissionais que poderão vir a utilizar a
NOC (com ênfase no grupo-alvo)
•
decreve a população-alvo de doentes para os quais a NOC foi
elaborada
•
identifica as intervenções clínicas e as práticas específicas incluidas
na NOC
•
identifica os resultados (outcomes) mais importantes ou as medidas
específicas da NOC
Métodos de selecção da
evidência científica
•
identifica com pormenor e classifica os métodos utilizados para
seleccionar a evidência científica que serviu de base à NOC
Fontes de evidência
científica
•
descreve as fontes bibliográficas da evidência científica (bases de
dados, CD-ROMs, WWW, etc.)
Metodologia de
avaliação crítica da
Esquema de
hierarquização da
•
descreve em pormenor os métodos utilizados para avaliar
criticamente a evidência científica que serviu de base à NOC
•
descreve os esquema de classificação da validade da evidência
científica e a força das recomendações nela baseadas (se justificável)
Métodos de análise e
validação da evidência
científica
•
descreve os métodos analíticos utilizados para os dados da evidência
científica (RCTs, meta-análises, revisões sistematizadas, estudos
retrospectivos, etc.), incluindo a sua validação interna e externa
•
identifica as organizações que apoiam formalmente as NOCs e as
suas recomendações depois de publicadas
Estratégia de
implementação
•
descreve os planos práticos para a implementação da NOC:
contextos, modalidades, avaliação
Recomendações
principais
•
descreve as recomendações principais, resumidas das que estão
incluidas no principal segmento do texto base
Título
Adaptação
Responsáveis
Fontes de financiamento
Comités e grupo
responsável
Objectivos
Tópico/doença
Categoria
Utilizadores potenciais
População-alvo
Intervenções / Práticas
Resultados (outcomes)
Apoiantes e subscritores
4
•
apresenta o algoritmo clínico que sintetiza as recomendações do
texto
•
descreve os problemas metodológicos identificados pelo grupo e
identifica áreas de incerteza da evidência, assim como os passos que
foram dados para a solucionar
Análise de custos
•
inclui análise económica, se possível
Benefícios potenciais
gerais e de sub-grupos
•
identifica os benefícios antecipados da aplicação das recomendações
em geral, assim como em sub-grupos específicos (se se justificar)
Riscos potenciais e em
sub-grupos
•
identifica os riscos antecipados da aplicação das recomendações em
geral, assim como em sub-grupos específicos (se se justificar)
•
descreve os meios em que a NOC será disponibilizada e a sua
localização (material impresso, CD-ROM, Internet)
•
identifica os documentos extra classificados como importantes pelos
responsáveis
•
identifica os recursos referentes a doentes que serão necessários
estar presentes para aplicação da NOC
Data de publicação
•
data em que foi disponibilizada publicamente
Revisões
•
datas em que estão previstas as revisões das recomendações
Algoritmo clínico
Reservas qualitativas
Disponibilidade
Documentação anexa
Recursos de doentes
5
TÍTULO
NORMA DE ORIENTAÇÃO CLÍNICA PRÁTICA PARA O TRATAMENTO DO USO E
DEPENDÊNCIA DO TABACO
INTRODUÇÃO
O uso de tabaco é uma importante causa de morbilidade e mortalidade, sendo referido como a
principal causa evitável de doença e morte nas sociedades avançadas (americana, por ex.). (1)
É uma causa reconhecida de cancro, doença cardíaca, acidente vascular cerebral, doença
pulmonar crónica obstrutiva e complicações na gravidez. (2)
Apesar dos perigos para a saúde que representa, o uso de tabaco permanece
surpreendentemente elevado. Em Portugal, 18 % de todos os adultos fumam. (3) Além disso, a
prevalência do uso de tabaco em adolescentes tem subido dramaticamente desde 1990. (4-6)
Uma percentagem significativa dos actuais fumadores está disposta a deixar de fumar (7,8)
criando uma enorme responsabilidade para todos os prestadores de cuidados de saúde: estes
deverão estar à altura do desafio, uma vez que há actualmente intervenções eficazes que
aumentam significativamente a taxa de sucesso das tentativas de abandono do uso de tabaco.
Os utilizadores de tabaco não devem ser deixados entregues a si próprios, mas sim
encorajados e ajudados activamente na terminação adequada da sua dependência, devendo
ser-lhes oferecidas as várias modalidades de tratamento que actualmente se sabe serem
efectivas.
A negligência e desatenção do sistema de saúde em relação a este problema custa um preço
elevado - em termos de doença evitável, vidas perdidas e custos económicos - que já nada
justifica, visto que nas últimas duas décadas a investigação clínica clarificou muitos aspectos
da dependência de tabaco e foram descobertas várias formas efectivas de terapêutica, quer
farmacológica quer de aconselhamento.
Pode-se afirmar que se verifica em relação ao uso de tabaco uma rara confluência de
circunstâncias:
• Ameaça para a saúde altamente significativa
• Tendência dos clínicos para não intervir consistentemente
• Existência de intervenções efectivas.
É difícil identificar qualquer outra condição que apresente uma mistura tal de letalidade,
prevalência e negligência, apesar da existência de intervenções efectivas e prontamente
acessíveis.
Outro aspecto a salientar é que os tratamentos de cessação do tabagismo são efectivos não só
clinicamente, mas também relativamente ao custo, nomeadamente em comparação com outras
intervenções de prevenção de doença e tratamentos médicos, como o tratamento da
hipertensão e hipercolesterolémia, e exames de rastreio como a mamografia periódica ou os
testes de Papanicolau. O tratamento da dependência de tabaco é considerado o “gold
standard” das terapêuticas preventivas (9-13).
6
Em países como os EUA há um reconhecimento crescente de que as intervenções em relação
ao uso de tabaco devem tornar-se parte integrante dos cuidados de saúde, constituindo um
modelo de boa prática (14). Para esta mudança de atitude contribuiu o aparecimento em 1996
de uma “guideline” intitulada ”Smoking Cessation Clinical Practice Guideline” (15), a que se
seguiu a publicação em 2000 de uma segunda versão resumida e actualizada, chamada
“Treating Tobacco Use and Dependence: A Clinical Practice Guideline” (14), que foi publicada
sob a forma de um ”United States Public Health Report”, dada a importância que é dada a
este problema nos EUA.
Existe a necessidade de também no nosso país mudar a atitude de todos os prestadores de
cuidados de saúde em relação a este problema, em particular dos que trabalham nos Cuidados
Primários: foi baseada nesta convicção que o Instituto da Qualidade em Saúde (IQS) decidiu
elaborar esta Norma de Orientação Clínica, destinada a sumariar e apresentar os dados
práticos mais recentes sobre a cessação do tabagismo.
Natureza da dependência de tabaco
Para muitos utilizadores, o tabaco resulta em verdadeira dependência, comparável à
dependência causada por opiáceos, anfetamina e cocaína, e, como no caso destas drogas,
apresenta muitas das características de doença crónica (16).
Uma minoria de utilizadores de tabaco consegue abstinência permanente numa primeira
tentativa de abandono, mas a maioria persiste no uso de tabaco e tipicamente passa por
múltiplos episódios de remissão e recidiva.
Reconhecer a cronicidade da dependência do tabaco permite uma aproximação mais correcta
do tratamento, levando a valorizar a necessidade de cuidado continuado e a dar importância
ao aconselhamento activo.
Apenas 7% dos fumadores conseguem abstinência a longo prazo, quando o tentam por si
próprios (17-18); a taxa de sucesso pode aumentar para 15 - 30% se apoiados por tratamentos e
intervenções efectivas (14), que fazem parte das recomendações desta NOC . Os tratamentos
mais eficazes são o aconselhamento intensivo associado a farmacoterapia, mas mesmo
intervenções tão breves como aconselhamento com duração inferior a 3 minutos, podem
aumentar significativamente a taxa de abstinência (14).
A maior parte dos utilizadores de tabaco são fumadores de cigarros. Por este motivo, grande
parte da atenção clínica e de investigação neste campo tem incidido sobre a avaliação e
tratamento dos fumadores de cigarros. Mas todos os produtos de tabaco têm efeitos
devastadores sobre a saúde das pessoas (19-20) e os médicos devem intervir em relação a todos
os utilizadores de tabaco (cachimbo, charutos, etc.): é esta a razão para a adopção do termo
“utilizador de tabaco” em vez de “fumador”. Há no entanto algumas recomendações para as
quais só existe evidência baseada em estudos sobre fumadores de cigarros. Nestes casos é
usado o termo “fumador” para reflectir o carácter limitado das recomendações.
Referências
1. Centers for Disease Control and Prevention. Perspectives in disease prevention and health
promotion. Smoking – attributable mortality and years of potential life lost – United States, 1984.
MMWR Morb Mortal Wkly Rep 1997; 46 (20): 444-51.
7
2. US Department of Health and Human Services. The health benefits of smoking cessation: A report
of the Surgeon General. Atlanta (GA): US Department of Health and Human Services. Public
Health Service, Centers for Disease Control, Center for Chronic Disease Prevention and Health
Promotion, Office of Smoking and Health. DHHS Publication Nº (CDC) 90-8416, 1990.
3. Eurotrials, nº 2, Setembro de 2000.
4. Centers for Disease Control and Prevention. Tobacco use among high school students – United
States, 1997. MMWR Morb Mortal Wkly Rep 1998; 47 (12): 229-233.
5. Centers for Disease Control and Prevention. Incidence of initiation of cigarette smoking – United
States, 1965 – 1996. MMWR Morb Mortal Wkly Rep 1998; 47 (39):837-40.
6. Gilpin E, Choi WS, Berry C, Pierce JP. How many adolescents start smoking each day in the
United States. J Adolesc Health 1999; 25:248-55.
7. Centers for Disease Control and Prevention. Health objectives for the nation cigarette smoking
among adults – United States, 1993. MMWR Morb Mortal Wkly Rep 1994; 43(50):925-30.
8. Centers for Disease Control and Prevention. Cigarette smoking among adults – United States,
1995. MMWR Morb Mortal Wkly Rep 1997; 46 (51): 1217 – 20.
9. Eddy DM. David Eddy ranks the tests. Harv Health Lett 1992; 11.
10. Cummings SR, Rubin SM, Oster G. The cost – effectiveness of counseling smokers to quit. JAMA
1989; 261 (1): 75-9.
11. Eddy DM. The economics of cancer prevention and detection: getting more for less. Cancer 1981;
47 (5 Suppl): 1200-9.
12. Eddy DM. Setting priorities for cancer control programs. J Natl Cancer Inst 1986; 76 (2): 187-99.
13. Oster G, Huse DM, Delea TE, Colditz GA. Cost – effectiveness of nicotine gum as an adjunct to
physician’s advice against cigarette smoking. JAMA 1986; 256 (10): 1315-8.
14. Fiore MC, Bailey WC, Cohen SJ, et al. Treating Tobacco Use and Dependence. Clinical Practice
Guideline. Rockville, Md: US Department of Health and Human Services. Public Health Service.
June 2000.
15. Fiore MC, Bailey WC, Cohen SJ, et al. Smoking Cessation: Clinical Practice Guideline nº 18.
Rockville, Md: US Department of Health and Human Services. Public Health Service, Agency for
Health Care Policy and Research; 1996. AHCPR publication 96 – 0692.
16. Jones H, Garrett B, Griffiths R. Subjective and physiological effects of intravenous nicotine and
cocaine in cigarette smoking cocaine abusers. J Pharmacol Exp Ther 1999; 288 (1): 188 – 97.
17. Centers for Disease Control and Prevention. Smoking cessation during previous year among
adults – United States, 1990 and 1991. MMWR Morb Mortal Wkly Rep 1993; 42 (26): 504-7.
18. Hatziandreu EJ, Pierce JP, Lefkopoulou M, Fiore MC, Mills SL, Novotny TE, et al. Quitting
smoking in the United States in 1986. J Natl Cancer Inst 1990; 82 (17): 1402-6.
19. National Cancer Institute. Cigars: Health effects and trends. Smoking and Tobacco Control
Monograph nº 9. Bethesda, Maryland, National Cancer Institute. NIH Publication nº 98 – 4302.
1998.
20. Iribarren C, Tekawa I, Sidney S, Friedman G. Effect of cigar smoking on the risk of cardiovascular
disease, chronic obstructive pulmonary disease, and cancer in men. N Eng J Med 1999; 340 (23):
1773-80.
ADAPTAÇÃO
Esta NOC não foi adaptada directamente de nenhuma recomendação, protocolo, consenso ou
“guideline” publicadas até à data.
FONTES DE FINANCIAMENTO
As fontes de financiamento para a elaboração desta NOC provêm exclusivamente do Instituto
da Qualidade em Saúde (IQS).
8
COMITÉS E GRUPO RESPONSÁVEL
Os autores desta NOC fazem parte da área das Normas de Orientação Clínica do IQS e são a
Dra. Isabel Soares e o Prof. António Vaz Carneiro (responsável da área das NOC).
OBJECTIVOS
Esta NOC tem por objectivo fornecer recomendações efectivas, baseadas na evidência
científica, sobre o tratamento do uso e dependência de tabaco.
TÓPICO/DOENÇA
A doença a que se refere esta NOC é a dependência de tabaco, seja qual for a forma de
utilização (cigarros, charutos, cigarrilhas, cachimbo).
CATEGORIA
É uma NOC de triagem/rastreio e de efectividade terapêutica.
UTILIZADORES POTENCIAIS
•
•
•
•
•
•
•
•
•
Médicos de família
Médicos do trabalho
Internistas
Cardiologistas
Pneumologistas
Obstetras
Pediatras
Enfermeiros
Psicólogos
POPULAÇÃO – ALVO
Todos os utilizadores de tabaco.
INTERVENÇÕES PRÁTICAS
As duas principais categorias de intervenções são as intervenções breves e as intervenções
intensivas. Tanto umas como outras incluem várias formas de aconselhamento e
farmacoterapia.
As intervenções breves são de 3 tipos, conforme se dirigem a um de três grupos de doentes:
• utilizadores de tabaco que desejam fazer de imediato uma tentativa de abandono
• utilizadores de tabaco que não desejam fazer para já uma tentativa de abandono
(intervenção motivacional)
• ex-utilizadores recentes de tabaco (intervenção para prevenção de recidiva)
9
As intervenções intensivas diferem das breves na duração, assim como na intensidade, do
aconselhamento.
RESULTADOS
O resultado (outcome) é o da cessação permanente do uso de tabaco.
MÉTODOS DE SELECÇÃO DA EVIDÊNCIA CIENTÍFICA
A selecção da evidência científica foi feita exclusivamente em fontes secundárias de
informação.
Definem-se como fontes de evidência científica secundária aquelas que, tendo seleccionado
os artigos, ensaios e estudos nas bases de dados primárias (Medline, EMBASE, CINAHL, por
exemplo), fazem sobre eles uma avaliação crítica baseada na sua estrutura metodológica,
seleccionando apenas aquelas que, pela sua validade, importância e relevância para a prática
clínica, constituem a evidência considerada a mais válida (ver adiante).
O critério base foi o das referidas fontes de evidência científica secundária serem
inequivocamente baseadas na evidência científica e estarem disponíveis sob a forma impressa
(artigos de revistas, livros) e/ou electrónica (CDROMs, Internet).
FONTES DE EVIDÊNCIA CIENTÍFICA
As fontes de evidência científica utilizadas como base desta NOC incluem artigos, revistas,
livros e páginas na Internet de organizações específicas. Seguem-se as indicações de cada
fonte individual.
ARTIGOS PUBLICADOS EM REVISTAS OU BASES DE DADOS ELECTRÓNICAS
•
The Tobacco Use and Dependence Clinical Practice Guideline Panel SaCR. A clinical practice
guideline for treating tobacco use and dependence. JAMA 2000; 283:3244-3254.
•
Lancaster T, Stead L, Silagy CA, Sowden A for the Cochrane Tobacco Addiction Review Group.
Effectiveness of interventions to help people stop smoking: findings from the Cochrane Library.
BMJ 2000; 321:355-358.
•
Tashkin DP, Kanner R, Bailey W, Buist S, Anderson P, Nides MA et al. Smoking cessation in
patients with chronic obstructive pulmonary disease: a double-blind, placebo-controlled,
randomised trial. Lancet 2001; 357:1571-1575.
•
Fiore MC, Bailey WC, Cohen SJ, et al. Treating tobacco use and dependence. Quick Reference
Guide for Clinicians. Rockville, MD: U.S. Department of Health and Human Services. Public
Health Service. 1st ed. 2000
•
Abbot NC, Stead LF, White AR, Barnes J, Ernst E. Hypnotherapy for smoking cessation
(Cochrane Review). In: The Cochrane Library, Issue 1, 2001. Oxford: Update Software.
•
Gourlay SG, Stead LF, Benowitz NL. Clonidine for smoking cessation (Cochrane Review). In: The
Cochrane Library, Issue 1, 2001. Oxford: Update Software.
•
Hajek P, Stead LF. Aversive smoking for smoking cessation (Cochrane Review). In: The
•
Hughes JR, Stead LF, Lancaster T. Anxiolytics for smoking cessation (Cochrane Review). In: The
10
•
Hughes JR, Stead LF, Lancaster T. Antidepressants for smoking cessation (Cochrane Review).
In: The Cochrane Library, Issue 1, 2001. Oxford: Update Software.
•
Lancaster T, Stead LF. Silver acetate for smoking cessation (Cochrane Review). In: The
•
Lancaster T, Stead LF. Mecamylamine (a nicotine antagonist) for smoking cessation (Cochrane
Review). In: The Cochrane Library, Issue 1, 2001. Oxford: Update Software.
•
Lancaster T, Stead LF. Individual behavioural counselling for smoking cessation (Cochrane
•
Lancaster T, Stead LF. Self-help interventions for smoking cessation (Cochrane Review). In: The
•
Lancaster T, Silagy C, Fowler G. Training health professionals in smoking cessation (Cochrane
•
Lumley J, Oliver S, Waters E. Interventions for promoting smoking cessation during pregnancy
•
Rice VH, Stead LF. Nursing interventions for smoking cessation (Cochrane Review). In: The
•
Serra C, Cabezas C, Bonfill X, Pladevall – Vila M. Interventions for preventing tobacco smoking in
public places (Cochrane Review). In: The Cochrane Library, Issue 1, 2001. Oxford: Update
Software.
•
Silagy C. Physician advice for smoking cessation (Cochrane Review). In: The Cochrane Library,
Issue 1, 2001. Oxford: Update Software.
•
Silagy C, Mant D, Fowler G, Lancaster T. Nicotine replacement therapy for smoking cessation
•
Sowden A, Arblaster L. Community interventions for preventing smoking in young people
•
Sowden AJ, Arblaster L. Mass media interventions for preventing smoking in young people
•
Stead LF, Hughes JR. Lobeline for smoking cessation (Cochrane Review). In: The Cochrane
Library, Issue 1, 2001. Oxford: Update Software.
•
Stead LF, Lancaster T. Interventions for preventing tobacco sales to minors (Cochrane Review).
In: The Cochrane Library, Issue 1, 2001. Oxford: Update Software.
•
Stead LF, Lancaster T. Group behaviour therapy programmes for smoking cessation (Cochrane
•
Ussher MH, West R, Taylor AH, McEwen A. Exercise interventions for smoking cessation
•
White AR, Rampes H, Ernst E. Acupuncture for smoking cessation (Cochrane Review). In: The
•
Stead LF, Lancaster T. Telephone counselling for smoking cessation (Cochrane Review). In: The
•
Rigotti NA, Munafo MR, Murphy MFG, Stead LF. Interventions for smoking cessation in
hospitalised patients (Cochrane Review). In: The Cochrane Library, Issue 2, 2001. Oxford: Update
Software.
•
Critchley J, Capewell S. Smoking cessation for the secondary prevention of coronary heart
disease (Protocol for a Cochrane Review). In: The Cochrane Library, Issue 2, 2001. Oxford:
Update Software.
•
van der Meer RM, Wagena EJ, Ostelo RWJG, Jacobs JE, van Schayck CP. Smoking cessation
for patients with chronic obstructive pulmonary disease (Protocol for a Cochrane Review). In: The
11
•
David S, Lancaster T, Stead LF. Narcotic antagonists for smoking cessation (Protocol for a
Cochrane Review). In: The Cochrane Library, Issue 2, 2001. Oxford: Update Software.
REVISTAS
•
Evidence-Based Medicine 2000-2001
•
ACP Journal Club 2000-2001
•
Evidence-Based Cardiovascular Diseases 2000-2001
•
Evidence-Based Practice 2000-2001
•
Evidence-Based Healthcare 2000-2001
•
Evidence-Based Obstetrics and Gynecology 2000-2001
•
Evidence-Based Oncology 2000-2001
•
Bandolier 2000-2001
LIVROS
•
Sackett DL, Haynes RB, Guyatt GH, Tugwell P. Clinical Epidemiology. 2 ed. Boston:
Little, Brown and Company, 1991.
•
Evidence Based Cardiology. 1st ed. London: BMJ, 1998.
•
Sackett DL, Straus SE, Richardson WS, Rosenberg W, Haynes RB. Evidence-Based
Medicine. How to practice and teach EBM. 2nd ed. Edinburgh: Churchill Livingstone,
2000.
•
Clinical Evidence 5. 5th ed. London: BMJ Publishing Group, 2001.
•
Making use of guidelines in clinical practice. 1st ed. Oxon: Radcliffe Medical Press,
1999.
•
Implementing clinical guidelines. 1st ed. Oxon: Radcliffe Medical Press, 1999.
CDROMs
•
Cochrane Library 2001-2. Update Software
•
Best Evidence 5
•
UpToDate 9.2, 2001
INTERNET
Site da WWW
URL
•
Agency for Research and Health
Quality (ARHQ), USA
http://www.ahrq.gov
•
Canadian Medical Association
Clinical Practice Guidelines
Infobase, Canada
http://www.cma.ca/cpgs
•
Scottish Intercollegiate Guidelines
Network, UK
http://www.rcpe.ac.uk/sign.html
12
•
National Guideline Clearinghouse,
USA
http://www.guideline.gov/index.asp
•
NHS Centre for Reviews and
Dissemination, UK
http://www.york.ac.uk
•
New Zealand Guidelines Group, New http://www.nzgg.org.nz
Zealand
•
St. George’s Hospital Medical
School Health Care Evaluation Unit,
UK
http://www.sghms.ac.uk
•
National Health and Medical
Research Council, Australia
http://www.ausinfo.gov.au
•
University of Alberta Guidelines
Appraisal Project, Canada
http://www.infoward.ualberta.ca/cpg
•
Netting the Evidence, UK
http://www.shef.ac.uk/uni/academic/RZ/scharr/ir/netting.html
•
Centre for Evidence-Based Medicine http://cebm.jr2.ox.ac.uk
at Oxford, UK
•
Filtros MBE para pesquisa
http://www.mssm.edu/library/ebm/ebmhedges.htm
•
Health Information Research Unit
McMaster, Canada
http://www.hiru.mcmaster.ca
•
ACP Journal Club
http://www.journalclub.org
•
UptoDate
http://www.uptodateinc.com/html/ordernow.htm
•
Inforetriever
http://www.infopoems.com
•
Medline
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
METODOLOGIA DE AVALIAÇÃO CRITICA DA EVIDÊNCIA
CIENTÍFICA
A evidência científica em que se baseia esta NOC é proveniente de fontes de evidência
científica secundária. Como já foi dito, estas são as que, tendo seleccionado os artigos,
ensaios e estudos nas bases de dados primárias (Medline, EMBASE, CINAHL, por exemplo),
fazem sobre eles uma avaliação crítica baseada na sua estrutura metodológica, seleccionando
apenas aquelas que, pela sua validade, importância e relevância para a prática clínica,
constituem a evidência considerada a mais válida.
Deste modo, e no que concerne esta NOC, a avaliação crítica da evidência científica dos
artigos originais – executada com base nos critérios da Medicina Baseada na Evidência – foi
realizada previamente pelos autores responsáveis pelas fontes secundárias. A evidência assim
produzida foi compilada, sintetizada e apresentada nos formatos acima descritos (publicações,
meios informáticos) e é sobre estes que esta NOC está construída.
13
ESQUEMA DA HIERARQUIZAÇÃO DA EVIDÊNCIA CIENTÍFICA
Quais são os critérios para a classificação da evidência científica em graus e que princípios
metodológicos lhe estão subjacentes?
A resposta encontra-se na operacionalização dos objectivos de conseguir definir a evidência
que seja a mais correcta (cientificamente falando) e que sirva de base ao médico, no sentido
de maximizar os aspectos positivos e minimizar os negativos das interacções clínicas com os
doentes (1-2).
Este desiderato consegue-se, por exemplo no caso de um esquema de tratamento, através da
convicção (que não pode ser provada inequivocamente) de que uma revisão sistematizada1
demonstrando homogeneidade dos resultados de RCTs (randomized clinical trials – ensaios
aleatorizados e controlados) de alta qualidade - que possuem aleatorização ocultada, duplaocultação na colheita e análise dos dados, follow-up exaustivo dos sujeitos de estudo e com
análise de intenção-de-tratar - fornece a evidência com o menor grau de viés na determinação
do efeito de uma intervenção terapêutica (3-4). A este tipo de evidência atribui-se o nível 1 e as
recomendações nele baseadas designam-se por grau A.
Quando a evidência existente é de menor qualidade - revisões sistematizadas com elevada
heterogeneidade, RCTs individuais com variável qualidade metodológica, estudos de coorte,
casos-controle ou opinião de peritos (designada por graus 2,3,4 e 5) - a graduação das
recomendações reflecte esse facto, sendo estas classificadas decrescentemente em niveis B, C
e D - o nível A é mais sólido que o nível B, o nível C que o D.
Este tipo de abordagem não é exclusivo da evidência terapêutica, já que pode também ser
utilizada na determinação dos níveis de evidência e graus de recomendação de manobras
preventivas e de etiologia ou iatrogenia (5).
1. Guyatt GH, Sackett DL, Sinclair JC, Hayward RSA, Cook DJ, Cook RJ et al. Users' guides to the
medical literature. IX. A method for grading health care recommendations. JAMA 1995; 274:18001804.
2. Guyatt GH, Cook DJ, Sackett DL, Eckman M, Pauker S. Grades of recommendation for
antithrombotic agents. Chest 1998; 114:441S-444S.
3. Guyatt GH, Sackett DL, Cook DJ, The Evidence-Based Medicine Working Group. Users' guides to
the medical literature. II. How to use an article about therapy or prevention. A. Are the results of
the study valid? JAMA 1993; 270:2598-2601.
4. Guyatt GH, Sackett DL, Cook DJ, The Evidence-Based Medicine Working Group. Users' guides to
the medical literature. II. How to use an article about therapy or prevention. B. What were the
results and will they help me in caring for my patients? JAMA 1994; 271:59-63.
5. Levine M, Walter S, Lee H, Haines T, Holbrook PR, Moyer VA et al. Users' guides to the medical
literature. IV. How to use an article about harm. JAMA 1994; 271:1615-1619.
1
Uma revisão sistematizada é uma revisão bibliográfica e científica sobre um determinado tema, executada de
tal maneira que os viéses se encontram reduzidos ao máximo. A característica fundamental de uma revisão
sistematizada é a explicitação clara e não ambígua dos critérios utilizados para a selecção, avaliação crítica e
inclusão da evidência científica naquela. Deste modo, uma revisão sistematizada apresenta objectivos formais e
precisos e os critérios de inclusão (e exclusão) dos estudos são explicitados detalhadamente. A revisão
sistematizada não apresenta, habitualmente, nenhuma representação gráfica determinada.
14
QUADRO A - Níveis de evidência e graus de recomendação terapêutica
Grau de
recomendação
Nível de
evidência
Análise metodológica
1a
RS* (com homogeneidade† interna) de EACs§
1b
EAC individuais (com IC# curtos)
1c
todos ou nenhuns¶
2a
RS* (com homogeneidade† interna) de estudos de coorte
2b
estudos de coorte individuais (incluindo EACs§ de baixa qualidade,
por ex. <80% de follow-up)
2c
investigação sobre resultados (“outcomes research”) §§
3a
RS* (com homogeneidade† interna) de estudos caso-controlo
3b
estudos caso-controlo individuais
C
4
estudos de séries de casos (e também estudos coorte e caso-controlo
de baixa qualidade**)
D
5
opinião de peritos sem explicitação prévia da metodologia de
avaliação crítica da evidência, ou baseada em investigação básica
(extrapolação), ou em “princípios primários” ††
A
B
Notas no final dos quadros
QUADRO B - Níveis de evidência e graus de recomendação sobre diagnóstico
Grau de
recomendação
A
Nível de
evidência
1a
RS* (com homogeneidade† interna) de estudos diagnósticos nível 1;
ou uma RPC∆ testada numa amostra de validação apropriada
1b
comparação independente e ocultada de uma gama de doentes
consecutivos, todos sujeitos ao teste em estudo assim como ao teste
comparativo considerado gold-standard
1c
SpPins e SnNouts absolutosΨ
2a
RS* (com homogeneidade† interna) de estudos diagnósticos ≥ nível
2
qualquer um dos seguintes:
2b
B
•
comparação independente ocultada e objectiva
•
estudo realizado numa gama de doentes ou não consecutivos ou
muito restrita (ou ambos) todos sujeitos ao teste em estudo assim
como ao teste comparativo considerado gold-standard
•
ou uma RPC∆ não-testada numa amostra de validação
apropriada
2c
3a
3b
comparação independente ocultada e objectiva de uma gama
apropriada de doentes, mas em que nem todos foram sujeitos ao teste
comparativo considerado gold-standard
15
qualquer um dos seguintes:
C
4
D
5
•
o teste comparativo considerado gold-standard não é objectivo,
mesmo que o estudo seja ocultado
•
independente
•
os testes positivos e negativos foram analisados por padrões
referenciais não idênticos
•
o estudo foi efectuado numa gama inapropriada de doentesΦ
(extrapolação), ou em “princípios primários”) ††
QUADRO C - Níveis de evidência e graus de recomendação sobre prognóstico
Grau de
recomendação
A
B
Nível de
evidência
1a
RS* (com homogeneidade† interna) de estudos com populações
iniciais bem definidas (inception cohort); ou uma RPC∆ testada
numa amostra de validação apropriada
1b
estudos de coorte em populações iniciais bem definidas (inception
cohort) com follow-up > 80% dos doentes
1c
todos ou nenhuns estudos de série de casos (case-series)
2a
RS* (com homogeneidade† interna) de estudos de coorte
retrospectivos ou grupos de controlo de RCTs não tratados
2b
estudos de coorte retrospectivos ou follow-up de doentes de grupos
de controlo de RCTs não tratados; ou uma RPC∆ não-testada numa
amostra de validação apropriada
2c
investigação sobre resultados (“outcomes research”) §§
3a
3b
C
4
estudos de séries de casos (case-series) (e também estudos de coorte
prognósticos de baixa qualidadeΘ)
D
5
(extrapolação), ou em “princípios primários”) ††
NOTAS REFERENTES AOS QUADROS
*RS: revisões sistematizadas
§
EACs: ensaios aleatorizados e controlados (RCTs: randomized controled trials)
†
Homogeneidade: é uma RS com um baixo grau de heterogeneidade na direcção e magnitude dos resultados dos
estudos individuais nela incluídos
∆
RPC: regra de predição clínica
#
IC: intervalos de confiança
¶
quando todos os doentes faleciam antes do tratamento estar disponível, mas alguns agora sobrevivem; ou
quando alguns doentes faleciam antes do tratamento estar disponível, mas nenhum agora morre quando o faz
**os estudos de coorte de baixa qualidade são os que não definiram claramente os grupos em comparação; e/ou
não mediram as exposições e resultados (outcomes) de maneira objectiva (de preferência em ocultação) em
ambos os grupos (expostos e não-expostos); e/ou não identificaram ou controlaram apropriadamente os
factores de confusão (confounders); e/ou não levaram a cabo um seguimento (follow-up) suficientemente
longo e completo. Os estudos casos-controle de baixa qualidade são aqueles que não definiram claramente os
grupos em comparação; e/ou não mediram as exposições e resultados (outcomes) de maneira objectiva (de
16
preferência em ocultação) em ambos os grupos (casos e controlos); e/ou não identificaram ou controlaram
apropriadamente os factores de confusão (confounders).
§§
a investigação sobre resultados (“outcomes research”) consiste – segundo a definição americana dos PORT –
nos estudos de coorte de doentes com idêntico diagnóstico (AVC, EAM, etc.) que relacionam os seus
resultados clínicos (clinical outcomes), sejam eles a mortalidade, morbilidade, eventos, etc., com os cuidados
médicos recebidos (aspirina, cirurgia, reabilitação); este tipo de investigação não utiliza EACs pelo que se
torna impossível a atribuição de efectividade a uma determinada manobra terapêutica. A vantagem desta
abordagem é que no permite reconhecer se os outcomes esperados correspondem aos encontrados na clínica
diária.
††
por princípios primários entendem-se os conceitos fisiopatológicos que presidem à prática médica (controle da
tensão arterial em doentes com dissecção da aorta, por exemplo); como é óbvio, estes princípios, se não
testados em estudos rigorosos, podem conduzir por vezes a práticas a práticas erradas
APOIANTES E SUBSCRITORES
•
•
•
•
•
Instituto da Qualidade em Saúde
Associação Portuguesa dos Médicos de Clínica Geral
-
ESTRATÉGIA DE IMPLEMENTAÇÃO
A estratégia de implementação desta NOC deve ser determinada pelo(s) organismo (s) que a
deseje utilizar.
RECOMENDAÇÕES PRINCIPAIS
AVALIAÇÃO DO USO DE TABACO
O primeiro passo no tratamento de uso e dependência de tabaco é identificar os seus
utilizadores.
Um grande número de utilizadores de tabaco consultam um médico pelo menos uma vês por
ano, colocando os clínicos numa posição privilegiada para intervir nesta situação.
A identificação efectiva do uso de tabaco não só abre as portas a intervenções com potencial
êxito, mas também orienta os médicos na escolha das acções apropriadas.
São quatro o número de respostas que se podem obter no rastreio do uso de tabaco:
• o doente usa tabaco e deseja fazer uma tentativa de abandono
• o doente usa tabaco, mas não deseja fazer para já uma tentativa de abandono
• o doente já usou tabaco, mas deixou de usar
• o doente nunca usou regularmente tabaco.
Esta NOC fornece respostas simples mas efectivas para todas estas situações (Fig. 1 e Quadro
1).
17
Quadro 1 - Estratégias breves para ajudar o doente que deseja abandonar o uso de tabaco –
Estratégia dos “5 As”
Acção
Implementar um sistema que assegure que,
para cada doente em cada consulta, o uso de
tabaco seja investigado e documentado
De uma maneira clara, persuasiva, forte e
personalizada, encorajar todos os
utilizadores de tabaco a abandonar
Interrogar cada utilizador de tabaco sobre se
está disposto a fazer uma tentativa de
abandono de imediato (ex.: dentro dos 30
dias seguintes)
Elaborar em conjunto com o doente um
plano de abandono do uso do tabaco
Fornecer aconselhamento prático
(ver Quadro 2)
Estratégias para implementação
Passo 1: Abordar – identificar sistematicamente todos os
utilizadores de tabaco em cada consulta
Expandir os sinais vitais para incluir uso de tabaco ou usar um
sistema de identificação universal alternativo.
SINAIS VITAIS
TA: ________ Pulso: ________ Peso: ________
Temperatura:________Frequência Respiratória: ________
Uso de tabaco: Actual Anterior
Nunca
(assinale um)
Passo 2: Aconselhar – incentivar com convicção todos os
utilizadores de tabaco a abandonar.
O aconselhamento deve ser:
• Claro – “Penso que é importante que abandone já e posso ajudálo. Reduzir apenas enquanto está doente não é suficiente”
• Forte – “Como seu médico quero que saiba que deixar de fumar
é a coisa mais importante que pode fazer para proteger a sua
saúde agora e no futuro. Estarei disponível para o ajudar”
• Personalizado – Associar o uso do tabaco à doença actual, e/ou
aos seus custos sociais e económicos, nível de
motivação/disponibilidade para deixar e/ou ao impacto do uso
de tabaco sobre crianças e outros membros do agregado
familiar
Passo 3: Avaliar – determinar se o doente deseja fazer uma
tentativa de abandono.
Avaliar a vontade do doente abandonar:
• Se o doente deseja fazer uma tentativa de abandono de imediato,
prestar assistência
• Se o doente deseja participar num tratamento intensivo, fornecer
o tratamento ou referenciar o doente para intervenção intensiva
• Se o doente claramente afirma que para já não deseja fazer uma
tentativa de abandono, fornecer uma intervenção motivacional
• Se o doente é membro duma população especial (adolescente,
mulher grávida, minoria racial/étnica), considerar fornecer
informação adicional
Passo 4 – Ajudar – ajudar o doente na sua tentativa de abandono.
Preparação do doente para a tentativa de abandono:
• Marcar uma data: idealmente a data de abandono deve ser
dentro de 2 semanas.
• Informar a família, amigos e colaboradores sobre a tentativa de
abandono, e pedir compreensão e apoio.
• Antecipar dificuldades que podem surgir durante a tentativa de
abandono, particularmente durante as semanas iniciais, mais
críticas. Entre elas, sintomas de abstinência de nicotina.
• Remover produtos de tabaco do ambiente antes de iniciar,
evitar fumar em lugares onde passa muito tempo (trabalho,
casa, carro).
Abstinência – a abstinência total é essencial
Experiência de tentativas de abandono anteriores – identificar
o que é que ajudou e o que é que correu mal em tentativas de
abandono prévias
Antecipar problemas ou dificuldades na tentativa de abandono
a iniciar – discutir problemas e dificuldades e como o doente
as vai vencer com êxito.
Alcool – o doente deve considerar limitar ou abster-se de
alcool, visto que o alcool pode causar recidiva.
Outros fumadores em casa – abandonar é mais difícil quando
há outros fumadores em casa. Os doentes devem encorajar as
18
Fornecer apoio social intra-tratamento (ver
Quadro 2)
Ajudar o doente a obter apoio social extratratamento (ver Quadro 2)
Recomendar o uso da farmacoterapia
aprovada, excepto em circunstâncias
especiais (ver Quadros 3 e 4)
Fornecer materiais suplementares
Programar consulta de seguimento,
pessoalmente ou via telefone
pessoas com quem vivem a abandonar com eles ou a não
fumar na sua presença .
Fornecer um ambiente clínico de apoio enquanto se encoraja o
doente na sua tentativa de abandono. “Estamos disponíveis para
vos ajudar”
Ajudar o doente a desenvolver suporte social para a sua tentativa
de abandono, no seu ambiente, fora do tratamento. “Peça à sua
família, amigos e colegas de trabalho para o/a ajudar na sua
tentativa de abandono”
Recomendar o uso de farmacoterapias efectivas. Explicar como é
que os medicamentos aumentam a probabilidade de sucesso e
reduzem os sintomas de abstinência. Os fármacos de 1ª linha
incluem: cloridrato de bupropiona de libertação retardada,
pastilhas mastigaveis de nicotina e adesivo transdérmico de
nicotina
Fontes:
Tipo: apropriadas para o doente, relativamente à sua cultura,
raça, educação e idade
Localização: prontamente acessíveis em cada local de consulta
médica
Passo 5: Acompanhar – agendar consulta de seguimento
Data – A consulta de seguimento deve ocorrer pouco depois da
data de abandono, de preferência durante a 1ª semana. Uma
segunda consulta de seguimento é recomendada dentro do 1º
mês. Programar consultas adicionais conforme indicado.
Acções durante a consulta de seguimento – Congratular
sucesso; se ocorreu uso de tabaco, rever as circunstâncias e
incentivar recompromisso com abstinência total; lembrar ao
doente que um lapso pode ser usado como uma experiência
de aprendizagem; identificar problemas já encontrados e
antecipar dificuldades no futuro imediato; avaliar uso e
problemas da farmacoterapia; considerar uso ou referência a
tratamento mais intensivo
INTERVENÇÕES CLÍNICAS BREVES
Esta secção da NOC apresenta estratégias específicas relativas a intervenções breves.
Estas intervenções breves podem ser postas em prática por qualquer clínico, mas são
particularmente importantes para os médicos de cuidados primários que vêm uma larga
variedade de doentes e têm fortes restrições de tempo na consulta.
Os objectivos das intervenções breves são claros: mudar a cultura clínica e os padrões de
prática, de modo a que cada doente que usa tabaco seja identificado e lhe seja oferecido
tratamento.
Há um tema central a estas estratégias: é essencial fornecer pelo menos uma intervenção
breve a todos os utilizadores de tabaco em cada visita clínica.
Embora muitos utilizadores de tabaco mostrem relutância em procurar programas de cessação
intensivos, nada deve impedir que recebam uma intervenção breve de cada vez que visitam
um médico. Além disso, estas intervenções devem ser usadas com todas as populações,
incluindo adolescentes, mulheres grávidas, idosos e minorias raciais e étnicas.
19
Apesar de não ser o objectivo desta NOC, é importante referir que para assegurar que todos os
doentes que usam tabaco sejam identificados para intervenção, são necessárias alterações
institucionais na prática clínica.
Este capítulo divide-se em 3 secções, cada uma com recomendações sobre intervenções
clínicas breves dirigidas a três tipos de doentes:
A. utilizadores de tabaco que desejam fazer de imediato uma tentativa de abandono
B. utilizadores de tabaco que não desejam fazer para já uma tentativa de abandono
C. ex-utilizadores recentes de tabaco
A – UTILIZADORES DE TABACO QUE QUEREM ABANDONAR DE IMEDIATO
Os médicos de Cuidados Primários observam todos os anos um grande número de utilizadores
de tabaco e por isso devem estar preparados para intervir em relação a estes doentes.
Os cinco passos principais de intervenção nos Cuidados Primários são (Quadro 1):
1.
2.
3.
4.
5.
Abordar o doente sobre se usa ou não tabaco
Aconselhar o doente a deixar de usar
Avaliar a vontade de fazer uma tentativa de abandono
Ajudar os que querem fazer uma tentativa de abandono
Acompanhar através de consultas de seguimento para prevenir recidivas
Estas estratégias foram concebidas para ser breves, necessitando de poucos minutos de tempo
directo do médico.
A cada doente que deseja fazer uma tentativa de abandono, deve ser fornecido tanto o
aconselhamento como o tratamento farmacológico.
Os três componentes do aconselhamento que são recomendados estão descritos no Quadro 2.
Quadro 2 -Elementos comuns de aconselhamento efectivo e terapeuticas comportamentais para cessação
de uso de tabaco
Componente
Exemplos
Aconselhamento Prático sobre o Tratamento
Afecto negativo
Identificar acontecimentos, estados de
Estar perto de outros fumadores
Ingerir alcool
espírito ou actividades que aumentam o
Sentir desejos de fumar
risco de fumar ou recair
Estar debaixo de pressão de tempo
Aprender a prever e evitar a tentação
Aprender estratégias cognitivas que reduzam os humores
Identificar e treinar aptidões de resolução de negativos
problemas. Tipicamente, estas aptidões
Introduzir alterações do estilo de vida que reduzam o stress,
destinam-se a defrontar situações críticas
melhorem a qualidade de vida ou produzam prazer
Aprender actividades cognitivas e comportamentais para
defrontar os desejos de fumar
Salientar o facto de que qualquer contacto com tabaco (mesmo
uma simples inalação) aumenta a probabilidade de recidiva
Fornecer informação básica acerca do
completa
tabagismo e das técnicas de abandono
A abstinência tipicamente atinge a máxima intensidade 1 a 3
semanas após o abandono
20
Os sintomas de abstinência incluem humor negativo, desejos de
fumar e dificuldade de concentração
Mencionar a natureza adictiva do hábito de fumar
Intervenções de suporte intra-tratamento
Referir que estão agora disponíveis tratamentos efectivos da
dependência do tabaco
Referir que actualmente metade das pessoas que alguma vez
Encorajar o doente na tentativa do abandono
fumaram, deixaram de o fazer
Comunicar confiança na capacidade do doente conseguir
abandonar
Perguntar como é que o doente se sente acerca da tentativa de
abandono
Exprimir directamente preocupação e vontade de ajudar
Comunicar cuidado e preocupação
Estar aberto à expressão pelo doente de receios relacionados com
o abandono, dificuldades experimentadas e sentimentos
ambivalentes
Interrogar sobre:
• razões que levam o doente a querer abandonar
Encorajar o doente a falar acerca do
• preocupações ou temores acerca do abandono
processo de abandono
• êxitos que o doente tenha conseguido
• dificuldades encontradas durante o processo de abandono
Intervenções de suporte extra-tratamento
Mostrar videos que exemplifiquem maneiras de obter apoio
Praticar modalidades de procura de apoio da família, amigos e
Treinar o doente para solicitar apoio
colaboradores
Ajudar o doente a criar uma casa livre de fumo
Ajudar o doente a identificar pessoas capazes de o apoiar
Telefonar ao doente para o incentivar a procurar apoio
Incentivar a solicitação de apoio
Informar o doente sobre recursos da comunidade (linhas de apoio
telefónico)
Enviar cartas para pessoas susceptíveis de apoiar
Telefonar a pessoas susceptíveis de apoiar
Arranjar apoio exterior
Convidar outros para sessões de cessação
Nomear doentes para serem “companheiros” uns para os outros
A terapêutica farmacológica deve ser oferecida a todos os doentes, excepto certos grupos que
requerem consideração especial (doentes com contra indicações médicas, os que fumam
menos de 10 cigarros por dia, mulheres grávidas e fumadores adolescentes).
O Quadro 3 descreve as recomendações gerais de terapêutica farmacológica e o Quadro 4
fornece instruções de prescrição sobre medicações específicas.
Quadro 3 - Normas de orientação clínica geral para prescrição de terapêutica farmacológica para
abandono do hábito de fumar
Quem deve receber terapêutica
farmacológica para abandonar o hábito de
fumar?
Quais são as terapêuticas farmacológicas de
1ª linha?
Que factores se devem considerar na
selecção das terapêutica farmacológicas de
1ª linha?
Todos os doentes em processo de abandono, excepto na presença
de circunstâncias especiais.
Deve ser dada consideração especial a populações seleccionadas:
os que têm contraindicações médicas, os que fumam menos de 10
cigarros/dia, mulheres grávidas e a amamentar e fumadores
adolescentes.
Cloridrato de bupropiona de libertação retardada e terapêuticas de
substituição de nicotina (pastilhas mastigáveis e adesivo
transdérmico).
Devido à inexistência de dados suficientes para escalonar estes
fármacos, a escolha de uma terapêutica farmacológica de 1ª linha
específica deve ser guiada por factores tais como:
• a familiaridade do clínico com os fármacos
21
•
•
•
Os tratamentos farmacológicos são
apropriados para fumadores ligeiros (ex.:
10-15 cigarros/dia)?
Quais são as terapêuticas farmacológicas de
2ª linha recomendadas?
Quando é que se devem usar agentes de 2ª
linha para tratar dependência do tabaco?
Quais as terapêuticas farmacológicas para
doentes particularmente preocupados com
aumento de peso?
Há terapêuticas farmacológicas que devam
ser especialmente consideradas em doentes
com história de depressão?
As terapêuticas de substituição de nicotina
devem ser evitadas em doentes com história
de doença cardiovascular?
As terapêuticas farmacológicas de
dependência do tabaco podem ser usadas a
longo prazo (6 meses ou mais?)
As terapêuticas farmacológicas podem ser
combinadas?
Quais as doses mais adequadas para as
terapêuticas de substituição de nicotina?
contraindicações para doentes seleccionados
preferência do doente
experiência prévia do doente com um fármaco específico
(positiva ou negativa)
• características do doente (ex.: história de depressão,
preocupações acerca do aumento de peso).
No caso de se decidir usar terapêutica farmacológica em
fumadores ligeiros, deve-se considerar reduzir a dose das
terapêuticas de substituição de nicotina de 1ª linha.
Não são necessários ajustamentos quando se usa cloridrato de
bupropiona de libertação retardada.
Cloridrato de clonidina e cloridrato de nortriptilina
Em doentes que não podem usar fármacos de 1ª linha, devido a
contraindicações, ou em doentes em que os fármacos de 1ª linha
não são úteis.
Os doentes devem ser monitorizados relativamente aos efeitos
adversos conhecidos dos agentes de 2ª linha.
Cloridrato de bupropiona de libertação retardada e terapêuticas de
substituição da nicotina, em particular pastilhas mastigáveis de
nicotina (que atrasam mas não impedem o aumento de peso)
Cloridrato de bupropiona de libertação retardada e cloridrato de
nortriptilina
Não: o adesivo transdérmico de nicotina, em particular, é seguro e
não causa efeitos cardiovasculares adversos. No entanto, a
segurança destes produtos para o período pós-enfarte agudo do
miocárdio imediato ou em doentes com angina grave ou instável
ainda não foi estabelecida.
Sim: esta aproximação pode ser útil com fumadores que
apresentem sintomas persistentes de abstinência durante o curso
da terapêutica farmacológica, ou que desejem terapêutica a longo
prazo. Uma minoria de doentes que deixam efectivamente de
fumar, usam fármacos de substituição de nicotina livremente a
longo prazo. No entanto, foi provado que 8 semanas de
terapêutica com o adesivo transdérmico de nicotina é tão eficaz
como regimes mais longos. O uso a longo prazo destas
medicações não apresenta um risco conhecido para a saúde. O
FDA aprovou o uso de cloridrato de bupropiona para manutenção
a longo prazo.
Sim: existe evidência de que combinar o adesivo transdérmico de
nicotina com pastilha mastigável de nicotina aumenta as taxas de
abstinência em relação ao uso de cada um destes fármacos
individualmente
No caso de pastilha mastigável pode ser usada em regime de dose
fixa ou numa base de dose livre.
Os fumadores altamente dependentes ou os que falharam com
2mg de pastilha mastigável, devem usar 4mg de pastilha
mastigável .
Não está provado que o uso de adesivo transdérmico de nicotina
em doses mais altas do que 22mg/24h seja mais eficaz em
conseguir abstinência a longo prazo.
Não está provado que redução gradual da terapêutica seja melhor
do que supressão abrupta.
22
QUADRO 4: Sugestões para o uso clínico de farmacoterapia para cessação do hábito de fumar
Fármaco
Apresentação
(preço
relativo por
unidade de
dosagem)
Cloridrato de
Bupropiona
(Zyban)
Comprimidos
de 150 mg (44
€)
Embalagem de
60
comprimidos
Nicotina pastilhas
mastigáveis
(Nicorette)
Dosagens: 2 e
4 mg (7€ e 12
€)
Embalagens de
30 e 105 p.
mastigáveis
Nicotina –
Sistema
terapêutico
transdérmico
(Nicotinell
TTS)
Dosagens: 10
cm2, 20 cm2 e
30 cm2
(0,7
mg/cm2/24h)
(66 €, 81€ e
87€)
Embalagens de
14 e 28
sistemas
Cloridrato de
Clonidina
(Catapresan)
Comprimidos
de 150 µg (1€)
Embalagens de
20 e 60
comprimidos
Dosagens: 25 e
50 mg (2 e 3
€)
Cloridrato de
Nortriptilina
(Norterol)
Precauções/
/Contraindicações
Efeitos
adversos
1ª LINHA
Convulsões
Contraindicações
absolutas: antecedentes Febre
Insónia
de convulsões, bulimia
Boca seca
ou anorexia nervosa,
Alterações
doença bipolar, tumor
do paladar
do SNC, cirrose
Rash
hepática grave,
supressão abrupta de
alcool ou
benzodiazepinas.
Contraindicações
relativas: alcoolismo,
diabetes tratada com
antidiabéticos orais ou
insulina, história de
traumatismo craneano,
uso de estimulantes ou
anorécticos ou fármacos
que reduzam o limiar de
convulsões*.
Interacções
medicamentosas:
fármacos que reduzem
o limiar de convulsões e
outrosФ.
Dores na
boca
Dispepsia
Reacção
cutânea
local
Insónia
2ª LINHA
Hipertensão “rebound”
Boca seca
Sonolência
Tonturas
Sedação
Risco de arritmias
Sedação
Boca seca
23
Dosagem
Duração
150 mg/dia, de
manhã, durante
6 dias; em
seguida, 150 mg
2 vezes /dia
7 a 12 semanas;
manutenção até
6 meses
(começar 1 a 2
semanas preinterrupção)
1-24
cigarros/dia: até
24 past. de 2
mg/dia
≥25
cigarros/dia: até
24 past. de 4
mg/dia
21 mg / 24 h
14 mg / 24 h
7 mg / 24 h
Até 12 semanas
0,15 – 0,75 mg/
dia
3 – 10 semanas
75 – 100 mg /
dia
12 semanas
4 semanas +
2 semanas +
2 semanas
ou
8 semanas
Embalagens de
20 e 50 comp.
de 25 mg;
Embalagem de
50 comp. de
50 mg
* Estes fármacos incluem: antipsicóticos, antidepressivos, antimaláricos, teofilina, corticosteroides sistémicos,
tramadol, quinolonas e anti-histamínicos sedativos.
Φ Estes fármacos incluem: β-bloqueantes, anti-arrítmicos tipo 1 c, captopril, loratadina, codeína, cimetidina,
valproato de sódio, orfenadrina, ciclofosfamida, levodopa e inibidores da monoaminooxidase.
B – UTILIZADORES DE TABACO QUE NÃO DESEJAM FAZER UMA
TENTATIVA DE ABANDONO
Para os doentes que não estão dispostos a fazer para já uma tentativa de abandono, deve ser
usada uma intervenção breve, concebida para promover a motivação para abandonar.
Podem ser diversas as razões para os doentes não quererem fazer uma tentativa de abandono:
falta de informação acerca dos efeitos nocivos do tabaco, receios acerca das consequências da
abstinência, falta de meios económicos ou ainda desmoralização por recidivas prévias.
Estes doentes podem responder a uma intervenção motivacional, delineada para educar,
reassegurar e motivar. Os componentes de uma intervenção deste tipo são descritos no
Quadro 5.
Quadro 5 - Aumentar a motivação para abandonar o uso de tabaco – Estratégia dos “5 Rs”
Relevância
Riscos
Recompensas
Encorajar o doente a descrever em que medida é que o abandono é pessoalmente
relevante, procurando ser tão específico quanto possível.
Informação motivacional tem o maior impacto se é relevante para o estado de
doença ou factores de risco do doente, situação familiar ou social (ex: existência
de crianças em casa), preocupação de saúde, idade, sexo e outras características
importantes do doente (ex.: experiência prévia de abandono, barreiras pessoais à
cessação).
O clínico deve pedir ao doente para identificar consequências negativas potenciais
do uso do tabaco. O clínico pode sugerir e esclarecer aquelas que parecem mais
relevantes para o doente. Deve salientar que fumar cigarros pobres em alcatrão ou
nicotina ou usar outras formas de tabaco (ex.: tabaco sem fumo, cigarrilhas,
cachimbo) não eliminam estes riscos.
Alguns exemplos de riscos:
Riscos agudos: dispneia, exacerbação de asma, prejuízo para a gravidez,
impotência, infertilidade, aumento dos níveis de monóxido de carbono do soro.
Riscos a longo prazo: enfarte do miocárdio, AVC, neoplasias do pulmão, outras
neoplasias (laringe, cavidade oral, faringe, esófago, pancreas, bexiga, cervix),
doenças pulmonares crónicas obstrutivas (bronquite crónica e enfisema),
incapacidade a longo prazo e necessidade de cuidado continuado.
Riscos ambienciais: risco mais elevado de neoplasia do pulmão e doença cardíaca
no cônjuge; taxas mais altas de fumadores em filhos de utilizadores do tabaco;
maior risco de baixo peso ao nascer, síndrome de morte súbita infantil, asma,
doença do ouvido médio, e infecções respiratórias, nos filhos de fumadores
O clínico deve pedir ao doente para identificar benefícios potenciais de suspender
o uso de tabaco, podendo sugerir e esclarecer aqueles que parecem mais
relevantes para o doente.
Exemplos de benefícios: melhor saúde; os alimentos sabem melhor; sentido do
olfacto mais apurado; diminuição dos gastos; sentir-se melhor consigo próprio; a
casa, o carro, a roupa e a respiração têm melhor cheiro; deixa de se preocupar
24
Resistências
Repetição
com o abandono; dá um bom exemplo aos filhos; os filhos são mais saudáveis;
deixa de se preocupar em expor outros a fumo; sente-se melhor fisicamente;
melhor desempenho nas actividades físicas; retarda o envelhecimento da pele
O clínico deve pedir ao doente para identificar barreiras ou impedimentos ao
abandono e indicar formas de tratamento (resolução de problemas,
farmacoterapia) dirigidas para a sua resolução.
Exemplos de dificuldades típicas: sintomas de abstinência, medo de falhar,
aumento de peso, falta de apoio, depressão, ter prazer no tabaco.
A intervenção motivacional deve ser repetida de cada vez que um doente não
motivado vem a uma consulta. Os utilizadores de tabaco que falharam em
tentativas de abandono prévias devem ser informados de que muitas pessoas
fazem tentativas de abandono repetidas até conseguirem ter êxito.
C – EX-UTILIZADORES DE TABACO RECENTES
Por causa da natureza crónica recorrente da dependência do tabaco, todos os ex-utilizadores
de tabaco devem receber tratamento breve de prevenção de recidiva.
Quando um clínico encontra um doente nestas circunstâncias, deve apoiar a decisão tomada
pelo doente, relembrar os benefícios da abstinência e ajudar o doente a resolver quaisquer
problemas resultantes do abandono do uso de tabaco.
A maior parte das recidivas ocorre precocemente, embora também possam ocorrer meses ou
mesmo anos após a data do abandono. As intervenções para prevenção das recidivas são por
isso especialmente importantes na fase inicial do processo de abandono, e podem ser
fornecidas por meio de consultas programadas, contactos telefónicos, ou em qualquer altura
em que um clínico encontre um ex-utilizador de tabaco.
Estas intervenções podem ser divididas em duas categorias:
• Intervenção mínima para todos os ex-utilizadores
• intervenções prescriptivas para doentes com problemas em manter a abstinência (Quadro
6)
Quadro 6 - Componentes de estratégias breves para impedir recidiva do uso de tabaco
Prevenção de recidiva prática mínima
Estas intervenções devem fazer parte de
todos os encontros com um doente que
abandonou recentemente o uso de tabaco
Todos os ex-utilizadores de tabaco devem ser felicitados pelos
sucessos e fortemente encorajados a permanecer abstinentes.
Quando se encontra um ex-utilizador recente devem ser usadas
perguntas “open-ended” com o objectivo de promover a
resolução de problemas pelo doente (ex.: Em que é que a
suspensão do uso de tabaco foi benéfica para si?).
O clínico deve encorajar a discussão activa pelo doente dos
seguintes tópicos:
•
os benefícios, incluindo potenciais benefícios de saúde, que
o doente pode obter da cessação.
•
qualquer sucesso que o doente tenha tido no processo de
abandono (ex.: duração da abstinência, diminuição dos
sintomas de abstinência)
•
os problemas encontrados ou dificuldades previsíveis em
manter a abstinência (ex.: depressão, aumento de peso,
álcool, outros utilizadores de tabaco em casa)
Prevenção de recidiva prescriptiva
25
Os componentes de prevenção de recidiva prescriptiva são individualizados na base da informação obtida acerca
de problemas que o doente está a ter em manter a abstinência. Estas intervenções de prevenção de recidiva mais
intensivas podem ser postas em prática durante consulta de seguimento programada (pessoal ou via telefone).
Seguem-se alguns problemas específicos que os doentes podem referir e respostas possíveis.
Problemas
Falta de apoio para a cessação
Respostas
Programar consultas de seguimento ou contactos telefónicos com
o doente.
Ajudar o doente a identificar fontes de apoio dentro do seu
ambiente.
Referenciar o doente a uma organização apropriada que ofereça
aconselhamento de cessação, ou apoio.
Humor negativo ou depressão
Se significativo, prestar aconselhamento, prescrever medicações
apropriadas ou referenciar o doente a um especialista.
Sintomas de abstinência fortes ou
prolongados
Se o doente refere desejo prolongado ou outros sintomas de
abstinência, considerar prolongar o uso de uma farmacoterapia
aprovada ou adicionar/combinar fármacos para reduzir sintomas
de abstinência fortes.
Aumento de peso
Recomendar iniciar ou aumentar actividade física; desencorajar
dieta estrita.
Reassegurar o doente de que algum aumento de peso após o
abandono é comum e parece ser auto-limitado.
Salientar a importância de uma dieta saudável.
Manter o doente com uma farmacoterapia que atrase o aumento
de peso (ex.: cloridrato de bupropiona de libertação retardada e
terapêuticas de substituição de nicotina, particularmente pastilhas
mastigáveis de nicotina).
Referenciar o doente a um especialista ou programa
especializado
Motivação em queda/sentimento de perda
Reassegurar o doente que estes sentimentos são comuns.
Recomendar actividades compensadoras.
Investigar para ter a certeza de que o doente não está envolvido
em uso periódico de tabaco.
Salientar que começar a fumar aumenta o desejo e torna o
abandono mais difícil.
INTERVENÇÕES CLÍNICAS INTENSIVAS
O tratamento intensivo da dependência de tabaco pode ser fornecido por qualquer clínico
treinado e que disponha dos recursos necessários para intervenções intensivas.
Há evidência substancial de que o tratamento mais intensivo é mais efectivo do que o
tratamento breve, por isso as intervenções intensivas são apropriadas para qualquer utilizador
de tabaco que deseje participar nelas, e não devem ser limitadas a qualquer subpopulação de
utilizadores de tabaco (ex:fumadores pesadamente dependentes, por exemplo).
No Quadro 7 estão descritos os componentes de uma intervenção intensiva.
26
Quadro 7 - Componentes de uma intervenção intensiva para abandonar o hábito de fumar
Componente
Estratégia de implementação
Avaliação
A avaliação deve assegurar que os usadores do tabaco desejam fazer
uma tentativa de abandono usando um programa de tratamento
intensivo.
Outras avaliações podem fornecer informação útil para o
aconselhamento (ex.: nível de stress, presença de comorbilidade)
Profissionais do Programa
Múltiplos tipos de profissionais são efectivos e devem ser usados.
Uma estratégia de aconselhamento seria colocar um médico a fornecer
mensagens acerca de riscos e benefícios para a saúde e a prescrever
farmacoterapia, e profissionais não médicos a fornecer intervenções
adicionais psicosociais ou de comportamento.
Intensidade do Programa
Por causa de evidência de uma forte relação dose – resposta, o
programa deve consistir de 4 ou mais sessões, tendo a sessão mais
longa uma duração superior a 10 minutos, para um tempo total de
contacto superior a 30 minutos.
Formato do Programa
Pode ser usado aconselhamento individual ou de grupo.
O aconselhamento telefónico pró-activo é também efectivo.
O uso de material de auto-ajuda adjuvante é opcional.
Devem ser usados processos de intervenção em avaliação de
seguimento.
Tipos de aconselhamento e
terapêuticas de comportamento
Terapêuticas de aconselhamento e de comportamento devem incluir
aconselhamento prático (resolução de problemas/treino de
desempenhos) e suporte social intra e extratratamento.
Farmacoterapia
Todos os fumadores devem ser encorajados a usar as farmacoterapias
mencionadas nesta NOC, excepto na presença de circunstancias
especiais.
Em populações seleccionadas (ex.: mulheres grávidas, adolescentes), o
uso de farmacoterapia deve ser sujeito a considerações especiais (ver
Quadro 3).
O clínico deve explicar ao doente de que modo estes fármacos
aumentam a taxa de sucesso de abandono do hábito de fumar e
reduzem os sintomas de abstinência.
Os agentes de farmacoterapia de 1ª linha incluem cloridrato de
bupropiona de libertação retardada e terapêuticas de substituição de
nicotina (pastilhas mastigáveis e adesivo transdérmico).
População
Os programas de intervenção intensiva podem ser usados com todos os
utilizadores de tabaco que desejem participar neles.
As recomendações referidas resultaram duma revisão e análise da literatura existente sobre
cessação do tabagismo, em que foram usadas apenas fontes secundárias de evidência
científica.
Importa nesta altura definir clara e explicitamente, para cada recomendação indicada nesta
NOC, os níveis de evidência em que aquela se baseia, de acordo com o esquema de
hierarquização atrás referido (ver secção intitulada “ESQUEMA DA HIERARQUIZAÇÃO
DA EVIDÊNCIA CIENTÍFICA”). A gradação atribuída é variável, já que parte das
recomendações têm por base meta-análises de ensaios aleatorizados e controlados (RCTs) por
27
ex., mas noutras partes, devido à inexistência de RCTs ou ensaios controlados, houve
necessidade de se recorrer a outro tipo de evidência científica.
As principais recomendações e respectiva classificação estão divididas em cinco secções:
• rastreio e avaliação
• estrutura e intensidade do tratamento
• elementos de tratamento
• populações especiais
• tópicos especiais
RASTREIO E AVALIAÇÃO
•
•
•
•
todos os doentes devem ser interrogados sobre o uso de tabaco e a sua situação em relação
ao uso de tabaco deve ser documentada numa base regular; a evidência mostra que esta
acção aumenta significativamente a taxa de intervenção dos clínicos (Força de
Evidência: A)
a inclusão nos sistemas de rastreio clínico da obtenção de informação sobre o tabagismo,
ou o uso de outros sistemas de detecção, são essenciais para a avaliação consistente,
documentação e intervenção relativamente ao uso de tabaco (Força de Evidência: B)
uma vez identificado um utilizador de tabaco, o clínico deve aconselhá-lo a abandonar e
deve avaliar a sua vontade de o fazer de imediato (Força de Evidência: D)
o tratamento da dependência de tabaco é efectivo e deve ser sempre disponibilizado ao
doente, mesmo que não tenham sido utilizadas, ou não se encontrem disponíveis, formas
específicas de avaliação especializada do doente utilizador de tabaco (Força de
Evidência: A)
Se o doente deseja fazer uma tentativa de abandono de imediato, devem ser iniciadas as
intervenções identificadas como efectivas nesta NOC.
Se o doente não deseja abandonar para já o uso de tabaco, deve ser fornecida uma intervenção
motivacional.
ESTRUTURA E INTENSIDADE DO TRATAMENTO
•
•
•
•
os médicos devem aconselhar veementemente cada doente que fuma a deixar de o fazer,
porque a evidência mostra que o aconselhamento médico para deixar de fumar aumenta as
taxas de abstinência (Força de Evidência: A)
mesmo intervenções mínimas (com duração inferior a 3 minutos) aumentam as taxas
globais de abstinência do tabaco; a cada utilizador de tabaco deve ser oferecida pelo
menos uma intervenção mínima, quer o doente venha ou não a ser referenciado para
intervenção intensiva. (Força de Evidência: A)
existe uma forte relação dose-resposta entre o tempo de contacto interpessoal das sessões
e os bons resultados do tratamento. Intervenções intensivas são mais efectivas do que
intervenções menos intensivas e devem ser usadas sempre que possível. (Força de
Evidência: A)
o tratamento feito através do contacto interpessoal, oferecido em 4 ou mais sessões,
parece ser especialmente efectivo em aumentar as taxas de abstinência. Assim, se
possível, os clínicos devem procurar encontrar-se 4 ou mais vezes com os doentes que
estão a fazer uma tentativa de abandono do uso de tabaco (Força de Evidência: A)
28
•
•
•
•
•
o tratamento efectuado pelos médicos aumenta as taxas de abstinência. Assim, todos os
médicos devem oferecer intervenções para cessação do tabagismo (Força de Evidência:
A)
os tratamentos prestados por vários tipos de profissionais de saude são mais efectivos do
que os fornecidas por apenas um tipo. Por isso, se possível, deve ser encorajada a
prestação de intervenções por mais do que um tipo de profissional de saude (Força de
Evidência: D)
o aconselhamento telefónico pro-activo (iniciado pelo médico) e o aconselhamento de
grupo e individual, são medidas efectivas e devem ser usadas nas intervenções para
cessação do tabagismo. (Força de Evidência: A)
as intervenções de cessação do tabagismo fornecidas em formatos múltiplos aumentam as
taxas de abstinência e devem ser encorajadas. (Força de Evidência: A)
todos os doentes que recebem uma intervenção para tratamento de dependência de tabaco
devem ser avaliados relativamente a abstinência no final do tratamento e durante
contactos clínicos subsequentes: a) doentes abstinentes devem receber o tratamento de
prevenção de recidiva referido nesta NOC; b) doentes que apresentam recidiva devem ser
avaliados para determinar se desejam fazer nova tentativa de abandono (Força de
Evidência: D)
Se o doente deseja fazer outra tentativa de abandono, fornecer ou referenciar para tratamento
adicional (referido nesta NOC).
Se o doente não deseja abandonar para já, fornecer uma intervenção motivacional (referida
nesta NOC).
ELEMENTOS DE TRATAMENTO
•
•
•
•
•
•
•
existem três tipos de aconselhamento e terapêuticas comportamentais que conduzem a
taxas de abstinência mais elevadas: a) fornecer aos fumadores aconselhamento prático
(aptidões de resolução de problemas/treino de desempenhos); b) fornecer suporte social
como parte do tratamento; e, c) ajudar os fumadores a obter suporte social fora do
tratamento. Estes tipos de aconselhamento e terapêuticas comportamentais devem ser
incluídas nas intervenções de cessação do tabagismo. (Força de Evidência: B)
todos os doentes que estão a tentar deixar de fumar devem ser encorajados a usar
farmacoterapias efectivas para cessação do tabagismo, excepto na presença de
circunstâncias especiais (Força de Evidência: A)
a utilização a longo prazo de farmacoterapia para cessação do tabagismo deve ser
considerada uma estratégia de redução da probabilidade de recidiva (Força de Evidência:
D)
a bupropiona de libertação retardada é uma terapêutica eficaz para cessação do tabagismo,
que os doentes devem ser encorajados a usar (Força de Evidência: A)
a nicotina sob a forma de pastilhas mastigáveis constitui uma terapêutica eficaz para
cessação do tabagismo, que os doentes devem ser encorajados a usar (Força de
Evidência: A)
os clínicos devem disponibilizar, a fumadores altamente dependentes, pastilhas
mastigáveis de nicotina doseadas a 4 mg em vez de 2 mg (Força de Evidência: B)
o adesivo transdérmico de nicotina é um tratamento de cessação do tabagismo eficaz, que
os doentes devem ser encorajados a usar (Força de Evidência: A)
29
•
•
•
•
a clonidina é um tratamento de cessação do tabagismo eficaz, que pode ser usado como
um agente de segunda linha, debaixo de supervisão médica, para tratar dependência de
tabaco (Força de Evidência: A)
a nortriptilina é um tratamento de cessação do tabagismo eficaz, que pode ser usado como
um agente de segunda linha, debaixo de supervisão médica, para tratar dependência do
tabaco (Força de Evidência: B)
a combinação do adesivo transdérmico de nicotina com uma forma auto-administrada de
terapêutica de substituição de nicotina (pastilhas mastigáveis de nicotina) é mais eficaz do
que uma única forma de substituição de nicotina; os doentes devem ser encorajados a usar
tais tratamentos combinados se forem incapazes de abandonar usando um único tipo de
farmacoterapia de 1ª linha (Força de Evidência: B)
a terapêutica com o adesivo transdérmico de nicotina de venda livre é mais eficaz do que
placebo, e o seu uso deve ser encorajado (Força de Evidência: B)
POPULAÇÕES ESPECIAIS
GRAVIDEZ
•
•
devido aos riscos sérios do tabagismo para a mulher grávida fumadora e para o feto,
devem ser oferecidas sempre que possível, às mulheres grávidas fumadoras, intervenções
alargadas para deixar de fumar, excedendo o aconselhamento mínimo (Força de
Evidência: A)
embora a abstinência desde o início da gravidez produza os melhores resultados para o
feto e mulher grávida, é benéfico deixar de fumar em qualquer momento da gravidez. Por
esta razão, os clínicos devem oferecer intervenções efectivas para cessação do tabagismo
na primeira consulta prenatal, assim como ao longo de todo o período da gravidez (Força
de Evidência: B)
MINORIAS RACIAIS E ÉTNICAS
•
•
os tratamentos de cessação do tabagismo têm sido eficazes em diferentes minorias raciais
e étnicas, pelo que os tratamentos considerados efectivos nesta NOC devem ser fornecidos
a estes pacientes (Força de Evidência: A)
os tratamentos de dependência do tabaco devem ser, sempre que possível, modificados ou
adaptados para se tornarem apropriados para as populações raciais e étnicas a que são
fornecidos (Força de Evidência: D)
FUMADORES HOSPITALIZADOS
•
os tratamentos de cessação do tabagismo têm-se provado eficazes em doentes
hospitalizados, pelo que devem ser oferecidos aos doentes internados (Força de
Evidência: B)
FUMADORES COM COMORBILIDADE PSIQUIÁTRICA E/OU DEPENDÊNCIA
QUÍMICA
•
a fumadores com condições psiquiátricas comórbidas devem ser oferecidos os tratamentos
identificados como efectivos nesta NOC (Força de Evidência: D)
30
•
•
a bupropiona de libertação retardada e a nortriptilina - tratamentos eficazes para cessação
do tabagismo na população geral - são também efectivos para tratar a depressão. Por esta
razão, estes fármacos devem ser especialmente considerados para o tratamento de
dependência do tabaco em fumadores com história actual ou passada de síndromes
depressivos (Força de Evidência: D)
a evidência indica que intervenções para cessação do tabagismo não interferem com a
recuperação da dependência química. Por esta razão, os tratamentos de cessação do
tabagismo considerados efectivos nesta NOC, incluindo aconselhamento e farmacoterapia,
devem ser oferecidos aos fumadores a receber tratamento para dependência química
(Força de Evidência: D)
CRIANÇAS E ADOLESCENTES
•
•
•
os clínicos devem interrogar os doentes pediátricos e adolescentes (assim como os seus
pais) a respeito do uso de tabaco, e devem transmitir uma forte mensagem sobre a
importância da abstinência total (Força de Evidência: D)
as intervenções de aconselhamento e comportamentais que são efectivas nos adultos,
devem também ser consideradas em relação a crianças e adolescentes. O conteúdo destas
intervenções deve ser modificado para se tornar apropriado ao grau de desenvolvimento
respectivo (Força de Evidência: D)
os clínicos a fazer consulta pediátrica devem oferecer aos pais aconselhamento e
intervenções para cessação do tabagismo, para limitar a exposição dos filhos a fumo em
segunda mão (Força de Evidência: B)
DOENTES IDOSOS
•
os tratamentos para cessação do tabagismo foram demonstrados como eficazes para
adultos idosos. Assim, estes devem receber os tratamentos de cessação do tabagismo
considerados efectivos nesta NOC (Força de Evidência: A)
TÓPICOS ESPECIAIS
AUMENTO DE PESO APÓS A CESSAÇÃO DO TABAGISMO
•
•
o clínico deve reconhecer que deixar de fumar é muitas vezes seguido por aumento de
peso. Adicionalmente, o clínico deve: a) salientar que os riscos para a saúde do aumento
de peso são pequenos, em comparação com os riscos da continuação do tabagismo; b)
recomendar actividade física e uma alimentação saudável; c) recomendar que os doentes
se devem concentrar em primeiro lugar sobre a cessação do tabagismo e não sobre o
controle de peso, até que os ex-fumadores se tornem confiantes sobre a sua abstinência.
(Força de Evidência: D)
para os fumadores altamente preocupados com o aumento de peso, pode ser apropriado
prescrever ou recomendar bupropiona de libertação retardada ou terapêutica de
substituição de nicotina, em particular pastilhas mastigáveis, que se provou atrasarem o
aumento de peso após a cessação (Força de Evidência: B)
OUTROS PRODUTOS DO TABACO
•
os utilizadores de charutos, cachimbos e outras formas combustíveis de tabaco devem ser
identificados, fortemente aconselhados a cessar o seu uso, e devem receber as mesmas
31
intervenções de aconselhamento recomendadas para os fumadores de cigarros (Força de
Evidência: D)
FORMAÇÃO DOS CLÍNICOS
•
todos os clínicos, incluindo os internos em formação, devem ser treinados em estratégias
efectivas para ajudar os utilizadores de tabaco que desejem fazer uma tentativa de
abandono, e para motivar os que não desejam abandonar para já (Força de Evidência: B)
ASPECTOS ECONÓMICOS DOS TRATAMENTOS DE DEPENDÊNCIA DO TABACO
•
•
os tratamentos de cessação do tabagismo considerados como eficazes nesta NOC (tanto
farmacoterapia como aconselhamento) são altamente efectivos relativamente ao custo, em
comparação com outros tratamentos (ex: tratamento de hiperlipidémia e mamografia de
rastreio) e devem ser fornecidos a todos os fumadores (Força de Evidência: A)
as intervenções intensivas de cessação do tabagismo são especialmente eficazes e custoefectivas e os fumadores devem ter pronto acesso a estes serviços, assim como a
intervenções menos intensivas (Força de Evidência: B)
ALGORITMO CLÍNICO
População
geral
O doente é presente
numa
consulta médica
Recidiva
Inquirir
(rastreio de uso
de tabaco)
Quadro 1
Utilizadores
correntes
Não
utilizadores
Prevenção
primária
Aconselhar
a abandonar
(Quqdro 1)
Avaliar a
vontade de
abandonar
(Quadro 1)
Sim
Ajudar no
processo de
abandono
(Quadros 1,2 e 3)
Programar
seguimento
(Quadro 1)
Não
Ex-utilizadores
Prevenção
de recidiva
(Quadro 6)
Incentivar
a motivação
para abandonar
(Quadro 5)
O doente agora
já deseja abandonar
O doente continua a não querer abandonar
32
Abstinência
RESERVAS QUALITATIVAS
Não se identificaram hiatos de conhecimento de dimensão significativa. A evidência científica
sobre a qual assenta esta NOC é de excelente qualidade, dado que existem múltiplas revisões
sitematizadas da Cochrane Collaboration, assim como estudos aleatorizados e controlados
(RCTs) de boa qualidade metodológica, com resultados consistentes e importantes.
ANÁLISE DE CUSTOS
Não foi efectuada nenhuma análise de custos dos diversos tratamentos possíveis para a
cessação do tabagismo.
A única informação financeira disponível é a dos preços médios diários dos diversos
esquemas terapêuticos.
BENEFÍCIOS POTENCIAIS GERAIS DE SUB-GRUPOS
Para a população em geral, os benefícios que podem advir da aplicação com sucesso das
recomendações desta NOC incidem sobre a prevenção de todas as patologias relacionadas
com o uso do tabaco (anteriormente indicadas). Deste modo, toda a população – mesmo a
saudável - poderá beneficiar destas medidas.
Os sub-grupos em que a cessação do tabaco trará maiores benefícios incluem: os doentes
cardíacos (especialmente coronários), os doentes vasculares (especialmente os doentes com
insuficiência arterial periférica), os doentes com DPCO, os diabéticos, os idosos, os
adolescentes e as grávidas.
RISCOS POTENCIAIS E DE SUB-GRUPOS
Não existem riscos potenciais significativos para nenhum grupo de pacientes ou de doentes
com a cessação do tabagismo. Os benefícios são universais.
DISPONIBILIDADE
O texto desta NOC será disponibilizado nos seguintes meios:
• impressão sob a forma de livro/manual
• publicação na revista do IQS
• publicação na página da Internet do IQS (www.iqs.pt)
DOCUMENTAÇÃO ANEXA
Não existe nenhuma documentação anexa integrada directamente com esta NOC, isto é, este é
um texto autónomo e completo.
RECURSOS DE DOENTES
Não se prevêm nenhuns recursos especiais por parte dos pacientes/doentes para poderem ser
alvo das intervenções recomendadas nesta NOC.
33
DATA DE PUBLICAÇÃO
Dezembro de 2001.
DATA DE REVISÃO PREVISTA
Esta NOC será revista, no todo ou em parte, no ano de 2003.
34
Centre for Evidence Based Medicine
University of Lisbon School of Medicine
Clinical Practice
Guideline on Smoking
Cessation
Inês Reis
Philip Fortuna
Raquel Ascenção
João Costa
António Bugalho
António Vaz Carneiro
CEMBE
Centro de Estudos de Medicina Baseada na Evidência
Faculdade de Medicina de Lisboa – Pisos 4/6
Av. Prof. Egas Moniz
1649-028 Lisboa
PORTUGAL
Tel. 217 940 424 or 217 985 135
Fax: 217 940 424
Email: [email protected]
Web: www.fm.ul.pt/cembe
Page 0 of 106
February 2008
TABLE OF CONTENTS
1. Introduction ........................................................................................................ 3
1.1 Epidemiology ............................................................................................... 3
1.2 Tobacco and cardiovascular and/or cerebrovascular risk ................. 4
1.3 Smoking, hypercholesterolemia and diabetes mellitus ........................ 5
1.4 Tobacco and pregnancy .......................................................................... 5
1.5 Smoking and pulmonary disease.............................................................. 7
1.6 Passive smoking ........................................................................................... 8
1.7 Other forms of smoking............................................................................... 9
2. Topic / Disease................................................................................................. 10
3. Objectives ........................................................................................................ 10
4. Category .......................................................................................................... 10
5. Adaptation....................................................................................................... 10
6. Target population............................................................................................ 10
7. Potential users of this CPG ............................................................................. 10
8. Sources of scientific methodology ............................................................... 11
8.1 Articles Published in Journals or Electronic Databases........................ 11
8.2 Books............................................................................................................ 19
8.3 Internet ........................................................................................................ 21
9. Methods for scientific evidence selection .................................................. 22
10. Methodology of critical evaluation of scientific evidence .................... 24
11. Hierarchy scheme for scientific evidence................................................. 26
12. Methods of analysis and scientific evidence validation......................... 28
12.1 Included studies....................................................................................... 28
12.2 Excluded trials .......................................................................................... 42
13. Practical interventions .................................................................................. 46
13.1 Pharmacological interventions ............................................................. 46
13.2 Non-pharmacological interventions .................................................... 50
13.3 Special populations................................................................................. 55
13.4 Role of health care providers ................................................................ 59
13.5 Special topics........................................................................................... 61
14. Outcomes....................................................................................................... 65
15. Implementation strategy.............................................................................. 65
16. Main recommendations............................................................................... 66
Page 1 of 106
16.1 Pharmacological interventions ............................................................. 66
16.2 Non-pharmacological interventions .................................................... 66
16.3 Role of health care providers ................................................................ 67
16.4 Special populations................................................................................. 67
16.5 Special topics........................................................................................... 69
17. Clinical algorithm .......................................................................................... 71
17.1 Screening and assessment of tobacco use........................................ 72
17.2 Brief clinical interventions ....................................................................... 72
17.3 Intensive clinical interventions ............................................................... 73
18. Qualitative reserves ...................................................................................... 74
19. Cost analysis................................................................................................... 74
20. General and subgroups potential benefits............................................... 74
21. General and subgroups potential risks ...................................................... 74
22. Availability ...................................................................................................... 74
23. Attached documents................................................................................... 75
24. Patients’ resources ........................................................................................ 75
25. Supporters and subscribers .......................................................................... 75
26. Committees and responsible group........................................................... 75
27. Funding sources............................................................................................. 75
28. Editorial independence ............................................................................... 76
29. Publication date............................................................................................ 76
30. Reviews ........................................................................................................... 76
31. Appendices.................................................................................................... 76
31.1 Fagerström scale (evaluation of the dependency level)................. 76
31.2 Synoptic tables......................................................................................... 77
31.3 The Agree Instrument.............................................................................. 89
31.4 The GLIA Instrument ................................................................................ 89
31.5 Glossary ..................................................................................................... 89
32. References ................................................................................................... 103
Page 2 of 106
1. Introduction
1.1 Epidemiology
Tobacco is produced in several areas of the world, and is legally marketed in
all countries. The World Health Report 2002 refers that at least one third of all
disease burden in industrialized countries of North America, Europe and Asia
is due to tobacco, alcohol abuse, hypertension, cholesterol increase and
obesity. In fact, more than three quarters of cardiovascular diseases (the
main cause of global mortality) are due to high levels of cholesterol,
tobacco, hypertension or their respective combination. Globally,
hypercholesterolemia causes more than 4 millions premature deaths per
year, tobacco around 5 millions and hypertension 7 million more.
Despite all efforts to reduce the selling and tobacco use, smoking is still
increasing, side by side with the world population. Nowadays, more than 15
billion cigarettes are consumed per day and it is estimated that one third of
the adult population has smoking habits1.
The European Report for Tobacco Control, launched in 2007 by the
World Health Organization (WHO), considers the prevalence of smokers (on a
daily basis and age ≥ 15 years) within Europe of 28.6%, 40% men and 18.2%
women. In young people under 15 the smoking habits prevalence (at least
one cigarette per week) is estimated by WHO, in the study Health Behaviour
in School-aged Children (2001/2002)2, as 2% from 11 to 13 years, 8% at 13,
and 24% at 15. The same study points out rates of prevalence in Portugal of
around 18 % in boys and 26% in girls.
In our country the most recent data comes form the 4th National Health
Enquiry (NHE) (conducted in 2005/2006), which estimates the smoking
prevalence (daily, ages >10) in mainland as 19.6% (28.7% men and 11.2%
women). In this geographical area there seems to exist a trend for a
decrease in male smokers and an increase in women, already verified in
previously conducted National Health Enquiries (1987, 1996, and 1998/1999).
In Madeira region, the present estimate of smoking percentages is similar to
the one found in the Continent. On the other hand, in Azores these
proportions are higher: 24% overall, 36.4% men and 11.9% women. The 4th NHE
was the first to include the whole national territory; therefore the Autonomous
Regions do not have results corresponding to periods preceding 2005/2006.
(National Health Enquiry 2005/2006).
Smoking has been identified as a major factor in diminishing health life
expectancy and increasing mortality. Smoking is the main risk factor for
premature death in Europe, being responsible for about 1.6 million deaths per
year. It is estimated that within the European region of WHO, tobacco is the
second more important risk factor, causing, in 2000, 12.3% of the total lost
years due to premature mortality and Quality Adjusted Life Years (QALYs),
Page 3 of 106
which equals the loss of around 18.6 million years of life. In 2002, in Portugal,
tobacco was also the second more important risk factor, contributing to
10.4% of QALYs 3.
Lung cancer related mortality is still increasing in European countries. In
spite of mortality rates due to lung neoplasia in women in Europe being lower
than the ones found in men, the actual increase in tobacco consumption
amongst teenagers and women is a worrying factor. Considering the time
interval between the beginning of smoking habits and the disease
manifestations, we can foresee an increase in cancer mortality in this group.
The diminishing of the prevalence of tobacco consumption in European men,
at least since 1980, has been reflected in the slight decrease noted in
mortality rates due to this neoplasic disease in men since 1990.
Nowadays, in Portugal there is an increase in both genders of mortality
rates due to respiratory system neoplasias. This fact is connected to the
increasing of tobacco consumption amongst women in our country. The nonoccurrence of a decrease in mortality rate in men due to these neoplasias is
explained by the time lapse between beginning of smoking and its reflex in
mortality and morbidity3.
The price of tobacco to governments, employers and environment
includes several kinds of costs such as social security and health systems,
absenteeism, diminishing productivity, deflorestation and collection of
cigarette-ends. In 1999, smoking was responsible for 6% of health expenses in
the United States of America 1.
According to the Family Budgets Enquiry, conducted in our country in
the year 2000 by the National Institute of Statistics, the family expenses with
tobacco was around 749 euros (4.2% of the total expense). (Information to
the Media, INE, 220 – accessed in May 2007).
The countries with lower Gross National Product (GNP) per capita
present smoking prevalence rates that are higher than 50%, when compared
to an average of 34% in richer countries. This fact is reverberated in the higher
mortality rate due to tobacco consumption in countries with lower GNP, in
individuals aged 35-69 years.
1.2 Tobacco and cardiovascular and/or cerebrovascular risk
Tobacco consumption is an independent risk factor to coronaropathy,
cerebrovascular disease and atherosclerotic disease, contributing to the
global mortality increase and due to cardiovascular causes 4.
The incidence of acute myocardial infarction (AMI) is increased six fold
in women and three fold in men who smoke 20 of more cigarettes per day,
comparing to individuals who never smoked. In the INTERHEART study,
smokers represented 36% of the population at risk to the first AMI5. In spite of
these data, more than 60% of 737 smokers did not believe they were at
higher risk to this nosologic entity.
Page 4 of 106
The risk of ischemic stroke also decreases, gradually, after smoking
cessation. In a series including smoking women, the accumulated risk
disappeared in two to four years after smoking cessation.
Among individuals with no known coronariopathy, the reduction of
cardiac events associated to smoking cessation varies between 7% and 47%.
The cardiovascular risk associated to tobacco smoke decreases shortly after
smoking cessation and this tendency is stable during the time of the eviction.
In a meta-analysis in which all patients had AMI, coronary artery bypass grafts
(CABG), angioplasty or other coronary disease, the relative risk of mortality of
smokers who stopped smoking comparing to smokers was 0.64, and this
benefit was not affected by age, gender, cardiac index, nationality or year
of the beginning of the study6 .
Tobacco use before CABG does not affect survival after surgery, but
smokers have an increased mortality risk by any cause (RR 1.68), cardiac
death (RR 1.75) and need to repeat revascularization (RR 1.14) comparing to
the ones who have stopped smoking at least a year before7.
After angioplasty, persistent smokers face a greater risk of death (1.76)
and of Q wave-AMI (2.08) comparing to the non-smokers, and an increased
risk of death from any cause and for cardiac causes (1.44 and 1.49
respectively) when compared with the ones who have stopped smoking8.
Among patients with left ventricular dysfunction (FE < 35%), tobacco
increases the all cause mortality (RR 1.41 comparatively to non-smokers or exsmokers) and the incidence of death and hospitalization due to cardiac
failure or AMI (RR 1.39)9.
1.3 Smoking, hypercholesterolemia and diabetes mellitus
Smoking is associated to an increase in serum concentrations of total
cholesterol and VLDL cholesterol, and to an increase of insulin resistance, and
diabetic patients who smoke have a greater difficulty in controlling glycemia,
a greater risk for end stage renal disease and a diminished survival rate as
soon as they begin dialysis10.
In diabetes type 1 patients, tobacco smoke is independently
associated with an increase in urinary albumin and non-proliferate
retinopathy and, if smoking is discontinued, there is a decrease in the
albuminuria to a level similar to the one found in non-smokers.
1.4 Tobacco and pregnancy
Smoking is the most important modifiable risk factor associated to a bad
prognosis during pregnancy. The prevalence of tobacco use during
pregnancy is around 10% - 20% (it varies according to the data collection
method), although it seems to be decreasing slightly. It is estimated that, in
populations with high smoking prevalence in women, cessation during
Page 5 of 106
pregnancy might prevent 10% of perinatal deaths, 35% of low weight birth
infants and 15% of pre-term labours. Furthermore, active and passive smoking
increase the risk for infertility, placenta rupture, premature rupture of this
membrane and placenta praevia.
The reduction in fetal oxygenation is the most studied
physiopathological cause for the adverse effects of smoking in pregnancy;
however, smoking may also damage the genetic material of the fetus, from
the direct toxicity of the more than 2500 deleterious constituents of
cigarettes.
A meta-analysis of 12 studies detected an increase of the risk of
infertility in smoking women, relatively to the non-smokers (OR 1.60) and
studies in women submitted to in vitro fertilization (IVF) have also shown a
reduction in the fertility of smokers, the pregnancy rate by number of cycles,
in IVF treatment, being significant smaller in this group (OR 0.66)11.
All pregnant women who smoke have 1.5 to 3.5 times greater
probability of having a low birth weight fetus (LBWF < 2500 g), and this risk
increases with the number of cigarettes consumed. The weight deficit
associated to a smoking mother varies between 200 to 300 g. At least 20% of
all LBWF are attributable to tobacco exposition during pregnancy, and
smoking in the third trimester seems to have a greater impact in this
pathology12.
There is significant evidence that smoking over 10 cigarettes per day
may be associated with an increase in the number of spontaneous abortions,
with a RR of 1.2 to 3.4. Large case-control and cohort studies have shown RR
of fetal death (after 28 weeks of gestation) of 1.2 to 1.4 in smoking women,
with larger risk with heavy smoking. A prospective study has shown,
furthermore, that non-smoking women passively exposed to tobacco smoke
are at greater risk of intra-uterine death than the ones not exposed (OR 1.53).
There is a considerable increase in the risk of preterm premature rupture of
membranes (PPROM) amongst smoking women, with a RR of 1.9 to 4.2.
Smoking also increases the risk of abruptio placenta with an adjusted relative
risk described from 1.4 to 2.5 and has been constantly associated with the
occurrence of placenta praevia with RR between 1.4 and 4.4.
Pregnant smoking women have 1.3 to 2.5 times a greater probability of
having a pre-term delivery, particularly before the 32nd week of gestation. It
should be noted that smoking and drug abuse are frequently the only
potentially modifiable risk factors associated to this intercurrence.
It is not clear yet that smoking effectively increases the risk of
congenital malformations but the risk of neonatal death (in the first 28 days of
life) seems increased in smoking women, with RR 1.2 to 1.4 and the sudden
infant death syndrome has been constantly associated to maternal smoking,
with a relative risk of children exposed in utero or during post natal life of 2.0
to 7.2. It has been suggested that pre natal exposure is a greater risk factor
than the exposure to passive smoke during childhood at home. Furthermore,
Page 6 of 106
as it was mentioned above, smoking increases other risk factors known as
SIDS such as pre term delivery and low birth weight.
The British Child Development Study data suggests that maternal
smoking habits during pregnancy are associated to an increased risk for
DM2 in offspring from 33 years of age on13.
Maternal smoking may also have long term implications in the exposed
reproductive healthof the offspring. Adult men subjected to tobacco
exposure in utero seem to have a 25% reduction of total count of
spermatozoids comparatively to the non-exposed, and it was also suggested
that there is a possible relationship between reduced feminine fertility and
pre natal smoking exposure14.
Also associated to maternal smoking is a precocious abandon of
maternal lactation and other morbidities such as respiratory infections,
asthma, otitis media, colic, bronchiolitis, small height, lower scores of reading
and speech, lower levels of attention, hyperactivity, school obesity and lower
school performance.
Finally, it should be mentioned that, in spite of the existence of metaanalysis that show a significant reduction of preeclampsia risk in smoking
pregnant women (OR 0.51), this benefit does not supersedes the many
clinical and obstetric problems previously described15.
All the risks mentioned above are insufficient to motivate cessation,
and it is estimated that only 20% to 40% women stop smoking completely
during pregnancy, and the majority does so before the first pre natal visit.
1.5 Smoking and pulmonary disease
Smoking alters the structure and function of central and peripheral airways,
parenchyma, capillaries and pulmonary immunological system, producing
an increase of respiratory symptoms amongst smokers. The increase risk of
several kinds of respiratory infections it is a well known fact, and smoking is an
important factor to the development of invasive pneumococcal disease in
non elderly immunocompetent adults. Furthermore, it seems to increase the
incidence of death due to tuberculosis.
Active smoking is by far the most important risk factor to chronic
obstructive pulmonary disease (COPD), being responsible to 80% to 90% of
the risk of developing this disease. It is also recognized that smoking is
associated to a doubling or tripling of decline rate in FEV1, and a 2 to 20 times
increase in the death risk by COPD16.
Tobacco is the main cause to the development of lung cancer (LC). It
is estimated that smoking is responsible for about 87% of LC cases, and it
should be underlined that LC is the most common death cause by neoplasia
in the world. Estimates of RR by LC in long time smokers, compared to nonsmokers, vary from 10 to 30 times17. The cumulative risk for cancer is
proportional to the total consumption of cigarettes, and it can attain 30% in
Page 7 of 106
smokers with marked smoking load, comparatively to the risk, lower or equal
to 1%, expected during the life of a non-smoking person17. Smoking cessation
clearly decreases the LC risk of ex-smokers, when compared to active
smokers. The size of this reduction is evident after 5 years from the beginning
of eviction and varies between 20 and 90%, according to the duration of the
abstinence. In smokers who are not able to stop smoking, the reduction
might have some effect in the reduction of LC risk. Epidemiological studies
have shown that non-smokers exposed to high levels of tobacco smoke
present an increased risk of LC when compared to lesser cumulative
exposures, and there is a dose-response relation between the intensity of the
exposure and the relative risk (as will be referred in the passive smoking
chapter).
Strong associations between smoking and the development of other
neoplasias (e.g. cancer of the mouth, larynx, oesophageal cancer, cancer
of the bladder, renal cell cancer, cancer of the pancreas, gastric cancer
and cervical cancer) have been found, although the risk is not as high as the
risk for LC. The manifestation of a second neoplasia connected to tobacco is
more likely to occur when there is a previous history of one of the mentioned
malignant tumours18.
1.6 Passive smoking
Nowadays, 1.3 billion adults in the entire world are smokers, meaning that
passive smoking, defined as the involuntary exposure of the non-smokers to
the tobacco smoke of active smokers, is inevitable for children or for the 2/3
of non-smoking adults.
The 2006 US Surgeon General’s Report confirms, explicitly, that any
exposure to tobacco smoke is harmful to human health. Several assessments
of nicotine levels conducted during the last decades show that passive
smoking has been largely prevalent in working places and homes. Lung
cancer has been increasing in non-smokers, and there are around 10.000
cases per year, from which it is estimated that about 2.000 to 3.000 are
caused by passive smoking, probably connected to the continuous exposure
to tobacco carcinogenic components, with the influence of genetic factors
not being excluded. A meta-analysis, including 52 trials, has shown a relative
risk of LC for non-smokers exposed to passive smoking of their partner of 1.21,
and other – which included 25 trials – referred that the relative risk in the
working place was 1.2219.
As far as cardiovascular disease is concerned, it is estimated that
passive smoking is responsible for about 40.000 deaths due to cardiac
disease every year in the United States of America20 and a meta-analysis of
the trials conducted to examine the association between passive smoking
and coronary disease (CD) estimated an excess of risk for CD of 27% in
passive smokers19. It was also shown in a study including 60.377 women in
Page 8 of 106
China, that there is an association between stroke and their active smoking
husbands.
In 2005, the Environment Protection Agency in California established
that 22.700 of the 69.000 deaths due to CD in 2000 were caused by passive
smoking. The 2006 Surgeon General’s Report refers a 25 to 30% increase in CD
risk due to passive smoking19.
Of the few data existent on the association between global mortality
and passive smoking, it was suggested an increase of about 15% in the
mortality of non-smokers living with smokers, comparative to non-smokers
living in a tobacco free household.
Although there is no scientific evidence of exceptional quality yet, all
available data suggests that there are clinically relevant consequences due
to passive smoking in adults with chronic respiratory disease.
Multiple reports in public health have identified specific risks associated
to infant passive smoking. In an inquiry involving around 17.448 children in the
USA, it was seen that children exposed to passive smoking had, in average,
two more days of activity restriction, one more day bed driven and 1.4 more
days of school abstinence than the non-exposed21. Children whose parents
are smokers present an increased risk of diseases of the lower respiratory tract
(the risk is increased in 50% if both parents are smokers), including a
significantly increased frequency of bronchitis and pneumonia during their
first year of life. The exposure to passive smoking during childhood is
associated to a greater prevalence and seriousness of infant asthma and
expression of the latter in adulthood. It is known that the smoking from
parents harms the development of pulmonary function during childhood and
that there is an association between that exposure and the occurrence of
medium otitis.
Passive smoking in healthy non-smoker teenagers may be associated
to lower levels of HDL cholesterol and the relation between total cholesterol /
HDL cholesterol. There is also increased evidence pointing out that passive
smoking influences future cardiovascular risk in children22.
1.7 Other forms of smoking
Epidemiologic studies have shown that cigarette brands that contain less tar
coal and nicotine reduce LC risk only marginally. Likewise, there was only a
small difference in the mortality rate between smokers of filter and non-filter
cigarettes18.
Cigar smoke contains the same toxic and carcinogenic compounds
found in cigarette smoke and the individuals who smoke four or more cigars
per day are exposed to a smoke amount equivalent to 10 cigarettes. Even
those who do not inhale cigarette smoke are subject to their own
environmental smoke. Cigar use is related to an increase of LC risk,
apparently less important than the one found with cigarette use (RR 2.1 and
Page 9 of 106
5.1 in two different trials), the threshold from which the LC risk increases not
being defined yet23.
Pipe tobacco use also increases LC risk, being this similar to the one
referred to the use of cigars.
2. Topic / Disease
The disease referred to in this CPG is tobacco dependence, regardless of the
way it is used (cigarettes, cigars, cigarillo, pipe, chewed, etc.).
3. Objectives
The purpose of the present CPG is to provide recommendations based in
scientific evidence relating to the use and dependence of tobacco
treatment.
4. Category
This is a CPG of therapeutic effectiveness.
5. Adaptation
This CPG was not directly adapted from any recommendation, protocol,
consensus or CPG published to date. It comes, partially, as an update of the
“Clinical orientation guideline to the treatment of tobacco use and
dependency” developed by the Institute of Quality in Health (IQS) and
CEMBE in 2002.
6. Target population
All users or individuals exposed to tobacco, regardless of gender and age.
7. Potential users of this CPG
•
•
•
•
•
•
Doctors (family doctors, occupational medicine, internal medicine,
cardiology, pneumology, obstetrics, paediatrics, etc.)
Dentists
Nurses
Psychologists
Pharmacists
Others.
Page 10 of 106
8. Sources of scientific methodology
The methodological sources of scientific evidence used as basis for this
CPG include articles, books and Internet pages of specific organizations.
These sources are common to all CPGs, and are included here as
information to the users who wish to elaborate this type of documents. It is
important to underline that only the ones deemed fundamental by the
authors of the present CPG are presented, so the list is, by definition,
incomplete.
8.1 Articles Published in Journals or Electronic Databases
•
ADAPTE: manual for guideline adaptation. ADAPTE Group; 2007. Available
by emailing [email protected].
•
Anonymous. Clinical practice guidelines and conflict of interest. CMAJ
2005;173(11):1297
•
Atkins D, Briss PA, Eccles M, Flottorp S, Guyatt GH et al. Systems for grading
the quality of evidence and the strength of recommendations II: Pilot
study of a new system. BMC Health Serv Res 2005, 5:25
•
Atkins D, Eccles M, Flattop S, et al. Systems for grading the quality of
evidence and the strength of recommendations I: Critical appraisal of
existing approaches. The GRADE Working Group BMC Health Serv Res
2004, 4:38
•
Bland JM. Sample size in guideline trials. Fam Pract 2000; 17:S17-S20
•
Boyd EA, Bero LA. Improving the use of research evidence in guideline
development: 4. Managing conflicts of interests. Health Res Policy Syst
2006,4:16
•
Brock WA. Development of protocols, guidelines, and critical pathways in
the intensive care environment. Intensive Care Med 1999; 5:321-325
•
Brook RH. Practice guidelines and practicing medicine. JAMA 1989;
262:3027-3030
•
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•
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8.2 Books
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8.3 Internet
•
Agency for Healthcare Research and Quality: www.ahrq.gov
•
•
American College of Physicians Clinical Practice Guidelines:
www.acponline.org/sci-policy/guidelines
•
Australian Government National Health and Medical Research Council:
www.nhmrc.gov.au
•
Clinical Knowledge Summaries (CKS) Prodigy Guidance:
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eGuidelines: www.eguidelines.co.uk
•
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www.gfmer.ch/000_Homepage_En.htm
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Guidelines International Network: www.g-i-n.net
•
Institute for Clinical Systems Improvement: www.icsi.org
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www.mja.com.au/public/guides/guides.html
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National Guideline Clearinghouse: www.guideline.gov
•
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•
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www.hlth.gov.bc.ca/msp/protoguides/index.html
•
Canadian Medical Association Infobase:
mdm.ca/cpgsnew/cpgs/index.asp
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Canadian Task Force on Preventive Health Care: www.ctfphc.org
•
Guidelines Advisory Committee: www.gacguidelines.ca
•
Public Health Agency of Canada guidelines: www.phacaspc.gc.ca/dpg_e.html
•
New Zealand Guidelines Group: www.nzgg.org.nz
•
NHS Health Technology Assessment Programme:
www.hta.nhsweb.nhs.uk/index.htm
•
Scottish Intercollegiate Guidelines Network: www.sign.ac.uk
•
Trip Database: www.tripdatabase.com/index.html
•
United States Preventive Services Task Force:
www.ahrq.gov/clinic/uspstfix.htm
9. Methods for scientific evidence selection
The sources of scientific evidence used as basis for the present CPG include
articles, books and Internet pages of specific organizations.
By means of identifying the main randomized and controlled clinical
trials, meta-analysis of clinical trials, systematic reviews and clinical practice
guidelines that would allow to answer the question on the interventions that
promote smoking cessation, we developed a research strategy that was
based on the following electronic databases:
• Medline (www.pubmed.com) (1966-3/2007)
• Cochrane Central Register of Controlled Trials (in Cochrane Library issue
1, 2007)
Page 22 of 106
• Cochrane Database of Systematic Reviews (in Cochrane Library issue 1,
2007)
• Database of Abstracts of Reviews of Effectiveness (in Cochrane Library
issue 1, 2007)
The research strategy developed for the 4 first mentioned databases
was the following:
#1. Smoking Cessation [MeSH]
#2. Tobacco Use Cessation [MeSH]
#3. Smoking/drug therapy [MeSH]
#4. Smoking/therapy [MeSH]
#5 OR/1-4
We applied research filters to the results to identify all randomized
clinical trials, meta-analysis of clinical trials, systematic reviews and guidelines.
Only the trials in adult population (over 18) were considered and they had to
be published in Portuguese, French or English. We obtained the synopsis of all
the trials identified by the research strategy, in order to select which ones
should be included in the analysis. This selection was made by 3 people. After
decision was made on which trials to include, the complete publications
were requested to be analysed. The research strategy also included the list of
references included in the identified trials.
The selection of the scientific evidence was made – additionally – in
secondary sources of information, which are defined as the ones that, having
selected the articles, papers and trials in the primary databases (Medline,
EMBASE, CINAHL, for example), perform critical evaluation of their quality,
based on their methodological structure, selecting only those that, through its
validity, importance and relevance to clinical practice constitute the
evidence considered as the most valid (see below). The base criterion was
that the referred sources of secondary scientific evidence were undoubtedly
based on scientific evidence and available in printing (journal articles, books)
and/or electronically (Internet).
For the final revision, the following secondary sources were included:
• ACP Journal Club
• ACP Medicine
• Agency for Health Care Research and Quality
• Bandolier
• Clinical Evidence
• DynaMed
• Evidence-Based Medicine
• Evidence Based Practice
• Guideline International Network
Page 23 of 106
• InfoPoems
• PIER from ACP
• Scottish Intercollegiate Guidelines Network
• UpToDate.
10. Methodology of critical evaluation of scientific
evidence
A critical evaluation of the evidence - in terms of its validity, importance and
applicability of the results - was an essential step in the scientific basis for the
preparation of this CPG. Indeed, without a guarantee of quality and scientific
methodology of the studies that form the basis of the CPG, the consistent
statement of the conclusions could be questioned. The following tables
formed the guides to critical evaluation, specific for the type of studies we
wanted to examine: in this case, only clinical trials and systematic reviews.
These tables are built up upon questions – guides – (primary and
secondary), that the trials under review had to respond in detail, so they
could be included (or not) in the final analysis and thus serve as scientific
basis to this CPG. The review process involved one of four types of possible
answers for each guide: yes, unclear/possibly, no or not applicable. To each
of these responses a numerical value of 2.1 or 0 was assigned (table 10.1).
Highlight
code:
TABLE 10.1 – Codification of responses
the
appropriate 2 – Affirmative response =
yes
1 – unclear / possibly
0 – negative response = no
n/a – not applicable
Each article was then sorted by a score, composed by the sum of all
the scores assigned to individual guides, standard for the No. of issues
applicable to the specific study, and the final classification was the ratio
between the total score and the maximum applicable (Table 10.2).
TABLE 10.2 – Calculation of the final classification of articles
Total score (sum of the assigned scores) ________ [A]
No. of issues applicable (max. 20) ________ [B]
Maximum possible score (2 x B) ________ [C]
FINAL STANDINGS (A/C in %) _________ %
Subsequently, an “evidence table” was built, on which each article
was individually included for the final analysis (table 10.3).
Page 24 of 106
TABLE 10.3 – Calculation of the final standings of the articles
Trial (authors
and year)
Design
Participants
Intervention and
comparison
Results
Final scores
Only the articles with the higher scores were included in the final
database of evidence for the present CPG.
TABLE 10.4 - Grid to the critical evaluation of an article describing a
prospective, randomized and controlled clinical trial
VALIDITY OF RESULTS
1. Was the range of patients well defined?
2. Was the disease diagnosis well characterized?
3. Are the inclusion and exclusion criteria logical and clear?
4. Were the patients randomized?
5. Was randomization blind?
6. Were the patients analyzed in the groups for which they
had been randomized initially (intend-to-treat)?
7. Was the randomization method explained?
8. Was the size of the sample statistically calculated?
9. Were the patients in comparison groups similar in terms of
known prognostic factors?
10. Except for the study drug, were all patients treated the
same way?
11. Were the patients blinded regarding the group they were
included into?
12. Were the investigators blinded regarding the study groups?
13. Were the data analyzers blinded regarding the study
groups?
14. Was final follow-up higher than 80%?
IMPORTANCE OF RESULTS
15. Was the therapeutic effect dimension (RRR, ARR and NNT)
important?
16. The effect estimate is precise enough (CI)?
17. Does that effect have clinical relevance?
APPLICABILITY OF RESULTS
18. Are the study patients similar to the clinical practice of the
individual doctor?
19. Were all important clinical results considered?
20. Do treatment benefits over impose to potential risks and
costs of implementation?
Y
2
2
2
2
2
?
1
1
1
1
1
N
0
0
0
0
0
2
2
2
1
1
1
0
0
0
n/a
n/a
n/a
2
2
1
1
0
0
n/a
n/a
2
2
1
1
0
0
n/a
n/a
2
2
1
1
0
0
n/a
n/a
2
2
1
1
0
0
n/a
n/a
2
1
0
n/a
2
1
0
n/a
2
2
1
1
0
0
n/a
n/a
n/a
n/a
n/a
n/a
Page 25 of 106
Table 10.5 - Grid to critical evaluation of a systematic review
VALIDITY OF RESULTS
1. Is the review centered on a clearly focused clinical issue?
Y
2
?
1
N
0
2. Are the inclusion (and exclusion) criteria for studies in the SR
appropriate?
3. Have all important and relevant studies been included?
2
1
0
2
1
0
4. Was the quality of the included studies correctly evaluated?
2
1
0
5. Were the critical evaluations of the studies reproducible
between the evaluators?
6. Were the studies’ results similar between them?
2
1
0
2
1
0
IMPORTANCE OF RESULTS
7. What are the global results of the SR?
2
1
0
8. What is the precision of the SR results?
2
1
0
2
1
0
2
1
0
2
1
0
APPLICABILITY OF RESULTS
9. Can the SR results be applied to our patients?
10. Were all clinically relevant outcomes duly considered, in view
of the question?
11. Do benefits of the practical application of results compensate
potential damages and costs?
n/a
n/
a
n/
a
n/
a
n/
a
n/
a
n/
a
n/
a
n/
a
n/
a
n/
a
n/
a
11. Hierarchy scheme for scientific evidence
The hierarchy system for scientific evidence used in the present CPG was
based in the recommendations of the Centre for Evidence-Based
Medicine, Oxford, United Kingdom. Nevertheless it is important to mention
that this system is not very different from the one that has been developed
internationally, named GRADE24. In this CPG we used an adaptation of
this system25, with recommendations good (level 1) or bad (level 2)
quality, according to the kind of scientific evidence it is based on, and this
evidence is classified with several levels of descending quality, raging
from A to D. As such, and for the purpose of the present document, a
recommendation graded as level A is considered to be based on high
quality evidence, while a level D recommendation only presents low
quality evidence.
Page 26 of 106
TABLE 11.1 - Levels of evidence and therapeutic or preventive
recommendation degrees
Degree of
Recommendation
A
B
Level of
evidence
1a
1b
1c
2a
2b
C
2c
3a
3b
4
D
5
Methodological analysis
SR* (with internal homogeneity†) of RCTs§
Individual RCTs (with short CI#)
All or none¶
SR (with internal homogeneity †) of cohort studies
Cohort individual studies (including low quality RCTs§, e.g.
< 80% follow-up)
Outcomes research §§ and ecological studies
SR* (with internal homogeneity†) of case-control studies
Individual case-control studies
Series of cases (as well as cohort and case control low
quality studies**)
Expert opinion with no previous explanation of the critical
evaluations of evidence methodology, o based in basic
investigation (extrapolations), or of “primary principles”††
Notes referring to tables
CI: confidence intervals
RCT: randomized controlled trials
§§ Outcomes research: consists in cohort studies with patients with identical diagnosis
(stroke, AMY, etc.) which relate their clinical outcomes, whether mortality, morbidity,
events, etc., with the received medical care (aspirin, surgery, rehabilitation); this kind of
investigation does not use RCT and therefore it is impossible to rate as effective a certain
therapeutic manoeuvre. The advantage of this approach is that it allows recognizing if
the expected outcomes correspond to the ones found in daily clinical practice.
† Homogeneity: low level of heterogeneity in the direction and magnitude of the result of
the clinical trials included
††By primary principles we consider the physiopathological concepts which preside to
medical practice (e.g. blood pressure control in patients with aorta dissection); obviously,
these principles, if not tested in rigorous trials, may sometimes lead to wrong practices.
* SR: Systematic review: a SR is a literature and scientific review on a certain subject,
done in such a way that all biases are reduced to a minimum. The fundamental
characteristic of a systematic review is the clear and non-ambiguous explanation of the
criteria used on the selection, critical evaluation and inclusion of evidence. As such, a
systematic review presents formal and precise objectives, and the inclusion (and
exclusion) criteria for the studies are thoroughly explained. The systematic review does
not usually present any determined graphic representation.
¶ when all the patients died before the treatment was available, but some of them now
survive with it; or when some patients died before the treatment was available, but none
now dies when using it.
#
§
As it was clear from the previous tables, the recommendation degrees
include four levels, in decreasing order of validity (A, B, C and D). Table
11.2 summarizes them, according to the underlying type of clinical trial.
Page 27 of 106
A
B
C
D
TABLE 11.2 – Degrees of recommendations
• Consistent level 1 trials
• Consistent level 2 or 3 trials or extrapolation of level
1 trials
• Level 4 trials or extrapolation of level 2 or 3 trials
• Level 5 trials or inconsistent / inconclusive at any
level
12. Methods of analysis and scientific evidence
validation
12.1 Included studies
12.1.1 Pharmacological interventions
12.1.1.1 Nicotine replacement therapy (NRT)
West R, Shiffman S. Effect of oral nicotine dosing forms on cigarette
withdrawal
symptoms
and
craving:
a
systematic
review.
Psychopharmacology 2001; 155(2):115-122
Systematic review of 12 clinical trials that concluded, with high degree of
evidence, that the oral nicotine dosing forms have reduced the
discomfort, irritability and anxiety caused by smoking cessation. It also
demonstrated that there is some evidence that these nicotine
replacements have a beneficial effect in the decrease of depressive
humour and smoking craving.
Hughes JR, Shiffman S, Callas P, Zhang J. A meta-analysis of the efficacy
of over-the-counter nicotine replacement. Tobacco Control 2003;
12(1):21-27.
Systematic review whose results have shown that the over-the-counter
nicotine replacement therapy has a wider effect in smoking cessation
comparing to placebo (OR 2.5, CI 95%, 1.8 to 3.6) and that it produced
smoking cessation rates similar, although inferior, to the prescription
nicotine replacement therapy (OR 1.4, CI 95%, 0.6 a 3.3).
Cepeda-Benito A, Reynoso JT, Erath S. Meta-analysis of the efficacy of
nicotine replacement therapy for smoking cessation: differences between
men and women. Journal of Consulting and Clinical Psychology 2004;
72(4):712-722.
This meta-analysis, which included 21 RCTs, showed that the long term
benefits of nicotine replacement therapy decreased more rapidly in
Page 28 of 106
women than in men. The association of intensive non-pharmacological
support to pharmacological therapy seemed more important in women.
Silagy C, Lancaster T, Stead L, Mant D, Fowler G. Nicotine replacement
therapy for smoking cessation: Cochrane Systematic Review. Cochrane
Database of Systematic Reviews 2004; Issue 3
Systematic review of 103 studies showed that all marketed forms of
nicotine were effective in smoking cessation. The OR for abstinence with
nicotine replacement therapy, compared to control, was of 1.77 (CI 95%,
1.66 to 1.88). In highly dependent smokers (Fagerström score >7) it was
shown that the 4 mg gums were more effective than the 2 mg ones. The
indirect comparison between the different kinds of nicotine replacement
therapy did not reveal a significant difference in their efficacy. There is low
evidence that the combination therapy with different forms of nicotine
replacement therapy is more effective comparing to the isolated use of
one formula. The efficacy of nicotine replacement therapy seems
independent of the duration or the context in which the therapy was
administrated, as well as the degree of additional support provided to the
smoker.
Etter JF, Stapleton JA. Nicotine replacement therapy for long-term
smoking cessation: a meta-analysis. Tobacco Control 2006; 15(4):280-285.
Meta-analysis, including 12 RCTs, that evaluated the effect a unique
course of nicotine replacement therapy in smoking cessation, at the end
of 2 to 8 years. The favourable OR to the nicotine replacement therapy,
versus control, was of 1.99 (CI 95% 1.50 to 2.64). There was no evidence
that the effect varies according to the follow-up time (2 years minimum
and 8 years maximum) or the duration go therapy. The rate of global
relapses after 12 months was 30.0% (CI 95% 23.5 to 37.5%) which represents
an overestimate of the benefit and cost-efficacy relative of nicotine
replacement therapy when the abandon rates are only evaluated at 6
and 12 months. Most relapses of tobacco use, after the first 12 months of
cessation, occurred during the first or second year, and they were not
detectable afterwards.
12.1.1.2 Antidepressants
Scharf D, Shiffman S. Are there gender differences in smoking cessation,
with and without bupoprion? Pooled - and meta-analyses of clinical trials
of Bupoprion SR. Addiction 2004; 99(11):1462-1469.
Meta-analysis of 12 RCTs that has shown that slow release bupoprion
effectively helps smoking cessation compared to placebo (OR 2.49 CI 95%
2.06 to 3.00), with the benefit of this drugs similar in both genders. On the
Page 29 of 106
other hand it was seen that women generally have an inferior success
rate in smoking cessation regardless of the treatment used.
Wagena EJ, Knipschild P, Zeegers MP. Should nortriptyline be used as a
first-line aid to help smokers quit? Results from a systematic review and
meta-analysis. Addiction 2005; 100(3):317-326.
Systematic review and meta-analysis where nortriptyline has shown a
significant superior rate of tobacco abstinence, after 6 months, than
placebo, with RR 2.4 (CI 95% 1.7 to 3.6), and RD 0.11 (CI 95% 0.07 to 0.15).
There was a lesser rate of smoking cessation with nortriptyline compared
to bupoprion, but this difference was not statistically significant. The use of
nortriptyline in smoking cessation proved to be well tolerated and safe.
Hughes JR, Stead LF, Lancaster T. Antidepressants for smoking cessation:
Cochrane Systematic Review. Cochrane Database of Systematic Reviews
2007; Issue 1.
Systematic review which included 53 RCTs, comparing antidepressant
drugs and placebo or other therapies for smoking cessation. It was
demonstrated that bupoprion and nortriptyline helped long term smoking
cessation and that, when used in monotherapy, double the rate of
eviction (OR 1.9, CI 95%. 1.72 to 2.19 and OR 2.34, CI 95%. 1.61 to 3.4
respectively), with adverse effects rarely serious or a cause to stop the
treatment. When comparing bupoprion versus nortriptyline, a benefit was
found, although not statistically significant (OR 1.43, CI 95%, 0.9 to 2.27).
Both drugs seem to be equally effective and have shown similar efficacy
as nicotine replacement therapy; nevertheless, there is no evidence that
they provide an additional long term benefit when used concomitantly
with nicotine replacement therapy. There was no significant long term
benefit with prolonged use of bupoprion to prevent a consumption
relapse. Concerning selective serotonin recapture inhibitors, there was no
evidence of a facilitator effect in the smoking cessation.
12.1.1.3 Nicotine receptor partial agonists
Wu P, Wilson K, Dimoulas P, Mills EJ. Effectiveness of smoking cessation
therapies: a systematic review and meta-analysis. BMC Public Health
2006; 6:300.
Systematic review to study the relative efficacy of the different available
therapies to smoking cessation (nicotine replacement therapy, bupoprion,
varenicline), using as primary result the cessation at 12 months. All the
methods displayed therapeutic effects. When directly and indirectly
compared, bupoprion was not superior to nicotine replacement therapy
(OR 1.14, CI 95% 0.20 to 6.42 and OR 0.92, CI 95%, 0.64 to 1.32,
respectively) and, on the other hand, varenicline was superior to
Page 30 of 106
bupoprion (OR 1.58, CI 95% 1.22 to 2.05) in smoking cessation at 12
months. In an indirect comparison, varenicline was superior to nicotine
replacement therapy when confronted with placebo (OR 1.66, CI 95%
1.17 to 2.36, p=0.004) or with controls (OR 1.73, CI 95% 1.22 to 2.45,
p=0.001) at the end of 12 months.
Cahill K, Stead LF, Lancaster T. Nicotine receptor partial agonists for
smoking cessation: Cochrane Systematic Review. Cochrane Database of
Systematic Reviews 2007; 24(1):CD006103.
Meta-analysis proving that varenicline increases long term smoking
cessation rates (12 months) compared to placebo (OR 3.22, CI 95%, 2.43
to 4.27) or bupoprion (OR 1.66, CI 95%, 1.28 to 2.16). Nevertheless, there is
no clear evidence of its efficacy in the prevention of a relapse. The main
adverse effect of varenicline was nausea (mild to moderate degree,
decreasing with the drug habituation).
12.1.1.4 Anxiolytics
Hughes JR, Stead LF, Lancaster T. Anxiolytics for smoking cessation:
2000; Issue 4.
A systematic review whith 6 RCTs, comparing anxiolytics (diazepam,
meprobamate, buspirone, metoprolol, oxprenolol) with placebo. It was
shown that there is no consistent evidence that anxiolytics significantly
contribute to smoking cessation. Nevertheless, it was not possible to
exclude a possible effect form these drugs in dependence cessation.
12.1.1.5 Clonidine
Gourlay SG, Stead LF, Benowitz ML. Clonidine for smoking cessation:
2004; Issue 3.
Systematic review analyzing 6 small RCTs, with potential bias sources,
comparing clonidine (oral and transdermal) and placebo. It was shown
that clonidine is effective in promoting smoking cessation. Nevertheless,
important dose-dependent adverse effects may limit its use for this
indication (particularly xerostomia and sedation).
12.1.1.6 Opioid antagonists
David S, Lancaster T, Stead LF, Evins AE. Opioid antagonists for smoking
cessation: Cochrane Systematic Review. Cochrane Database of
Systematic Reviews 2006; Issue 4.
Based on the limited data from 4 RCTs, it was not possible to confirm or
exclude naltrexone’s role in smoking cessation or abstinence in the long
term.
Page 31 of 106
12.1.2 Non-pharmacologic interventions
12.1.2.1 Complementary therapies
12.1.2.1.1 Acupuncture
White A.R., Rampes H., Campbell J.L. Acupuncture and related
interventions for smoking cessation: Cochrane Systematic Review.
Cochrane Database of Systematic Reviews 2006; Issue 1
Systematic review including 24 RCTs showing that there is no consistent
evidence that acupuncture or related techniques (acupression, laser
therapy or electro stimulation) are effective interventions in smoking
cessation.
12.1.2.1.2 Hypnotherapy
Abbot NC, Stead LF, White A.R., Barnes PC. Hypnotherapy for smoking
Systematic Reviews 1998; Issue 2
Systematic review which has not demonstrated a superior effect of
hypnotherapy in smoking cessation rates at six months versus other
interventions or the absence of treatment.
12.1.2.2 Behaviour interventions
12.1.2.2.1 Self-help
Lancaster T, Stead LF. Self-help interventions for smoking cessation:
2005; Issue 3
Review based on 60 RCTs demonstrating that the use of self-help material
(leaflets or audiovisual media) increases sligthly the smoking cessation
rates, when compared to non-intervention. There was no evidence that
when associated with other interventions – such as counselling by a health
care provider or nicotine replacement therapy – the success rate
increases. There is evidence that the use of personalized material is more
effective comparatively to the use of non-personalized one, but the
effect is still of small dimension.
12.1.2.2.2 Group therapy
Stead LF, Lancaster T. Group behaviour therapy programmes for smoking
Systematic review of 55 RCTs showing that group therapy in smoking
cessation presents better results than self-help programmes and other less
intensive interventions (with material support but no support face-to-face)
– OR 2.04, CI 95%, 1.60 to 2.60; as well as non-intervention – OR 2.17, CI
Page 32 of 106
95%, 1.37 to 3.45. Nevertheless, there is no sufficiently strong evidence to
evaluate if this therapy is more effective or more cost-effective than an
individual counselling equally intensive; or even if it produces a
supplementary benefit with additional forms of therapy (such as
counselling by a health care provider or the use of nicotine replacement
therapy).
12.1.2.2.3 Telephone support
Solomon LJ, Marcy TW, Howe KD, Skelly JM, Reinier K, Flynn BS. Does
extended proactive telephone support increase smoking cessation
among low-income women using nicotine patches? Preventive medicine
2005; 40(3):306-313
The results of this RCT are consistent with a meta-analysis of other 4 RCTs,
and suggest that proactive telephone counselling, when added to
replacement therapy with nicotine OTC patches, has a favourable effect
on the smoking abstinence rates in the short term. There was no significant
effect in the long term.
Pan W. Proactive telephone counselling as an adjunct to minimal
intervention for smoking cessation: a meta-analysis. Health education
research 2006; 21(3):416-427
Meta-analysis of 22 trials studying the proactive telephone counselling as
an adjunct to minimal intervention for smoking cessation. It was found that
this type of intervention is effective in light smokers and younger men.
Stead LF, Perera R, Lancaster T. Telephone counselling for smoking
According to the 48 trials analyzed by the authors of this systematic
review, proactive telephone counselling increased the success rate of
smoking cessation, and there is a dose-response relation. The support lines
are an important help source for smokers who wish to stop smoking. The
completion of three or more calls increased the probability of cessation
comparatively to a minimum intervention (self-help material, counselling
minimal intervention, isolate pharmacotherapy).
12.1.2.2.4 Individual counselling
Lancaster T, Stead LF. Individual behavioural counselling for smoking
Systematic review that selected 21 trials related to the individual
counselling role in smoking cessation. It was shown that this type of
intervention, supplied by trained professionals in smoking cessation,
Page 33 of 106
outside the usual clinical practice environment and lasting over 10
minutes, helps smokers in eviction. There is no evidence of a doseresponse benefit for interventions longer than 10 minutes, but the
possibility of the existence of a clinically useful effect was not excluded.
12.1.2.2.5 Sequencial based behavioural intervention
Riemsma RP, Pattenden J, Bridle C, Sowden AJ, Mather L, Watt IS, Walker
A. Systematic review of the effectiveness of stage based interventions to
promote smoking cessation. BMJ 2003; 326(7400):1175-1177
The authors of this review, which included 23 RCTs, have concluded that
evidence suggests that stage based interventions are not more effective
than interventions that do not consider the behaviour changes stages or
non-intervention.
12.1.2.2.6 Relapse prevention
Hajek P, Stead LF, West R, Jarvis M, Lancaster T. Relapse prevention
Systematic review in which the authors concluded that there is not
sufficient evidence to support the use of any kind of strategies to prevent
relapses in abstinent smokers for a short period of time, in any smoking
cessation context. Most trials analyzed cognitive and behavioural
strategies to the development of competencies related to the
identification of high risk situations for relapse.
12.1.2.3 Aversive therapy
Hajek P, Stead LF. Aversive smoking for smoking cessation: Cochrane
Systematic
Review. Cochrane Database of Systematic Reviews 2001; Issue 3
Systematic review with 25 RCTs, comparing aversive therapies
(interventions that add unpleasant stimuli to the act of smoking, trying to
extinguish the latter), using inactive procedures or aversive therapies of
different intensities for smoking cessation. Based on these results, we can
conclude that the presently available evidence is insufficient to determine
the efficacy of “rapid smoke” (aversive therapy method that requires
several smoke inhalations within very few seconds between each
inhalation) or the existence of a dose-response to the aversion stimulation.
Other aversion methods (lighter forms of the “rapid smoke” method) do
not seem to have specific efficacy. In order to achieve a correct
evaluation of aversion therapy, we would have to conduct more trials
with the adequate methodology.
Page 34 of 106
12.1.3 Special populations
12.1.3.1 Cardiovascular patients
Wiggers LC, Smets EM, de Haes JC, Peters RJ, Legemate DA. Smoking
cessation interventions in cardiovascular patients. European Journal of
Vascular and Endovascular Surgery 2003; 26(5):467-475.
Systematic review which analysed the few available trials on smoking
cessation in cardiovascular patients. In this group, there was no evidence
of efficacy for most interventions (nicotine replacement therapy or other
pharmacological therapy, self-help materials, individual, group or
telephone counselling). There is limited evidence of the efficacy of
medical or nurse counselling.
Ludvig J, Miner B, Eisenberg MJ. Smoking cessation in patients with
coronary artery disease. Am Heart J 2005; 149(4):565-572
A systematic review of 33 randomized, double-blind clinical trials
demonstrated that the auxiliaries to smoking cessation (nicotine in the
several marketed forms, bupoprion and behavioural therapy) cause, in
patients with coronary artery disease, a modest increase in abstinence
rate at 12 months, versus placebo.
Barth J, Critchley J, Bengel J. Efficacy of psychosocial interventions for
smoking cessation in patients with coronary heart disease: a systematic
review and meta-analysis. Annals of behavioural medicine: a publication
of the Society of Behavioural Medicine 2006; 32(1):10-20
Systematic review of 19 RCTs evaluating the efficacy of psychosocial
interventions in smoking cessation in patients with coronary heart disease.
It was seen that psychosocial interventions (behavioural approaches,
telephone support, self-help material) have a positive role in smoking
cessation with OR of 1,66 (CI 95%, 1,24 to 2,21), vs. the usual treatment of
patients, but they have to be provided during a minimum period of 1
month.
12.1.3.2 Pregnancy
Lumley J, Oliver SS, Chamberlain J, Oakley L. Interventions for promoting
smoking cessation during pregnancy: Cochrane Systematic Review.
Systematic review of 64 trials (including 51 RCTs) related to the smoking
cessation interventions during pregnancy. The smoking cessation
programmes reduced the proportion of smoking women, the occurrence
of low weight at birth and pre term labour. The analysis relating to the
change in the occurrence of very low weight at birth, stillborns and perior neonatal death was not statistically significant.
Page 35 of 106
12.1.3.3 Psychiatric disease
Hitsman B, Borrelli B, McChargue DE, Spring B, Niaura R. History of
depression and smoking cessation outcome: a meta-analysis. Journal of
Consulting and Clinical Psychology 2003; 71(4):657-663
Meta-analysis of 15 trials which showed that the existence of previous
history of major depression does not seem to be an independent risk
factor for the cessation failure, in the short or long term, in a smoking
cessation programme.
Prochaska JJ, Delucchi K, Hall SM. A meta-analysis of smoking cessation
interventions with individuals in substance abuse treatment or recovery.
Journal of Consulting and Clinical Psychology 2004; 72(6):1144-1156
Systematic review of 19 RCTs showing that the smoking cessation
interventions with individuals in substance abuse treatment programmes
where effective in the short term, whether to patients in treatment or in
recovery, being nevertheless ineffective in the long run. It was also seen
that these interventions seem to promote alcohol or illicit substances long
term abstinence.
12.1.3.4 Young people
Sussman S, Sun P, Dent CW. A meta-analysis of teen cigarette smoking
cessation. Health psychology: official journal of the Division of Health
Psychology, American Psychological Association 2006; 25(5):549-557
Systematic review of 48 trials analyzing the smoking cessation rates in
teenagers. There were superior rates of cessation in the short and long run
in patients included in smoking cessation programmes; the rates were
slightly superior in the programmes lasting longer than 5 sessions, which
included a motivational component, cognitive behavioural techniques
and social influence approaches, conducted in scholar clinics and within
the school class.
Grimshaw GM, Santon. Tobacco cessation interventions for young people.
Systematic review of 15 randomized and non-randomized clinical trails,
evaluating the smoking cessation strategies efficacy in young people
under 20. There was no consistent evidence of efficacy of any
intervention to increase the rates of smoking cessation for 6 months in a
row. Nevertheless, multiple component interventions have shown a
degree of persistent abstinence (30 days of occasional abstinence
prevalence at 6 months), particularly the one that included elements of
the “change stages” model. Presently, there is no available evidence
Page 36 of 106
supporting the use of pharmacological therapy (nicotine or bupoprion) in
teenager smokers.
12.1.3.5 Hospitalized smokers
Rigotti NA, Munafo MR, Murphy MFG, Stead LF. Interventions for smoking
cessation in hospitalised patients: Cochrane Systematic Review.
Systematic review of 17 trials related to interventions in hospitalised
patients. It was shown that behavioural interventions - which include
contact during hospitalization and at least one month of follow-up - are
effective in promoting smoking cessation in hospitalised patients. Nicotine
replacement therapy increased smoking cessation rates.
12.1.3.6 Preoperative patients
Møller A, Villebro N. Interventions for preoperative smoking cessation:
2005; Issue 3
Systematic review of 4 trials related to preoperative smoking cessation. It
was seen that preoperative interventions for smoking cessation were only
effective in the peri-operative period; the abstinence was not significantly
kept in the long run. The data on the smoking cessation effects in the
postoperative complications are contradictory.
12.1.3.7 Chronic obstructive pulmonary disease (COPD) patients
Van der Meer RM, Wagena EJ, Ostelo RWJG, Jacobs JE, Van Schayck CP.
Smoking cessation for chronic obstructive pulmonary disease: Cochrane
Systematic Review. Cochrane Database of Systematic Reviews 2001; Issue
1
Systematic review including 5 RCTs, 2 with high quality, analyzing the
smoking cessation efficacy in chronic obstructive pulmonary disease
(COPD) patients. The authors have concluded that the combination of
pharmacological and psychosocial therapy was superior to the
psychosocial therapy isolated or the absence of treatment. Nevertheless,
there was no sufficiently strong evidence that isolated psychosocial
therapy increases the success rate for smoking cessation in COPD
patients, when compared to the non-existence of therapy.
12.1.4 Role of health care providers
Gorin SS, Heck JE. Meta-analysis of the efficacy of tobacco counselling by
health care providers. Cancer epidemiology, biomarkers & prevention
2004; 13(12):2012-2022
Based on 37 trials’ results it was seen that contact and counselling from
health care providers increased smoking cessation rates. The most
Page 37 of 106
effective interventions were performed by doctors,
multidisciplinary teams, dentists and, finally, nurses.
followed
by
Mojica WA, Suttorp MJ, Sherman SE et al. Smoking-cessation interventions
by type of provider: a meta-analysis. Am J Prev Med 2004; 26(5):391-401
Meta-analysis in which the interventions from psychologists, doctors or
nurses have increased smoking cessation rates. Nicotine replacement
therapy increased, approximately to the double, the intervention efficacy
with most professionals.
Sinclair HK, Bond CM, Stead LF. Community pharmacy personnel
Systematic review of 2 RCTs concluding that there is evidence (although
with a limited weight) that counselling plus support programme with data
registry given by trained professionals in the context of a communitarian
pharmacy, may have a positive effect on the smoking cessation rates.
Lancaster T, Stead LF. Physician advice for smoking cessation: Cochrane
4
Systematic review of 39 RCTs, where a brief doctors’ counselling
compared to the non-existence of counselling, has shown a small yet
significant effect in smoking cessation rates (OR 1.74, CI 95%, 1.48 to 2.05).
There was no sufficient evidence, from indirect comparisons, to establish a
significant difference in medical counselling with the intensity of the
intervention, the amount of available follow-up or the use of support
materials. A comparison between intensive counselling and minimum
counselling has shown a small advantage in the first one (OR 1.44, CI 95%,
1.24 to 1.67). The direct comparisons have also shown a small benefit in
follow-up visits.
Carr AB, Ebbert JO. Interventions for tobacco cessation in dental setting.
Cochrane
Database of Systematic Reviews 2006, Issue 1
Systematic review of 6 clinical trials evaluating the efficacy of dentists’
interventions in smoking cessation, whether in practice or within the school
health context. The available evidence suggests that behavioural
interventions made by oral health professionals, together with a
component of oral/dental evaluation, can increase smoking cessation
rates among users of non-smoked types of tobacco (e.g. chewing
tobacco). Only one trial included real smokers, and therefore we have no
Page 38 of 106
sufficient evidence to draw any conclusion on the efficacy of the
intervention in that group.
Rice VH, Stead L. Nursing intervention and smoking cessation: metaanalysis update. Heart & lung: the journal of critical care 2006; 35(3):147163
Systematic review of 34 randomized clinical trials. Is spite of the
heterogeneous results, it has shown that nursing interventions, whether in
the hospital or in ambulatory, increased the smoking cessation probability.
12.1.5 Special topics
12.1.5.1 Community interventions
Secker-Walker RH, Gnich W, Platt S, Lancaster T. Community interventions
for reducing smoking among adults: Cochrane Systematic Review.
Systematic review of 37 controlled trials comparing communities with
smoking cessation intervention programmes with control communities. It
was shown that there is no impact of community interventions in smokers’
prevalence. This work suggests that community approach will remain as
an important part in health promotion activities but we have to consider
its limited effect when planning the magnitude of projects and resources
to use.
12.1.5.2 Workplace interventions
Fichtenberg CM, Glantz SA. Effect of smoke-free workplaces on smoking
behaviour: systematic review. BMJ 2002; 325:188-190
The analysis of 26 clinical trials showed that totally smoke-free workplaces
are associated to reductions of smoking prevalence of 3.8% (CI 95%, 2.8%
to 4.7%) and less 3.1 (2.4 to 3.8) smoked cigarettes per day in workers who
maintain smoking habits.
Smedslund G, Fisher KJ, Boles SM, Lichtenstein E. The effectiveness of
workplace smoking cessation programmes: a meta-analysis of recent
studies. Tobacco control 2004; 13(2):197-204
Meta-analysis of 19 clinical trials, showing that workplace interventions for
smoking cessation have a short term benefit. This was found both in the
randomized and in the non-randomized groups of trials, and they both
presented an adequate statistical homogeneity. The beneficial effect
seems to vanish with time, disappearing after 12 months.
Page 39 of 106
Moher M, Hey K, Lancaster T. Workplace interventions for smoking
Review studying the efficacy of workplace interventions for smoking
cessation; all the interventions already considered effective, such as
group therapy, individual counselling and nicotine replacement therapy
have shown to be equally effective in the workplace. Self-help methods
have been less effective. Prohibition and smoking restrictions in workplace
have reduced smoking incidence in workplace but it was not clear that
the active use prevalence or total smoking load have been reduced.
Social and environmental interventions, incentives, competitions and
programmes with different types of interventions do not present evident
advantages.
12.1.5.3 Incentives
Kaper J, Wagena EJ, Severens JL, Van Schayck CP. Healthcare financing
systems for increasing the use of tobacco dependence treatment:
2005; Issue 1
Systematic review analyzing RCTs, CTs and ITS that has shown evidence
(although with a limited weight) that the use of financing systems that
eliminate the smoking cessation programme costs for the patient may
increase smoking cessation rates in the long term, when compared to
systems that only reduce or do not change that treatment cost. Presently,
there is no sufficient evidence in order to evaluate the effects of monetary
incentives given to health care providers in order to identify and treat
smoking people.
Hey K, Perera R. Competitions and incentives for smoking cessation:
2005; Issue 2
Systematic review of 15 RCTs, concluding that economical incentives and
competitions do not seem to increase smoking cessation rates in the long
term; nevertheless, they may increase recruiting rates for cessation
attempt, and indirectly the absolute number of individuals that
successfully cease smoking.
Hey K, Perera R. Quit and Win contests for smoking cessation: Cochrane
2
4 RCT selected to study the impact of contests “Quit and Win” in smoking
cessation. The authors concluded that local and regional contests seem
to increase smoking cessation rates; nevertheless, the impact in the
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smoking prevalence in the population is small. These contests can induce
deception levels in the participants that may compromise the validity of
the intervention. International contests may be an effective mechanism,
mainly in developing countries, but we can not draw safe conclusions, as
there are no adequate studies available.
12.1.5.4 Biomedical risk assessment
Bize R, Burnand B, Mueller Y, Cornuz J. Biomedical risk assessment as an aid
for smoking cessation: Cochrane Systematic Review. Cochrane Database
of Systematic Reviews 2005; Issue 4
Systematic review of 8 RCTs, concluding that, to date, there is no good
evidence on the biomedical risk assessment efficacy (physiological
parameters determination aiming to provide smokers with a measure of
the smoking harmful effects) as an incentive to smoking cessation.
12.1.5.5 Partner support
Park E-W, Schultz JK, Tudiver F, Campbell T, Becker L. Enhancing partner
support to improve smoking cessation: Cochrane Systematic Review.
Systematic review of 9 RCTs, in which the interventions to enhance nonsmoking partner support to improve smoking cessation do not show
increases in long term cessation rates. Nevertheless, we can not draw
conclusions on the real impact of this strategy, since limited data from
some trials suggest that these interventions did not successfully change
the support provided by the partners.
12.1.5.6 Physical exercise
Ussher M. Exercise interventions for smoking cessation: Cochrane
1
Systematic review in which only 1 of the 11 RCTs analysed presented
evidence that exercise was beneficial to smoking cessation on the long
term. All the other trials presented several methodological limitations or
included only a moderate exercise programme, insufficient to attain the
desired level of exercise; therefore, we can not trustworthily exclude an
effect of this type of intervention.
12.1.5.7 Health care provider training
Lancaster T, Silagy C, Fowler G. Training health professionals in smoking
This review concluded that specifically trained professionals in smoking
cessation have a greater probability of identifying smokers and
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consequently to propose abstinence strategies. Nevertheless, there is no
significant evidence that the mentioned training may in any way change
the smoking habits of their patients.
Anderson P, Jane-Llopis E. How can we increase the involvement of
primary health care in the treatment of tobacco dependence? A metaanalysis. Addiction 2004; 99(3):299-312
Systematic review of 19 trials in which primary health care professionals
were involved in the treatment of smoking addiction increasing the
tracing rates, counselling and cessation of their patients. The
administration of educational interventions, to learning professionals, and
the combination of these with practical support, to established
professionals, has proven to be an efficient strategy.
12.1.5.8 Passive smoking
Roseby R, Waters E, Polnay A, Campbell R, Webster P, Spencer N. Family
and career smoking control programmes for reducing children's exposure
to environmental tobacco smoke: Cochrane Systematic Review.
Systematic review of 18 RCTs on all kinds of mechanisms eventually
involved in the prevention of children’s exposure to environmental
tobacco smoke, including active children care providers (0-12 years).
Presently we have no sufficient evidence to conclude which is the most
effective intervention to reduce parents’ smoking within children health
practice environment.
12.2 Excluded trials
Stead LF, Hughes JR. Lobeline for smoking cessation: Cochrane Systematic
This drug is not available in Portugal.
Lancaster T, Stead LF. Silver acetate for smoking cessation: Cochrane
3
Lancaster T, Stead LF. Mecamylamine (a nicotine antagonist) for smoking
Page 42 of 106
Rosen CS. Is the sequencing of change processes by stage consistent
across health problems? A meta-analysis. Health psychology: official
journal of the Division of Health Psychology, American Psychological
Association 2000; 19(6):593-604
This review refers only to the analysis of the intervention method by stage
per si.
Melvin CL, Dolan-Mullen P, Windsor RA, Whiteside HPJ, Goldenberg RL.
Recommended cessation counselling for pregnant women who smoke: a
review of the evidence. Tobacco control 2000; 9 Suppl 3: III80-III84
This study was excluded since it was a narrative review.
Wilson K, Gibson N, Willan A, Cook D. Effect of smoking cessation on
mortality after myocardial infarction: meta-analysis of cohort studies. Arch
Intern Med 2000; 160(7):939-944.
This study approaches the benefits but not the smoking cessation
methods.
Khuder SA, Mutgi AB. Effect of smoking cessation on major histologic types
of lung cancer. Chest 2001; 120(5):1577-1583
methods.
McClure JB. Are biomarkers a useful aid in smoking cessation? A review
and analysis of the literature. Behavioural medicine (Washington, DC)
2001; 27(1):37-47
Wagena EJ, Zeegers MP, Huibers MJ, Chavannes NH, Van Schayck CP.
Bupoprion: an effective new aid for smoking cessation. Nederlands
tijdschrift voor geneeskunde 2001; 145(2):103-104
The article was written in Dutch, there was no international language
translation available.
Sansores RH, Ramirez-Venegas A, Espinosa-Martinez M, Sandoval RA.
Treatments to quit smoking, available in Mexico. Salud pública de México
2002; 44 Suppl 1:S116-S124
Le Foll B, Aubin HJ, Lagrue G. Behavioural and cognitive therapy to break
the smoking habit. Review of the literature. Annales de médecine interne
2002; 153(3 Suppl):1S32-1S40
Page 43 of 106
Maeda K, Noguchi Y, Fukui T. The effects of cessation from cigarette
smoking on the lipid and lipoprotein profiles: a meta-analysis. Preventive
medicine 2003; 37(4):283-290
methods.
Tingle LR, DeSimone M, Covington B. A meta-evaluation of 11 schoolbased smoking prevention programmes. The Journal of school health
2003; 73(2):64-67
This review evaluates only the programmes but not their outcomes.
Polanska K, Hanke W, Sobala W. Meta-analysis of prenatal smoking
cessation interventions. Przeglad Epidemiologiczny 2003; 57(4):683-692
The article was written in Polish, there was no international language
translation available.
Huibers MJH, Beurskens AJHM, Bleijenberg G, Schayck CP. Psychosocial
interventions delivered by general practitioners: Cochrane Systematic
Review to evaluate the efficacy of psychosocial interventions by the
family doctor in a wide range of disturbances, including only 2 trials on
smoking cessation, one of which was of low quality. The existence of other
works with scientific evidence of excellent quality that have evaluated
directly this counselling, determined the exclusion.
Critchley J, Capewell S. Smoking cessation for the secondary prevention
of coronary heart disease: Cochrane Systematic Review. Cochrane
Database of Systematic Reviews 2003; Issue 4
methods.
Lee PN, Sanders E. Does increased cigarette consumption nullify any
reduction in lung cancer risk associated with low-tar filter cigarettes?
Inhalation toxicology 2004; 16(13):817-833
methods.
Mooney M, White T, Hatsukami D. The blind spot in the nicotine
replacement therapy literature: assessment of the double-blind in clinical
trials. Addictive behaviours 2004; 29(4):673-684
Page 44 of 106
This study focuses the methodology of selection of papers on nicotine
replacement therapy, but does not mention other smoking cessation
methods.
Park EW, Tudiver F, Schultz JK, Campbell T. Does enhancing partner
support and interaction improve smoking cessation? A meta-analysis.
Annals of family medicine 2004; 2(2):170-174
The existence of a systematic review, with scientific evidence of excellent
quality, published in Cochrane Library, including the same authors and
more recently published studies, has determined the exclusion.
Rice VH, Stead LF. Nursing interventions for smoking cessation: Cochrane
1
The existence of an updated version of this systematic review, included in
the present CPG, has determined the exclusion.
Woodward M, Lam TH, arzi F et al. Smoking, quitting, and the risk of
cardiovascular disease among women and men in the Asia-Pacific
region. Int J Epidemiol 2005; 34(5):1045-1046
methods.
White A, Moody R. The effects of auricular acupuncture on smoking
cessation may not depend on the point chosen--an exploratory metaanalysis. Acupuncture in medicine 2006; 24(4):149-156.
This meta-analysis was developed based on controlled non-randomized
trials. Given the existence of a systemic review, exclusively based in RCTs,
on the same subject, we chose to exclude this article.
Stead LF, Lancaster T. Nicobrevin for smoking cessation: Cochrane
Systematic
Green JP, Jay Lynn S, Montgomery GH. A meta-analysis of gender,
smoking cessation, and hypnosis: a brief communication. The International
journal of clinical and experimental hypnosis 2006; 54(2):224-233
Excluded study as it approaches the gender role in the hypnoses success
and not the hypnoses technique role per si in smoking cessation.
Page 45 of 106
13. Practical interventions
13.1 Pharmacological interventions
As previously discussed, tobacco is a risk factor for several diseases, and
smoking cessation is a challenge, both to smokers and health
professionals who guide and stimulate their attempts to stop smoking.
Presently there are several pharmacological therapies available to
smokers aiming to reduce the smoking craving and decrease abstinence
symptoms.
13.1.1 Nicotine replacement therapy (NRT)
Nicotine replacement therapy is largely used to replace the nicotine
levels smokers acquire by inhaling tobacco smoke. The NRT efficacy in
smoking eviction was proven in many studies.
In the West and Shiffman26 review, published in 2001, 12 clinical trials
were included, evaluating the NRT effects in abstinence symptoms and in
smoking craving. Based on the results, the authors concluded that there is
strong evidence that NRT reduces discomfort (6 out of 7 trials), irritability (9
out of 9 trials) and anxiety (3 out of 4 studies) and some evidence of a
beneficial effect in decreasing depressive humour and smoking craving
(in the latter, nicotine gums were not so effective). Nevertheless, they
underline the need for trials with better methodological quality and more
comprehensive descriptions.
According to the analysis conducted by Etter and Stapleton27,
including 12 RCTs with placebo, a unique course of NRT for a period
varying between 2 to 8 years has also shown benefit in smoking cessation,
without evidence that this effect varies according to the duration of the
initial therapy or the follow-up periods. The global relapse rate after 12
months was 30%, drawing attention to the possibility of an over estimate of
the benefit and cost-effectiveness of the replacement treatment, when
we only evaluate quit rates at 6 and 12 months. Most relapses after the
first 12 months have occurred during the first or the second year, and
were not detectable later. Nevertheless, and in spite of the exceptions
related to the bias induced by short follow-up periods (6 and 12 months),
smoking cessation benefits were confirmed by a systematic review,
published in 2006 by Wu et al28, that compared different smoking
cessation therapies (NRT, bupoprion, varenicline) at 12 months. In 70 RCTs,
comparing NRT to a control group, a significant benefit with NRT was
found, confirmed by the advantage of NRT versus placebo in 49 RCTs.
As there are several pharmaceutical forms of nicotine replacement
therapies, Silagy29 evaluated, in 2004, 103 RCTs demonstrating that all
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marketed pharmaceutical forms are effective in smoking cessation and
that there is no evidence, by indirect comparison, of a significant
difference between the different forms, namely in transdermal patches or
gums. These results seem to be independent of the duration or context in
which the therapy is applied and the intensity of additional support
provided to the patient. Also according to this publication, the association
of different forms of NRT recommended by the U.S. Department of Health
and Human Services CPG30, was proven to be beneficial, although this
evidence is presented with some reserve, due to the heterogeneity of the
available studies. The combination of nicotine patches with a selfadministered form of NRT may be recommended to smokers who are not
successful with a single type of 1st line pharmacotherapy. In highly
dependent smokers (Fagerström score ≥7) a significant benefit was found
with the use of 4 mg gums, instead of 2 mg, and, in this group, there was a
low quality evidence supporting the combination of different forms of NRT.
Only one clinical trial compared NRT with other pharmacological
treatments, showing higher rates of smoking cessation when bupoprion
was associated to a placebo patch comparatively to the use of nicotine
patches plus a placebo tablet. More studies are needed to evaluate the
association of NRT with other drugs.
Assuming that the efficacy of NRT is independent of the association
with non-pharmacological therapies, Hughes et al31 published in 2003 the
results of a meta-analysis of 4 RCTs which proved NRT over the counter
(OTC) efficacy versus placebo. This review included two randomized
studies and two non-randomized trials, comparing NRT subject and nonsubject to medical prescription, which presented non-homogenous
results, but that, when combined via random effects mode, have
produced a OR higher that 1 (1.4, CI 95%, 0.6 to 3.3); the authors could
therefore conclude that OTC NRT was as effective as NRT subject to
medical prescription.
Comparing the efficacy of this therapy in men and women,
Cepeda-Benito32 evaluated 21 double blind, randomized trials versus
placebo, showing that NRT, together with non intensive nonpharmacological support, is more effective than placebo in men at 3, 6
and 12 months. In women, the benefit was only found at 3 and 6 months,
so it was concluded that in this group the association of intensive
pharmacological support is even more important.
13.1.2 Antidepressants
The idea that smoking cessation may induce depression and that nicotine
itself may have an antidepressant effect has promoted the use of
bupoprion and nortriptyline in smoking cessation attempts.
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We have identified four systematic reviews discussing this issue. In
the first one, a meta-analysis of 12 RCTs published by Scharf and
Shiffman33 in 2004 in the journal Addiction, the differences between
genders in smoking cessation were analyzed with or without bupoprion; in
the second one, published in 2005, also in Addiction by Wagena34, 5 RCTs
were analyzed, comparing nortriptyline with bupoprion or placebo; the
third one, published in 2006 by Wu et al28, compared the result of different
smoking cessation therapies (nicotine replacement therapy, bupoprion,
varenicline) at 12 months; the fourth one was published in Cochrane
Library in 2007, by Hughes et al35, studying the efficacy of antidepressant
therapy in smoking cessation, and it included 53 trials (40 of which on
bupoprion and 8 on nortriptyline).
So, when used isolated, and according to Scharf33 and Hughes35
reviews, bupoprion presents an effective aid effect to smoking cessation
comparatively to placebo. The first study has demonstrated that the
benefit of this drug is equal in men and women; however, there was
evidence that women presented a lower success rate regardless of the
treatment used.
Also in Hughes and Wagena studies, nortriptyline has shown benefit
compared to placebo in the smoking abstinence rate evaluated at 6 and
12 months. The second study certified this difference as higher in the first
months of treatment, and the number of abstinent people increased
faster in smokers taking nortriptyline. Both studies showed that bupoprion
achieved greater abstinence rates comparing to nortriptyline, but the
difference was not statistically significant.
When compared to NRT, bupoprion and nortriptyline seem to have
a similar efficacy, and there is no evidence that adding these
antidepressants to NRT increases long term cessation (Hughes et al.).
Through a direct and indirect comparison, Wu et al did not demonstrate
as well a statistically significant advantage of bupoprion versus NRT.
These two antidepressants are effective regardless of the present or
former history of depression, and the adverse effects are rarely serious or
causing the treatment withdrawl, if the usual recommended dosage to
smoking cessation is respected.
There was no evidence of a significant benefit, in the long term, of
the prolonged use of bupoprion to prevent relapses35.
In what concerns selective inhibitors of serotonin recapture, there
was no significant benefit in smoking cessation > 12 months, with this class
of drugs35.
13.1.3 Partial agonists of nicotine receptors
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Partial nicotine agonists aim at reduction of smoking abstinence
symptoms and the pleasure gained by tobacco smoke, and varenicline is
the only molecule of this group available in the Portuguese market.
In 2007, Cahill et al36, published in Cochrane Library a systematic
review evaluating the efficacy and tolerability of partial agonists of
nicotine receptors, including 5 RCTs. The authors have identified a
significant increase in smoking cessation rates in the long term (12
months), in patients treated with varenicline compared to placebo or
bupoprion.
Likewise, in the reviews by Hughes et al35 and Wu et al28, quoted
above, varenicline proved to be, by direct comparison, superior to
bupoprion. In the last trial it was also seen a greater efficacy of varenicline
face to NRT by indirect comparison, versus placebo and all the control
groups.
In spite of the evidence of varenicline efficacy in smoking cessation,
several authors consider it necessary to conduct comparative trials
between varenicline and NRT and more trials versus bupoprion, as well as
more trials to evaluate its efficacy in the treatment of relapses.
13.1.4 Anxiolytics
Anxiety may be an important component in the failure of smoking
cessation attempts, so several authors have pondered the use of
anxiolytics as helper in smoking cessation.
In a systematic review published in 2000 in Cochrane Library,
Hughes, Stead and Lancaster37, reviewed 6 RCTs studying different
anxiolytics (diazepam, meprobamate, motoprolol, oxprenolol and
buspirone) but none of the trials has shown evidence of a beneficial
effect from any of these drugs. Nevertheless, the confidence intervals
were wide, so the exclusion of a possible favourable effect can not be
definitive. More trials are required in order to clarify the real role of this
class of drugs.
13.1.5 Other pharmacological classes
13.1.5.1 Clonidine
Clonidine belongs to the central alfa-2 agonists class, used primarily as
anti-hypertensive therapy and the treatment of opioid abstinence; its use
has been recently proposed for smoking cessation.
Gourlay e Stead38 evaluated the use of clonidine in smoking
cessation therapy, after 12 months of follow-up, through 6 RCTs that
included potential bias sources, and the benefit of this therapy was
statistically significant versus placebo. Nevertheless, adverse effects such
as xerostomia or sedation were very frequent. According to these authors,
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transdermal clonidine may be indicated as a 2nd line drug, and its
sedative effect may be useful in specific patients. It requires a careful
vigilance in order to adjust the dose and monitor potential serious adverse
effects.
13.1.5.2 Opioid antagonists
Assuming the role of the opioid system in the pleasure of smoking, David
et al39, conducted a systematic review to evaluate the role of the opioid
antagonists in smoking cessation. They did not identify studies with long
term follow-up of therapies with naloxone or buprenofine. Based on the
data of only 4 RCTs, there was no significant difference between
naltrexone and placebo in quit or long term abstinence rates (OR 1.26 CI
95%, 0.80 to 2.01). Nevertheless, since the confidence interval is very wide,
evidence does not allow the exclusion of some efficacy of this drug, and
so it is necessary to conduct larger clinical trials in order to make practical
recommendations.
13.2 Non-pharmacological interventions
13.2.1 Complementary therapies
13.2.1.1 Acupuncture
White et al40 review, exclusively based in RCTs, has shown that there is no
consistent evidence that acupuncture and related techniques (digit
pressure, laser therapy and electro stimulation) are effective interventions
in smoking cessation, since it is not possible to prove that the effect of
these techniques is a placebo effect. Nevertheless, the selected studies
are heterogeneous and present several methodological flaws, thus
justifying the need for further trials in order to draw firm conclusions.
13.2.1.2 Hypnotherapy
The systematic review by Abbot et al41, published by Cochrane Library,
has not shown a superior effect of hypnotherapy in smoking quit rates at
six months versus another interventions, or the absence of treatment.
Nevertheless, some consideration has to be made relating to the
evaluation of this technique. Firstly, in order to identify a positive effect of
hypnotherapy in smoking cessation, versus the absence of treatment, we
should exclude the non-specific effects conditioned by the presence of a
therapist. This verification is made difficult by the non-existence of a
suitable placebo. Secondly, since it was not possible to prove the efficacy
of other behavioural interventions, the comparison of the latter with
hypnotherapy becomes a problem.
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In future trials, the investigators should consider the definition and
description of the type of hypnotherapy used and the comparison with
active interventions (preferably with an equivalent duration of contact
with the therapist).
13.2.2 Behavioural interventions
All the studies published within this area agreeon the methodological
difficulties associated with the evaluation of different behavioural
interventions.
The evaluation of efficacy of behavioural therapy is more difficult
than the pharmacological therapy. This fact is related to the difficulty in
defining an adequate control and keeping the necessary conditions for a
double blind trial (the smoker and the therapist usually know the group
which they belong to). The standardization of the health care providers’
attitude is a complex process, and many times it is accepted that the
same method, applied by different professionals, may lead to different
results. Whenever the therapeutic method is known by those who apply it
and there is a formed opinion on the efficacy of each one of the
interventions being studied, a performance bias may be induced. This is
also possible whenever the same therapists apply different methods.
The design of trials of behavioural interventions, usually with multiple
treatment arms to identify the effective therapeutic element, makes it
difficult to explicitly predefine control groups. Nevertheless, and in
opposition to what is seen when evaluating pharmacological
interventions, the choice of an adequate control for a behavioural
intervention poses serious problems, since it will hardly be equivalent to
the non-specific effects of the study method.
13.2.2.1 Self-help
There is evidence, in a small dimension, of the systematic review of
Lancaster e Stead42 in Cochrane Library, that self-help materials for
smoking cessation can increase the number of individuals who stop
smoking, comparatively to the absence of treatment. These materials
were defined as leaflets, audiovisual media or computer programmes,
which may be used by smokers as adjuvant factors in the attempt of
quitting smoking without the help of a health care provider, therapist or
therapy group.
Personalized self-help materials seem to be the most effective. They
can produce a superior effect relatively to the non-personalized ones,
being more attractive and easier to read, and they can be used by a
higher number of people. Nevertheless, it is difficult not to confuse this
type of materials with the ones that require additional contacts. On the
other hand, it was seen that help advices to smoking cessation are
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currently widely spread among the entire population. This
“contamination” may complicate the demonstration of the standard selfhelp programmes, since the control group and the experimental one may
have suffered similar interventions.
The necessary evidence to determine which are the theoretical
models and the most important elements to the individualization of the
materials is insufficient. All studies suggest that the supply of self-help
materials, together with health care providers counselling, does not
improve the results. Likewise, there is small evidence of the effect of
adding self-help materials to nicotine replacement therapy.
There were no studies with direct comparison between self-help
materials and minimal counselling interventions.
The authors consider that self-help interventions are probably most
suitable to smokers who are not in contact with the health system (since
individualized interventions depend on the capacity to obtain baseline
data). All smokers who seek help will probably benefit more from a brief
counselling or personalized materials. Internet may be an important
vehicle to provide smokers access to individualized resources.
13.2.2.2 Group therapy
Stead e Lancaster43 analyzed group therapy as an aid to smoking
cessation, in the systematic review published by the Cochrane Library.
They enumerate several particularities that hinder the evaluation of the
role of group therapy in smoking cessation, namely the difficulty to
explicitly define experimental groups (different approaches are tested in
one single study), the non-existence of an adequate control group and
variations in the characteristics of the groups. There is not sufficient
evidence to identify which elements in group therapy are the most
important to the success of smoking cessation.
In spite of these interventions having at first glance a more
favourable cost-effectiveness relatio than one individual one, there are no
trials to consubstantiate a comparative efficacy between the two
approaches.
On the other hand, to attend a therapy group the smoker must
have not only the will to quit smoking, but also the time and effort needed
to participate in the sessions.
The comparison between a therapy group and another with no
intervention supports the conclusion that the group programmes may
help smoking cessation, in spite of not providing evidence on the specific
benefit of this therapy.
There is reasonable evidence that group therapy is superior to selfhelp in smoking cessation, but there is no evidence that the meeting with
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other smokers, alone, is superior to brief or intensive individual counselling,
and that its association with NRT is superior to its use alone.
One can assume that behavioural and pharmacological
interventions contribute in an independent way, to the success of smoking
cessation. As such, group therapy may be considered as one of the
constituents to include in a multifactorial intervention.
13.2.2.3 Telephone counselling
Three systematic reviews were identified, studying the role of telephone
counselling in smoking cessation. A rigorous evaluation of reactive
services, such as aid telephone lines, has been made difficult since it is not
possible to develop randomized trials in which the adequate support is
denied to some individuals who contact those services, preventing the
formation of a comparative group.
In the systematic review from Cochrane Library, conducted by
Stead et al44 the role of telephone counselling was evaluated, whether
pro-active (initiated by the health care provider) or reactive (initiated by
the smoker, through aid lines); there was a slight benefit in adding
telephone counselling to pharmacotherapy. It provides smokers with a
route of access to smoking cessation support and the call-back
counselling increases their utility. Within this counselling there is a doseresponse relationship, that is, the accomplishment of three or more
telephone calls increases the odds of quitting, comparatively to a minimal
intervention (self-help material, counselling minimal intervention, isolated
pharmacotherapy).
The meta-analysis, conducted by Pan45, evaluated 22 trials and the
pro-active telephone counselling role as adjuvant to minimal intervention
to smoking cessation. It was seen that this type of intervention is effective
in younger males who smoke <10 cigarettes per day.
Solomon et al46 review concluded that pro-active telephone
counselling, when added to transdermal patches of NRT provided at no
cost, has a favourable effect on the short term abstinence rates. There
was no long term significant result.
13.2.2.4 Individual counselling
The systematic review by Lancaster et al47 studied the role of individual
counselling to smoking cessation. Individual counselling was defined as a
face-to-face meeting between a smoker and a therapist with trained
competencies to help him stop smoking. Different types of behavioural
approaches were accepted and all the interventions initiated by
professionals within their usual practice context were excluded, in order to
avoid a possible confounding bias. Individual counselling (lasting over ten
minutes) was more effective than the control with a minimum contact
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(lasting less than ten minutes) with the therapist. There was no evidence of
a dose-response effect with the increase in counselling intensity over the
10 minutes period (in spite of, statistically, not being possible to exclude
the possibility of a clinically useful effect).
There was no significant additional benefit when individual
counselling was provided to smokers under NRT. This fact can only
indicate that, in this context, additional relative benefit is small, since quit
rates in control groups were increased by the use of effective
pharmacotherapy.
It is concluded that interventions such as individual counselling,
given by smoking cessation trained professionals, outside the scope of
usual clinical practice and lasting over 10 minutes, help smokers in
smoking cessation.
13.2.2.5 Stage based behavioural intervention
The stage based intervention is a type of behavioural intervention in which
individuals are classified in five stadiums: pre-contemplation,
contemplation, preparation, action, maintenance. This type of
intervention is based on the hypothesis that the actions that consider the
stage of the behavioural change process where the individual is will be
more effective and efficient than an identical intervention in all stages.
In the trials selected for the systematic review by Riemsma et al48,
the efficacy of stage based behavioural interventions showed a
heterogeneous methodological quality of the trials; few referred the
validation of the scale used to determine the change stage; there was no
homogeneity in the type of intervention defined for each of the stages;
and the description of the interventions was sometimes very limited and
not sufficient to draw conclusions on the adequacy to the defined stage.
13.2.2.6 Prevention of relapse
Different strategies to prevent relapses after a well succeeded smoking
cessation process were evaluated. It should be noted that there is no
clear distinction between treatments to prevent relapses and prolonged
treatments for smoking cessation. Nevertheless, we consider interventions
to prevent relapses, those that explicitly seek to reduce relapse rates after
the end of an initial well succeeded treatment phase, or after the date of
abandon of a self motto attempt.
The behavioural and cognitive strategies to the development of
competencies related to the identification of high risk situations for
relapsing are the most common studies.
In the systematic review by Hajek et al49, there was no evidence to
support the use of any type of strategies to avoid relapses in abstinent
smokers, nevertheless, there were methodological and contents
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limitations that may have contributed to this result. This conclusion is
related, particularly, with the traditional treatments based on identifying
and attempting to solve the problems with minimal interventions.
Currently, and until the release of further data, it seems more
efficient to concentrate efforts in attempts of early smoking cessation.
13.2.3 Aversion therapy
Hajek and Stead50 review evaluated the aversion therapy role in smoking
cessation. This technique is based on classical animal conditioning
experiments and it consists of adding unpleasant stimuli to the smoking
action, in an attempt to extinguish it.
The authors found a large number of published articles on this
subject, but most papers had several methodological flaws that could
origin false-positive results. As such, it was concluded that the available
evidence is insufficient to determine the efficacy of the “rapid smoke”
(aversion therapeutic method which requires several smoke inhalations
within a few seconds) or the existence of a dose-response to the aversion
stimulation. Other aversion methods (lighter forms of the “rapid smoke”
method) do not seem to present any specific efficacy. It is justified,
nevertheless, to conduct a larger number of trials with adequate
methodology in order to achieve a correct evaluation of this type of
approach.
13.3 Special populations
It is important to consider the particularities of some specific populations,
in which the harmful effects of tobacco may have more serious
consequences (such as pregnant women or cardiovascular patients), or
that may represent a more favourable context for smoking cessation. On
the other hand, the groups where the efficacy of the interventions
generally used may be questioned deserve a more careful approach,
and/or the pertinence of the use of different methodologies should also
be more carefully evaluated.
13.3.1 Cardiovascular patients
There are three systematic reviews published relating to smoking cessation
as a strategy to secondary prevention in smokers with cardiovascular
disease.
Only the work by Wiggers et al51, published in 2003, refers
cardiovascular disease in general, and does not show evidence of benefit
in most interventions (nicotine replacement therapy or other
pharmacological therapy, self-help materials, individual group or
telephone counselling) in these patients. There was just limited evidence
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of efficacy of medical or the nursing team counselling. The number of
studies available then in cardiovascular patients was small and the effects
very limited (only 5 of the 12 analyzed trials showed significant results).
More recently, two systematic reviews were performed, focusing on
smokers with coronary heart disease. The review of 33 randomized
double-blind clinical trials, included in the review by Ludvig et all52,
demonstrated that each of the smoking cessation aids (nicotine in its
several forms, bupoprion and behavioural therapy) increases modestly
the abstinence rates at 12 months in coronary patients, comparatively to
placebo. There is no evidence showing a significant difference in the
efficacy of several aids. The meta-analysis by Barth et al53, published in
2006, states that psychosocial interventions (behavioural approaches,
telephone support, self-help material) have a positive effect in smoking
cessation in patients with ischemic disease, versus the usual treatment, if
applied for a minimum period of 1 month. The analyzed studies were
randomized heterogeneous trials, using the model of random effects.
In what concerns adverse effects of smoking cessation drugs in
patients with cardiovascular disease, several RCTs were analyzed
individually in the review by Ludvig and the work of Silagy et al29, already
mentioned in the pharmacotherapy chapter. It was seen that high levels
of nicotine may be a risk factor to cardiac events. Nevertheless, the risk
from nicotine within the replacement drugs currently marketed is probably
not superior to the risk of smoking per se. The transdermal patch, through
its slow release and reduced nicotine concentrations, was safe in patients
with stable coronary disease, and it did not increase the number of
events, being considered therefore as a viable option in patients following
an acute myocardial infarction (after 2 weeks).
There was no available evidence of quality relating to the safety of
gums and inhalers but, considering that they are immediatly released,
they should not be recommended to high risk cardiac patients. Bupoprion
was considered safe in coronary disease patients.
13.3.2 Pregnancy
Considering the serious risks associated to smoking in pregnant women,
several studies were conducted in order to evaluate the efficacy of
smoking cessation interventions, when integrated in pre-natal care.
Polanska et al54 meta-analysis, published in 2003, confirms that the
interventions in prenatal smoking significantly increase the smoking
cessation rates at the end of pregnancy, and they refer a greater
efficacy in interventions including specific material to pregnant women.
In the systematic review by Lumley et al55, published in 2004, the
analysis of 48 randomized and non randomized clinical trials, having
significant statistical heterogeneity, has shown that the application of
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smoking cessation programmes lead to a reduction of the proportion of
women who keep on smoking at the end of their pregnancy. All 16 trials
that included information on prenatal outcomes, with demonstrated
homogeneity, have revealed a reduction in the occurrence of low weight
at birth and pre-term labour. The analysis relating to the occurrence of
very low weight at birth, still born babies and peri or neonatal death did
not present an adequate statistical power. This review also included 5
trials relating to relapses prevention (800 women) that did not show a
significant reduction of relapses.
Concern of use of NRT in pregnant, puerperal or breast feeding
women, is centered on the fear of adverse effects on the foetus. In the
above mentioned review, NRT did not present a significant advantage
over other types of intervention to smoking cessation during pregnancy.
On the other hand, the number of trials conducted to date evaluating the
drug safety in pregnancy is very small.
Also, there are no published articles on the use of bupoprion as
smoking cessation drug during pregnancy.
We might possibly consider the use of pharmacotherapy in smoking
pregnant or breast feeding women who cannot cease smoking only with
psychosocial interventions, after considering the risks and the fact that its
efficacy is not known, opposing to the risks of keeping on smoking. If this is
the case, the lower dose of the established therapeutic interval should be
used30.
13.3.3 Psychiatric disease
The results of a meta-analysis with 15 clinical trials, published in 2003 by
Hitsman et al56, suggest that the existence of personal history of major
depression is not an independent risk factor to cessation failures in the
short or long term in a smoking cessation programme. Consequently,
these patients should be offered the interventions identified as effective in
this CPG. Considering that slow release bupoprion and nortriptyline –
effective treatments to smoking cessation in the general population – are
also effective to treat depression, these drugs should be specially
considered to the treatment of tobacco dependency in smokers with
current or previous history of depressive syndromes.
Prochaska et al57 meta-analysis indicates that there is a strong
evidence that all smoking cessation interventions in individuals involved in
treatment programmes for other forms of dependency are effective in the
short term, both for patients undergoing treatment as for patients in
recovery; however, they are not effective in the long run. These
interventions seem to promote as well the long term abstinence of alcohol
or illicit drugs.
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13.3.4 Young people (adolescents)
Considering the young population, Sussman et al58 meta-analysis,
published in 2006 and including 48 clinical trials, led to the conclusion that
young people included in smoking cessation programmes present higher
abandon rates in short and long term. It was also seen that these rates are
relatively higher in programmes lasting longer than 5 sessions, those that
include a motivational component, cognitive behavioural techniques,
social influence approaches, or programmes conducted in scholar clinics
and within their school class.
Grimshaw and Santon58 published in the same year in the Cochrane
Library a systematic review of 15 randomized and non randomized clinical
trials, to evaluate the efficacy of smoking cessation strategies in young
people under 20, with an average of at least one cigarette per week
(defined as regular smokers). No intervention has shown an increase in
smoking cessation rates up to six months, nevertheless the so-called
complex interventions (including multiple components – psychological,
social, cognitive behavioural), with some persistence of abstinence (30
days or occasional abstinence prevalence at 6 months), and particularly
the ones that included elements of the “change stages” model, had
some success.
The evidence currently available does not permit to consider that
the efficacy, effectiveness and neuropharmacological safety would be
different in young people relatively to other smoking groups; however, the
only two trials that studied pharmacological interventions (nicotine
replacement therapy isolated or combined with bupoprion) in this group
of individuals, were small in size and did not present a statistically
significant benefit in smoking cessation rates.
13.3.5 Elderly patients
As with younger smokers, smoking cessation in the elderly may reduce the
risk of acute myocardial infarction, death due to coronary disease and
pulmonary neoplasia30. It can also enable faster recoveries from diseases
exacerbated by smoking and improve the brain circulation.
The recommended interventions to the general population have
also proved beneficial to the elderly; however, due to some individuals’
difficulties of mobility and transportation, the pro-active telephone
counselling is especially indicated in this population.
13.3.6 Hospitalized smokers
In the particular context of hospitalized patients, it was seen that smoking
cessation treatments are effective.
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The publication in 2002 of the Rigotti et al59 meta-analysis, analyzing
17 randomized and randomized clinical trials to interventions in
hospitalized patients, showed that behavioural interventions which
include contact during hospitalization and at least one month of follow-up
are effective in promoting smoking cessation in hospitalized patients.
Nicotine replacement therapy increased smoking abandon rates.
13.3.7 Preoperative patients
Moller et al60, identified 4 statistically heterogeneous clinical trials related
to preoperative smoking cessation, and their analysis, as a systematic
review, concluded that the preoperative interventions to smoking
cessation are only effective in the perioperative period, without a long
term significant effect. The available data on the smoking cessation effect
in postoperative complications are contradictory, and we need more
research in order to issue a valid opinion.
13.3.8 Chronic obstructive pulmonary disease (COPD) patients
Smoking cessation is presently considered the most important therapy of
COPD smokers; therefore, it is pertinent to know the efficacy of the
different interventions to smoking cessation in this particular group of
patients.
In a systematic review, published in 2001, 5 RCTs analyzing smoking
cessation in patients with COPD were included; two of them were of high
quality. The authors concluded that the combination of pharmacological
and psychosocial therapy was superior than the isolated use of
psychosocial therapy or the absence of therapy in these patients.
Nevertheless, there is no satisfactory level of evidence proving that
isolated psychosocial therapy increases the success rate of smoking
cessation in patients with COPD61.
13.3.9 Ethnic and racial groups
Certain ethnic and racial groups present susceptibilities to some diseases
susceptible to tobacco use (cardiovascular disease, neoplasias, among
others).
According to Fiore et al30 CPG, these individuals usually have little
access to health care and they are not aware of the harms caused by
tobacco. Studies have demonstrated that the strategies used in general
populations, may be adapted, considering the language and cultural
differences.
13.4 Role of health care providers
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All health care providers are potential agents for smoking cessation. Over
the last several years many reviews have been done on the efficacy of
the intervention of several types of health professionals.
The meta-analysis from Gorin e al62, has shown that counselling from
health care providers leads to a small increase in smoking cessation rates.
Within the promotion of smoking cessation, the doctors have shown to be
the most effective, when compared to multidisciplinary teams, dentists
and nurses; nurses seem to be the less effective, although the tendency is
not statistically significant; and there was no significant difference
between dentists and multidisciplinary teams, although the number of
studies involving dentists is rather small. There was also a statistical
tendency towards a higher smoking cessation with a larger number of
health care providers involved.
Mojica63 meta-analysis, published in 2005, also involving several
types of health care providers, showed that the interventions performed
by psychologists, doctors or nurses are effective in smoking cessation.
Lancaster et al64 systematic review, published in 2004, studied 39
RCTs (31.000 smokers) relating to the medical counselling role in promoting
smoking cessation. It was demonstrated, through the analysis of 17 RCTs,
that a brief counselling from the doctor, when compared to the absence
of counselling, has a small but significant effect in smoking cessation rates.
There was no sufficient evidence, from indirect comparisons, to establish a
significant difference in the efficacy of medical counselling related to the
interventions intensity, the amount of follow-up given or the use of support
materials. The direct comparison between intensive and minimum
counselling suggested a small advantage from the first one, but the results
presented some degree of heterogeneity. Direct comparison also showed
evidence of a small but significant benefit of follow-up visits.
The 2006 update of the Rice et al65 meta-analysis, initially published
in 2004 by Cochrane Library, identified 34 randomized clinical trials relative
to interventions of nurse professionals in smoking cessation. It was shown
that a structured intervention from this class (including counselling, and/or
behavioural therapy) in hospital or in clinic, increases the probability of
smoking cessation, comparatively to the usual health care. Counselling
during tracing or multifactorial secondary prevention programmes has
proven to be the less effective. The results of the several trials were
heterogeneous, but using a random effects model, there was no change
in the estimate of a statistically significant effect.
The role of pharmacists in smoking cessation was analyzed in the
systematic review by Sinclair et al66, comparing a counselling and support
programme with data registration, provided by previously trained
professional in a communitarian pharmacy, with the support usually given
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at the pharmacy. The small number of studies and the significant statistical
heterogeneity of results only allowed the conclusion that there is limited
evidence that the referred interventions in community pharmacies may
have a positive effect in smoking cessation rates.
Carr and Ebbert67 have published a systematic review of 6 clinical
trials, to evaluate the efficacy of interventions by dentists in their practice
or in the context of school health. The available evidence suggests that
behavioural interventions provided by oral health professionals, along with
an oral/dental evaluation component, may increase the smoking
abstinence rates among users of non-smoked tobacco. Only one of the
analyzed studies included smokers, so there was not enough evidence to
conclude on the efficacy of these interventions in that group.
13.5 Special topics
13.5.1 Communitarian interventions
The systematic review by Secker-Walker et al68, which included only
controlled trials, studied community interventions regarding the promotion
of smoking cessation. It was shown that, comparing communities with
smoking cessation intervention programmes and control communities,
there is no impact of those initiatives in the smokers’ prevalence.
The community approach will remain an important part of the
health promotion activities, but we should consider the limited effect of
these initiatives when planning the magnitude of projects and resources
to use.
13.5.2 Workplace interventions
“Smoke free” environments and more specifically “smoke free”
workplaces, protect non-smokers from the increasingly known harmful
effects of passive smoking and may create an environment that
encourages active smokers to cease or reduce consumption. The
efficacy of interventions for smoking cessation and the effects of smoking
restrictions in the workplace, were recently studied in 3 systematic reviews.
The work by Fichtenberg et al69, published in 2002, studied the
differences in consuming and prevalence before and after a workplace
becoming “smoke free”, or between comparable samples with and
without smoke restrictions. The analysis of the 26 selected trials (cohort,
cross sectional and population trials) has shown that workplaces totally
smoke free are associated to reductions in smoking prevalence of 3.8%
and less 3.1 cigarettes smoked per day by working people who keep on
smoking.
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Smedslund et al70 meta-analysis, published in 2004, and involving 19
controlled clinical trials, has shown that interventions to smoking cessation
in the workplace are effective in the short run (6 months). However, the
effect seems to diminish with time, disappearing after 12 months. The
effect described was found in both trial groups (randomized and nonrandomized), that presented adequate statistical homogeneity. The data
found were also consistent with the results of Fisher 1990 meta-analysis, the
only one previously conducted on the effects of workplace smoking
cessation programmes.
Recently, in 2005, Moher71 group confirmed some of the main
conclusions of the previous work, showing that interventions directed to
the smoker, already proven efficient (group therapy, individual
counselling and nicotine replacement therapy) are likewise effective
when provided in the workplace. Only the self-help methods seem to be
less effective. The authors also found limited evidence that the use of
incentives and competitions increased the participation in smoking
cessation programmes. These results were found only in randomized, but
highly heterogeneous, trials. This study also concluded that prohibitions
and smoking restrictions reduce smoke incidence in the workplace, but it
was not clear that they reduce the prevalence of active smoking or the
total smoking load of the working people. This last conclusion opposes the
results of Fitchenberg et al, which showed a reduction in the prevalence
and daily consumption of cigarettes.
Thus, as it decreases the smoke incidence in the workplace (and
consequently passive smoking) and possibly the smoking prevalence and
the total smoking load of smokers, we would strongly advise transforming
workplaces in “smoke free” environments.
The incentives to smoking cessation may be given in different forms:
economical, competitions and financing systems to smoking cessation
programmes.
Hey and Perra72 systematic review, included 15 RCTs and proved
that economical incentives and competitions provided within the
community context, health service and workplace, do not increase long
term smoking cessation rates. Nevertheless, they may increase recruitment
rates for a smoking cessation attempt, and indirectly, the number of
individuals who successfully quit smoking. Given the impossibility of
showing the efficacy of these interventions, it simply is not possible to
estimate the respective cost-efficacy relationship. Specifically, regarding
contests as Quit and Win (created in 1980 by Minnesota Cardiovascular
Health Programme and conducted since 1994 twice a year as an
international contest) it was shown, in a second systematic review by the
same investigators73, that local and regional proofs seem to increase
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smoking cessation rates in spite of the reduced impact in the population
smoking prevalence. The international level contests may become an
effective intervention to smoking cessation, but it is not possible to draw
safe conclusions from the currently available data.
Relating to the financing programmes for smoking cessation
programmes (which eliminate costs to the patient), a systematic review
by Kaper et al74 concluded that total financing of smoking cessation
programmes increased the number of ex-smokers, the number of
participants trying to quit and the use of low cost smoking cessation
treatments, comparatively to the partial financial beneficial or the
absence of financial intervention; the methodological quality of these
trials was low, and there was also some heterogeneity between contexts,
interventions and selected participants, which represent some limitative
factors, so the results should be interpreted with caution.
13.5.3 Biomedical risk determination
Calculating biomedical risk consists of measuring physiological
parameters (e.g. respiratory function tests, measurement of exhaled
carbon monoxide, etc.) aiming to supply smokers with a measure of the
harmful effects of smoking.
According to the results of the systematic review by Bize et al75,
based in 8 RCTs, there is no quality evidence allowing to draw conclusions
on the efficacy of the biomedical risk determination as an incentive to
smoking cessation.
13.5.4 Partner support
The systematic review by Park et al76, of 9 RCTs studied the role of the
partner in smoking cessation strategies. It was shown that in interventions
for gaining partner’s support in smoking cessation programmes did not
increase long term cessation rates. Nevertheless, we cannot draw
conclusions on the impact of this strategy, since that interventions
capable of successfully changing the support given by partners to
smokers who wanted to quit smoking are lacking.
13.5.5 Physical exercise
In Ussher77 systematic review, only one of the eleven selected trials has
shown a positive effect of exercise as an auxiliary for long term smoking
cessation. Thus, there is no sufficient evidence to recommend physical
exercise as a specific auxiliary to smoking cessation. Nevertheless, all trials
that did not shown a significant effect presented limitations, namely
insufficient sample size to exclude an effect of the interventions,
methodological flaws, inadequate interventions (e.g. the exercise level
was not sufficiently intense to produce the necessary changes).
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There is some evidence that points to the recommendation of
physical exercise as a specific auxiliary to reduce symptoms of smoking
abstinence and smoking craving. More trials are needed to exclude the
psychophisiological basis of this effect.
13.5.6 Training of health care providers
Since the efficacy of the interventions of health care providers in
increasing smoking cessation rats is established, it seems coherent to
increase the number and the quality of the mentioned interventions,
especially if we consider the reduced number of smokers who presently
receive counselling from this professional group. The training of health
professionals in smoking cessation may become a means to attain that
purpose and was studied in two well elaborated systematic reviews.
The results of the Lancaster et al78 review, published in 2002,
concluded that trained professionals have a greater probability of
identifying smoking patients and consequently to propose smoking
cessation strategies. However, there was no significant evidence that this
training actually changes the smoking habits of their patients.
Andeerson et al79 systematic review, published in 2004,
complements the previous one, showing that interventions on increasing
primary health care professional involvement are effective, both in
increasing smoking cessation rates in patients, as in tracing and
professional counselling rates. Training programmes were more effective
to training doctors than to more differentiated doctors. It was also
concluded that, to training professionals, educational programmes are
the most effective ones, and that for established doctors, educational
interventions and combined practices are the ones that achieve the
better results.
13.5.7 Passive smoking
Currently, there is no evidence to draw conclusions on the most effective
intervention to reduce parental smoking, within pediatric health practice,
and we cannot extrapolate the usually successfull brief medical
counselling used for the adult health context. This information is based on
the results of a systematic review designed by Roseby et al76, and
published in 2002, that studied 18 RCTs on several mechanisms eventually
involved in the prevention of environmental smoking exposure in children,
including paediatricians (0-12 years).
In spite of the information mentioned above, and the fact that
there is not currently sufficient evidence of its effectiveness, it makes sense
in the context of the paediatric appointment to provide counselling to
smoking cessation directed to parents, in order to limit their children
exposure to passive smoking.
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13.5.8 Weight gain after smoking cessation30
Weight gain after smoking cessation is an important concern for many
smokers and this may lead to intervention failure. Most ex-smokers gain
less than 4.5 kg, but around 10% gain around 13.5 kg or more.
Some evidence suggests that rigorous dieting during the beginning
of smoking cessation may later induce failure. There are also data which
permits to state that a moderate increase in physical activities may slow
the weight gain.
Bupoprion therapy or the use of NRT delays weight gain. However,
after finishing the therapy, ex-smokers gain approximately the same
weight they would gain if they had not used the therapy. There is also
evidence that after a relapse, smokers have tendency to loose the weight
gained during the abstinence period. As such, and according to Fiore et
al30, the health care provider should not deny the possibility of a weight
gain, nor minimize the importance of that fact to the patient; he should
prepare the patient to this eventuality; the greater benefit of smoking
cessation should also be stressed out in face of the weight gain; during
the smoking cessation attempt it should be stressed the importance of not
taking any rigorous measures to avoid weight gain, since the latter can
make smoking cessation even more difficult, and, finally, the health care
provider should offer to help the patient to loose weight, after an effective
smoking abstinence.
13.5.9 Other tobacco products30
As tobacco smoke, the use of chewing tobacco or other forms of
tobacco (cigar, cigarillo, pipe) increases the risk of stomach,
cardiovascular, pulmonary and neoplasic disease.
The available evidence is limited, but it shows benefit of using the
described therapies for smoking cessation in smokers of other forms of
tobacco. Since the majority of studies focused smoked tobacco in the
form of a cigarette, the benefit of pharmacological therapies in smokers
of other forms of tobacco it is not precisely known.
14. Outcomes
The outcome is the long term cessation of tobacco use.
15. Implementation strategy
This CPG does not describe, or recommend, a specific implementation
strategy.
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The users of this document are the agents who naturally will
implement the respective recommendations. Nevertheless, in the present
CPG appendices, the GLIA (Guideline Implementability Appraisal)80
instrument is described, and it may be used as a basis to practical
implementation schemes.
16. Main recommendations
16.1 Pharmacological interventions
•
•
•
•
•
•
Nicotine replacement therapy (NRT) should be recommended to
patients who wish stop smoking (Recommendation level: A)
• All the available forms of nicotine can be recommended, since
they
all
are
equally
effective
in
smoking
cessation
(Recommendation level: A)
• The choice of NRT type should consider the patient needs,
tolerance and cost (Recommendation level: D)
• In highly dependent smokers (Fagerström score ≥7) the 4 mg gums
should be administered instead of the 2 mg gums
• In women, it is more important to associate to NRT an intensive nonpharmacological support. (Recommendation level: B)
• The combination of transdermal patches with a self-administered
NRT form may be recommended in patients who cannot abandon
tobacco with a single type of 1st line pharmacotherapy
(Recommendation level : B)
Bupoprion is an effective drug and should be recommended to
patients who want to stop smoking (Recommendation level A)
Nortriptyline is an effective drug and should be recommended to
patients who want to stop smoking (Recommendation level: A)
Varenicline is an effective drug and should be recommended to
patients to want to stop smoking (Recommendation level: A)
Nicotine replacement therapy, varenicline, bupoprion and nortriptyline
should all be considered as first line drugs, to use separately
(Recommendation level A); considering, in the drug choice, the needs
of the patient, tolerance and cost. (Recommendation level: D)
Clonidine is an effective drug and should be prescribed, under
medical supervision, as a second line drug, to patients who want to
stop smoking (Recommendation level: A). It’s sedative effect may be
useful in specific patients (Recommendation level: D)
16.2 Non-pharmacological interventions
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•
•
•
•
•
Self-help materials should be supplied to smokers who are not
receiving other type of interventions for smoking cessation. It is more
useful to supply brief counselling or individualized self-help materials to
smokers who seek help (Recommendation level A)
The smoker who is motivated to abandon smoking should have the
possibility of attending therapy groups (Recommendation level: A)
Pro-active telephone counselling should be given to smokers interested
in quitting smoking, as there is a dose-response relationship. The
response telephone call with counselling increases the usefulness of
support telephone lines (Recommendation level: A)
Individual counselling should be supplied by smoking cessation trained
professionals outside the clinical practice environment and lasting over
10 minutes (Recommendation level: A)
Physical exercise may be recommended to individuals with greater
intolerance to abstinence symptoms and craving. (Recommendation
level: D).
16.3 Role of health care providers
•
•
•
•
•
Any health care provider (doctor, nurse, psychologist or
multidisciplinary professional teams) should cooperate to smoking
cessation with smokers they usually have contact with
(Recommendation level: A). Dentists should also perform these
interventions whenever possible. (Recommendation level: B).
Doctors, as the most effective professionals in smoking cessation,
should be the priority elements in the application of interventions to this
purpose. (Recommendation level: A)
All doctors should offer their patients counselling regarding smoking
cessation (Recommendation level: A), and perform, if possible, at least
one follow-up appointment (Recommendation level: B)
Nurses should, whenever possible, provide smokers, hospitalized or not,
with a structured intervention to smoking cessation, including
counselling and/or behavioural therapy (Recommendation level: A)
All health professionals working in community pharmacies should,
whenever possible (and after previous training), provide their smoking
patients counselling to smoking cessation. This counselling should, if
possible, be accompanied by a support programme with data
registration. (Recommendation level: B)
16.4 Special populations
16.4.1 Cardiovascular patients
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•
•
•
The methods of smoking cessation considered in this CPG should be
recommended to patients with cardiovascular disease who smoke
Patients with worsening cardiac disease or acute myocardial infarction
should only make behavioural therapy and/or bupoprion
(Recommendation level: B)
Patients with coronary disease or stable cardiac disease should take
bupoprion, nicotine patches and/or behavioural therapy, and abstain
from inhaled nicotine or nicotine gums. (Recommendation level: B)
16.4.2 Pregnancy
•
•
Behavioural evaluation and smoking cessation programmes should be
implemented in every context of pre-natal care, and the pregnant
women should be offered all interventions that exceed minimal
counselling (Recommendation level: A)
The use of pharmacotherapy in pregnant or breast feeding women
can be considered whenever the smoking cessation is not achieved
with only psychosocial interventions, and when the probability of
cessation and the associated potential benefits overcome the risks. In
this case, the lowest dose of the established therapeutic interval should
be used (Recommendation level: D).
16.4.3 Psychiatric disease
•
•
•
In presence of a previous history of major depression, all the
interventions identified as effective in this CPG should be used,
including counselling and pharmacotherapy. (Recommendation level:
A)
Slow release bupoprion and nortriptyline should be specially
considered in treating tobacco dependence in smokers with current or
previous history of depressive syndromes (Recommendation level: D)
The smoking cessation interventions considered effective in the present
CPG, including counselling and pharmacotherapy, should be offered
to smokers being treated or recovering from other dependencies
(Recommendation level: A).
16.4.4 Young people
•
All counselling and behavioural interventions to smoking cessation
considered effective to the adult population in the present CPG may
also be applied to teenage smokers. The programmes should include
multiple components, namely motivational, cognitive-behavioural
techniques, social influence approaches and/or interventions within
the school/class environment. (Recommendation level: B).
16.4.5 Elderly
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•
All smoking cessation treatments were proven effective in elderly
adults. Thus, these should receive the smoking cessation treatments
considered effective in the present CPG. (Recommendation level: A).
16.4.6 Hospitalized smokers
•
The hospitalized patients should be offered smoking cessation
behavioural interventions including contact during the internal periods
and at least one month of follow-up (Recommendation level: A). If
possible, all other types of strategies considered valid in the present
CPG can be used as well.
16.4.7 Preoperative patients
•
Preoperative patients should be offered the smoking cessation
interventions considered valid in the present CPG (Recommendation
level: B).
16.4.8 Chronic obstructive pulmonary disease (COPD) patients
•
COPD patients should receive combined pharmacological and
psychosocial therapy to smoking cessation (Recommendation level:
A).
16.4.9 Ethnic and racial groups
•
•
All smoking cessation treatments have been effective in different racial
and ethnic groups, so all treatments considered effective in the
present CPG should be supplied to these patients (Recommendation
level: A)81
The tobacco dependency treatments should be, whenever possible,
changed or adapted to become appropriate to the specific racial
and ethnic population to whom they are supplied (Recommendation
level: D)81.
16.5 Special topics
16.5.1 Workplace interventions
•
•
•
All workplaces should be smoke free. (Recommendation level: A)
The smoking cessation interventions considered effective in this CPG
should, if possible, be offered in workplaces. (Recommendation level:
A)
Incentives and competitions can be used to increase smoking
cessation programmes adherence in workplaces (Recommendation
level: B).
16.5.2 Training of health care providers
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•
•
Smoking cessation training programmes should be provided to primary
health care providers who can have an active role in this area.
Training programmes for doctors in training should include preferably
an educational component; the programmes to differentiated doctors
should include combined interventions with a practical and
educational component. (Recommendation level: A).
16.5.3 Passive smoking
•
The paediatricians should offer parents smoking cessation counselling
to limit their children’s exposure to passive smoking (Recommendation
level: D).
16.5.4 Weight gain after smoking cessation
•
•
The health professional should recognize that smoking cessation is
frequently followed by weight gain. Additionally, he should: a)
underline that the health risks related to weight gain are small,
comparing to the risks associated to the persistence of smoking; b)
recommend physical activity and a healthy diet; c) recommend that
patients should focus primarily in smoking cessation and not weight
control, until ex-smokers become confident on their abstinence
(Recommendation level: D)
In case of smokers highly concerned with weight gain, it may be
appropriate to prescribe or recommend slow release bupoprion or
nicotine replacement therapy, especially chewing gums, which
proved to delay the weight gain after cessation. (Recommendation
level: B).
16.5.5 Other tobacco products
•
Cigar, pipe and other combustible forms of tobacco users should be
identified and strongly advised to quit, and should get the same
counselling interventions recommended to cigarette smokers.
(Recommendation level: D)
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17. Clinical algorithm
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17.1 Screening and assessment of tobacco use
The first step to smoking cessation consists in identifying smokers30, 81.
Doctors have a privileged position, since a large number of tobacco
consumers go to the doctor at least once a year, and a large percentage
of smokers – about 70% according to Fiore et al30 – want to quit. In spite of
smokers quoting medical intervention as an important stimulus to the
cessation, most clinicians do not recognize them or do not advice and/or
offer help to smoking cessation in a regular basis.
The awareness of doctors in identifying and giving support to
smokers in their attempt to smoking cessation opens doors to interventions
with potential success and guides the clinician to the type of intervention
to supply each individual smoker. Thus, there are four types of responses
that may be obtained within screening for tobacco use:
•
•
•
•
The patient smokes and wishes to quit
The patient smokes, but does not wish to quit for the moment
The patient has smoked but he has already stopped
The patient was never a regular consumer of tobacco.
According to the situation of the patient, there are different interventions
that may be lead by the doctor and which we will describe in the next
paragraphs.
17.2 Brief clinical interventions
The brief interventions30,81 may be conducted by any health care
provider, but are primarily directed to primary care doctors. They are an
effective strategy in smoking cessation and have as a purpose to change
the clinical culture and practice standards, in a way that each smoker is
identified and offered treatment, at the same time that they consider the
difficulties of managing the short time available for each patient’s
appointment. As such, it is essential that all tobacco users are subject to a
brief intervention in each appointment, even if they are not available to
intensive interventions.
This chapter describes the brief intervention according to the
response obtained during the smoker’s evaluation:
A. Smokers who wish to make and attempt to quit immediately
B. Smokers who do not wish to make an attempt to quit at this
moment
C. Recent ex-smokers.
Page 72 of 106
17.2.1 Smokers who wish to make an attempt to quit immediately
The five main steps (the “5 A’s”) of intervention in smoking cessation within
the primary healthcare context are (see Table 31.2.1):
1. Approach the patient on tobacco consumption;
2. Advise the patient to stop smoking;
3. Assess the will to try to quit;
4. Assist the quitting attempt;
5. Accompany through follow-up appointments to prevent relapses.
These strategies were conceived to be brief. Pharmacological
therapy should be provided to all smokers beyond counselling (see Tables
31.2.2 and 31.2.3), except in special circumstances, namely
contraindications described above.
17.2.2 Smokers who do not wish to make an attempt to quit at the moment
The evaluation of tobacco use should be done as a routine. Smokers who
do not wish to quit may not be aware of the damaging effects of
tobacco, may have fears relating to the consequences of abstinence,
may lack economical resources, or may be demoralized by previous
relapses. These patients have the possibility of responding to a
motivational intervention, designed to educate, reassure and motivate
(see Table 31.2.4). The motivational interventions are more effective when
the doctors have an emphatic posture, promote the patient autonomy
(e.g. choice between different options), avoid arguments and support the
patient individual performance (e.g. by identifying previous successes in
behavioural changes).
17.2.3 Recent ex-smokers
Tobacco dependency should be seen as a chronic disease, and relapses
have been identified mainly in the two first years after the beginning of
smoking cessation (Wu et al28). According to Hajek et al49 review, there
was no consistent evidence of the benefit of prevention of relapse.
Nevertheless, we may recommend minimal interventions based on the
reinforcement of the importance of cessation and the availability of
helping to solve obstacles that can make the maintenance of smoking
cessation difficult. (see Table 31.2.5).
17.3 Intensive clinical interventions
In the systematic review by Lancaster et al47 it was not possible to establish
a statistical significant benefit of intensive clinical interventions.
Nevertheless, it is not possible to exclude a dose-response relationship, so,
Page 73 of 106
in motivated individuals may be beneficial to supply this type of
interventions performed by professionals specialists in smoking cessation
that have the necessary resources to intensive interventions30. In Table
31.2.6 the components of an intensive intervention are presented.
18. Qualitative reserves
We did not find hiatus of knowledge of significant dimension. The scientific
evidence on which this CPG is based upon is of an excellent quality, since
there are multiple systematic reviews (of Cochrane Collaboration
amongst others), as well as randomized and controlled trials (RCTs) of
good methodological quality, with consistent and relevant results.
19. Cost analysis
There was no cost analysis performed to determine the costs of the
possible treatments to smoking cessation. The only economic information
available is the daily average prices of the several therapeutic schemes.
20. General and subgroups potential benefits
To the population in general, the benefits that may be gained of the
successful application of the present CPG recommendations regard the
prevention of all diseases related to the use of tobacco (previously
mentioned). Thus, all population – including the healthy individuals – may
benefit from these measures.
The subgroups in which smoking cessation will present greater
benefits include cardiac patients (especially coronary), vascular patients
(specially the patients with peripheral arterial impairment), patients with
pulmonary disease (namely COPD), the diabetics, the elderly, young
people and pregnant women.
21. General and subgroups potential risks
There are no significant potential risks for any patient groups or smoking
cessation patients. The benefits are universal.
22. Availability
This CPG text will be available as follows:
• Printed as a book/manual;
• Available on-line at the official site of CEMBE and others
• As a CD-ROM in Portuguese and English.
Page 74 of 106
23. Attached documents
The decision algorithm will be available individually, in order to allow all
potential users of the present CPG to have a fast and effective access to
a synthesis of the recommendations of the present CPG.
24. Patients’ resources
There are no resources specifically directed to patients who wish to quit
smoking permanently available.
25. Supporters and subscribers
•
•
•
•
•
•
•
•
•
COPPT
IPPT
Sociedade Portuguesa de Pneumologia
Sociedade Portuguesa de Cardiologia
Associação Portuguesa de Médicos de Clínica Geral
Ordem dos Médicos
Ordem dos Médicos Dentistas
Ordem dos Farmacêuticos
Faculdade de Medicina de Lisboa
26. Committees and responsible group
The entity responsability for the elaboration of the present CPG is from the
Center for Evidence Based Medicine (CEMBE) at the University of Lisbon
School of Medicine in Portugal.
The authors of the present CPG are part of the Clinical Practice
Guidelines Department Group from CEMBE and they are: Inês Reis MD,
Philip Fortuna MD, Raquel Ascenção MD, António Bugalho MD, João
Costa MD and António Vaz Carneiro MD, PhD.
27. Funding sources
The economic support to this CPG came exclusively from Pfizer, as an
“unrestricted grant”. This kind of financing implies that the sponsor has had
no influence whatsoever whether in the scientific methodology, whether
in the final contents of the present CPG, being both the exclusive
responsibility of CEMBE from FML.
Page 75 of 106
28. Editorial independence
The present CPG is the intellectual property of the authors, who declare
that they do not have any conflicts of interest on their part and and with
their relationship with the sponsor, government, insurance companies,
scientific and professional societies, patient associations or any other
entity.
The expressed points of view and the final recommendations are
the exclusive responsibility of CEMBE, and they were not influenced by
any means by any institution or individuals not related to the authors.
29. Publication date
Completed in August 2007 and reviewed and published in October 2007.
30. Reviews
The present CPG will be reviewed, partially or globally, in 2012.
31. Appendices
31.1 Fagerström scale (evaluation of the dependency level)
Question to ask
How soon after you wake up do you smoke your first
cigarette?
< 5 minutes
6-30 minutes
31-60 minutes
> 61 minutes
Do you find it difficult to refrain from smoking in places
where it is forbidden? (e.g. theatres, airplanes, hospitals)
Yes
No
3. Which cigarette would you most hate to give up?
First in the morning
Any other
4. How many cigarettes per day do you smoke?
< 10 (less than half a pack)
11 - 20 (half to one pack)
21 - 30 (one pack to a pack and a half)
Points
3
2
1
0
1
0
1
0
0
1
2
Page 76 of 106
> 31 (more than one pack an a half)
5. Do you smoke more frequently during the first hours after
waking than during the rest of the day?
Yes
No
6. Do you smoke even if you are so ill that you are in bed
most of the day?
Yes
No
3
1
0
1
0
Scores:
• 7 - 10 = very high nicotine dependence
• 4 - 6 = medium nicotine dependence
• less than 4 = low nicotine dependence
31.2 Synoptic tables
31.2.1 Brief strategies to help the patient who wishes to quit smoking – “5
A’s” Strategy
Action
Strategies for implementation
Step 1. Approach – systematically identify all tobacco users at each appointment
Implement a system that assures
that, for each patient in each
Add to the appointment notes a field relating to the
appointment, tobacco use is
use of tobacco
investigated and documented
Step 2. Advise – incentive all tobacco users to quit with conviction
Counselling should be:
• Clear – “I believe it is important for you to quit
immediately and I can help you. To reduce only when
you are ill is not enough.”
• Strong - “As your doctor I want you to know that stop
In a clear, persuasive, strong
smoking is the most important thing you can do to
and personalized way,
protect your health right now and in the future. I will
encourage all tobacco users to
be available to help you.”
quit
• Personalized – Associate the use of tobacco to the
present disease, and/or to its social and economic
costs, level of motivation/availability to quit and/or the
impact of tobacco use on the children and other
members of the family
Step 3. Assess – determine if the patient wishes to try to quit
Ask each tobacco user if he is
Assess the patient’s will to quit:
willing to attempt to try to quit
• If the patient wishes to make an attempt to quit
immediately (e.g.: within the
immediately, provide the necessary assistance
following 30 days)
• If the patient wishes to participate in an intensive
treatment, supply the treatment or refer the patient to
Page 77 of 106
intensive intervention
• If the patient clearly states that he does not want,
for the moment, to make an attempt to quit, supply a
motivational intervention
• If the patient is a member of a special population
(teenager, pregnant women, racial/ethnic minority),
consider supplying additional information
Step 4. Assist – assist the patient in his attempt to quit
Preparation of the patient to the abandon attempt:
• Schedule a date: ideally, the abandon date should
be within two weeks
• Inform the family, friends and co-workers on the
abandon attempt, and demand understanding and
support
Elaborate, together with the
• Anticipate difficulties that may arise during the
patient, a plan to abandon the
use of tobacco
abandon attempt. Particularly in the first weeks, the
most critical ones. Among these, nicotine abstinence
symptoms
• Remove tobacco products from the environment
before starting, avoid smoking in places where you
spend a lot of time (workplace, home, car)
• Abstinence – total abstinence is essential
• Experience of previous abandon attempts – identify
what helped and what went wrong in previous
abandon attempts
• Anticipate problems or difficulties in the abandon
attempt to be started – discuss challenges / stimulus
and how the patient can overcome them with
success
Supply practical counselling
• Alcohol – the patient should consider to limit or
abstain drinking alcohol, since its use may lead to
relapses
• Other smokers at home – abandon is more difficult
when there are other smokers at home. Patients
should encourage the people they live with to quit at
the same time or not to smoke in their presence
Supply a supportive clinical environment when
Supply social support intraencouraging the patient in his attempt to quit “We are
treatment
available to help you”
Help the patient to develop social support to his
Help the patient to obtain social
abandon attempt, in this environment, outside the
support extra-treatment
treatment. “Ask your family, friend and co-workers to
help you in your attempt to quit”
Recommend the use to effective pharmacotherapy.
Recommend the use of
Explain how drugs increase the probability of success
approved pharmacotherapy,
and reduce abstinence symptoms. 1st line drugs
except in special circumstances include: varenicline, bupoprion, nicotine
replacements and nortriptyline.
• Type: appropriate to the patient, relating to his
culture, race, education, age and motivation
Supply self-help materials
• Location: readily accessible in each clinical practice
Page 78 of 106
Step 5: Accompany – Schedule follow-up appointment
• Date – The follow-up appointment should be
scheduled shortly after the abandon date, preferably
during the 1st week. A second follow-up appointment
is recommended in the 1st month. Schedule additional
appointments as needed.
• Actions during the follow-up appointment –
Congratulate success; if tobacco has been used,
Schedule follow-up
review the circumstances and incentive new
appointment, either personally
commitment with total abstinence; remind the patient
or by telephone
that a lapse my be used as a learning experience;
identify problems already found and anticipate
difficulties in the immediate future; evaluate the use
and problems of pharmacotherapy; consider the use
or reference to a more intensive treatment.
Table adapted from Fiore MC, Bailey WC Cohen SJ, et al. Treating Tobacco Use and Dependence,
Clinical Practice Guideline. Rockville, MD: U.S. Department of Health and Human Services. Public
Health Service. June 2000, pp 28-31.
31.2.2 General clinical practice guidelines to prescribe pharmacological
therapy to smoking cessation
Who should receive
pharmacological therapy
to smoking cessation?
What are the 1st line
pharmacological
therapies?
What factors should be
considered when
choosing a 1st line
pharmacological
therapy?
What are the
recommended 2nd line
pharmacological
therapies?
All patients in process of somoking cessation,
except in the presence of special
circumstances: clinical contraindications,
pregnant and breast feeding women and
teenagers
Varenicline, slow release bupoprion
chloridrate, nortriptyline and nicotine
replacement therapies (chewing gums and
transdermal patches)
Due to the non-existence of sufficient data to
order these drugs, the choice of a specific 1st
line pharmacological therapy should be
guided by factors such as:
• familiarity of the doctor with the drugs
• contraindications to selected patients
• preferences of the patient
• previous experience of the patient with a
specific drug (positive or negative)
• characteristics of the patient (e.g.: history
of depression, concerns with weight gain)
Clonidine chloridrate
Page 79 of 106
When should 2nd line
agents be used to treat
tobacco addiction?
What are the
pharmacological
therapies most adequate
to patients concerned
with weight gain?
Are there
pharmacological
therapies that should be
specially considered in
patients with history of
depression?
Can pharmacological
therapies for smoking
cessation be used in
patents with history of
cardiovascular disease?
Can smoking cessation
pharmacological
therapies be used in the
long term (6 months or
more?)
Can pharmacological
therapies be combined?
In patients who cannot use 1st line drugs due
to contraindications, or in patients in whom
the 1st line drugs are not useful. Patients
should be monitorized relating to clonidine
adverse effects.
Slow release bupoprion chloride and nicotine
replacement therapies, in particular nicotine
chewing gums (that delay but do not
prevent weight gain)
Slow release bupoprion chloride and
nortriptyline chloride
Yes. Patients with coronary disease or other
stable cardiac diseases, should take
bupoprion or nicotine patches, not inhaled
nicotine or nicotine gums. Patients with
worsening of the cardiac disease or recent
acute myocardial infarction (< 2 weeks)
should only use bupoprion.
Yes. This approach can be useful in smokers
who present persistent symptoms of
abstinence during the course of the
pharmacological therapy, or that want to
use long term therapy. Nevertheless, it was
verified that 8 weeks of therapy using the
nicotine transdermal patch, is as effective as
the longer regimens. The long term use of
these drugs does not present a known health
risk.
Yes. There is limited evidence that combining
nicotine transdermal patch with nicotine
chewing gum increases the abstinence rates
relatively to the use of each of these drugs
individually.
The chewing gums can be used in a fixed
dosage regimen or in a free dose basis.
Page 80 of 106
What are the most
appropriate dosages for
nicotine replacement
therapies?
Highly dependent smokers or the ones who
failed with 2 mg chewing gum, should use
the 4 mg gum.
It is not been shown that the use of the
nicotine transdermal patch in doses higher
than 22mg/24h is more effective in achieving
long term abstinence.
There is no evidence that the gradual
reduction of therapy is better than the
abrupt suppression.
Table adapted from Fiore MC, Bailey WC Cohen SJ, et al. Treating Tobacco USE and Dependence,
Clinical Practice Guideline. Rockville, MD: U.S. Department of Health and Human Services. Public
Health Service. June 2000, pp 26-27
Page 81 of 106
31.2.3 Drugs available in Portugal with recognized efficacy in smoking cessation
Drug
Pharmaceut
ical form
Dosage
Trade
Mark®
Pack
1,5mg
Nicopass
2mg
Nicorrett
e
12, 36 or
96 units
30 or 105
units
Gums/Chewi
ng Gums
4mg
1st
Nicotinell
fruit
Nicotinell
mint
Niquitin
Nicorett
e
Nicotinell
mint
Nicotinell
fruit
Niquitin
24 or 96
units
72 units
30 or 105
units
24 or 96
units
Dosage
Recommendati
ons
Adverse
Reactions
Contraindications
• Initiate: 2 mg if
habits < 20
cigarettes/day
• Initiate: 4 mg if
habits ≥ 20
cigarettes/day
• Initially: 8-12
units/day
• Maximum
dosage:
50mg/day
• Tt duration: 812 weeks
• Initiate tt on the
stipulated day for
cessation
• Do not smoke
concomitantly
• Slow and cyclic
chewing until
obtaining a
strong flavour;
then promote
contact with
bucal mucosa
• Average
duration each
unit ±30 min
• No intake food
or drinks (except
water) 15 minutes
before and
during the
chewing process
• Tempormandibular
articulation
pain
• Unpleasant
taste
• Oral
ulceration
• Hiccups
• Odinofagia
• Nausea
• Meteorism
• Dyspepsia
• Headaches
• Initiate: one
patch of
21mg/24h or
15mg/16h
during 4-6
weeks if habits ≥
20
cigarettes/day
• Initiate: one
patch of
14mg/24h or
10mg/16h
during 4-6
weeks if < 20
cigarettes/day
• Initiate tt on
day stipulated to
cessation
• No
concomitant
smoking
• Apply in the
morning on
healthy, clean
and dry skin
• Place
preferably in the
chest or any
members
proximal portion
• Skin irritation
• Pruritus
• Mialgia
• Headache
• Vertigo
• Insomnia
•
Somnolence
• Nausea
• Vomit
• Dyspepsia
• Palpitations
•
Tachycardia
•
• Non smokers
• Maintenance
of smoking habits
• AMY <4 weeks
• Unstable
angina
• Serious
arrhythmia
• Stroke in
evolution
• Pregnancy
• Breast feeding
• <18 years
• Oropharynx
disease
• Tempormandibular
articulation
disease
• Dental
changes
• Dental protesis
• Non smokers
• Maintenance
of smoking habits
• AMY <4 weeks
• Unstable
angina
• Serious
arrhythmia
• Stroke in
evolution
• Pregnancy
• Breast feeding
• <18 years
• Serious
dermatological
72 units
Nicotine
L
I
N
E
21mg/24h
14mg/24h
Transdermal
system
7mg/24h
15mg/16h
Nicotinell
TTS 30
Niquitin
clear
Nicotinell
TTS 20
Niquitin
clear
Nicotinell
TTS 10
Niquitin
clear
Nicorett
e
15
14 or
units
7 or
units
14 or
units
7 or
units
14 or
units
7 units
28
14
28
14
28
14 or 28
units
Page 82 of 106
10mg/16h
5mg/16h
Bupoprion
1st
L
I
N
E
Slow release
tablets
150mg
Nicorett
e 10
Nicorett
e5
Zyban
14 units
14 units
60 units
• Subsequent
therapeutic
periods of 2-4
weeks with
gradual
reduction to
transdermal
system with
lower dose of
nicotine release
• Initiate: 150
mg/day during
3 days
• Day 4:
increase to
150mg 12/12h
• Maximum
dosage:
450mg/day
• Duration: 7-12
weeks (after
cessation)
• Maintained
AE, renal or
hepatic
impairment,
cardiopathy
ischemia,
diabetes
mellitus, >65
years:
maintenance
dosage
150mg/day
• Change local
of application,
avoiding
panniculus
adiposus, breasts
and articular
areas
• Replace patch
after 24h
• If insomnia
remove 24 h
patch in the
evening or
choose the 16h
ones
• Initiate tt 2
weeks before the
stipulated date
for cessation.
• Administrate
with food
• In case of
insomnia,
anticipate the 2nd
daily dose to 8h
after the first
• In some patients
tt can be
maintained until a
maximum of 6
months after
cessation
• It can be
associated to NRT
Precordialgia
•
Hypertension
disease
• Insomnia
• Xerostomia
• Tremor
• Weight loss
• Headaches
• Irritability
• Anxiety
• Nausea
•
Constipation
•
Hypertension
• Hypersensitivity
• Epilepsy or
convulsions
• Anorexia or
bulimia
• Concomitant
use of MAO
inhibitors
• Alcoholic or
sedatives
abstinence
• Bipolar
disorders
• AMY <4 weeks
• Pregnancy
• Breast feeding
Page 83 of 106
Vareniclin
e
0,5mg
28 or 56
units
0,5mg+1m
g
11 units
0,5mg +
14 units
1,0mg
Tablets
Champix
1mg
28 or 56
units
25mg
Nortriptylin
e
Coated
tablets
10 or 60
units
Norterol
50mg
60 units
• Initiate:
0,5mg/day 3
days
• 4th to 7th day:
0,5mg 12/12h
• >7th day: 1mg
12/12h
• Tt duration: 12
weeks (if tt
effective after
the 1st 3 months,
consider 12
additional
weeks with
1mg/day)
• AE
maintained or
serious renal
impairment:
maintenance
dose 0,5mg
12/12h
• Initiate tt 1-2
weeks before the
stipulated date
for cessation
• Administrate
with or without
food
• Insomnia
•
Somnolence
• Nightmares
• Irritability
• Headaches
• Nausea
• Fatigue
• Increased
appetite
• Terminal renal
impairment
• <18 years
• Pregnancy
• Breast feeding
• Initiate
25mg/day 3
days
• 4th to 7th day:
50mg/day
• >7th day:
75mg/day
• Maximum
dosage:
150mg/day
• Initiate tt 10-14
days before the
scheduled date
to cessation
• Sedation may
influence driving
ability
• Overdose may
lead to
cardiotoxicity
•
Somnolence
• Xerostomia
• Tremor
• Urinary
retention
• Arrhythmia
• Blurred
vision
•
Hallucinations
• Restlessness
•
Constipation
• concomitant
use of MAO
inhibitors
• AMY <4 weeks
• Pregnancy
Page 84 of 106
• Nausea
2nd
L
I
N
E
Clonidine
Tablets
0,15mg
Catapre
san
20 or 60
units
• Initiate:
0,15mg 12/12h
• Growing
titulation of
0,15mg/day
each 7 days if
necessary
• Maximum
dosage:
0,9mg/day
• Initiate tt ≤3
days previous to
the stipulated
date to cessation
• Therapy should
not be stopped
abruptly
• Sedation may
influence driving
• Dose
adjustment in
renal impairment
• Xerostomia
•
Somnolence
• Dizziness
• Vertigo
•
Constipation
• Depression
• Hydrosaline
retention
• Orthostatic
hypotension
• Bradicardia
sinusal
•
Atrioventricul
ar block
• Sinusal knot
disease
• 2nd and 3rd
degree
atrioventricular
block
• Cerebral and
peripheral
hypoperfusion
• Concomitant
use of β-bloquers
• Syndrome of
abstinence if
sudden
suspension
• Pregnancy
• Breast feeding
Page 85 of 106
31.2.4 Increase the motivation to smoking cessation – “5 Rs” strategy
Relevance
Risks
Rewards
Resistances
Repetition
Encourage the patient to describe in what measure is the abandon personally
relevant, trying to be as specific as possible.
The motivational information has a greater impact if it is relevant to the state
of the disease or risk factors to the patient, family or social status (e.g.
existence of children at home), health concern, age, sex and other important
characteristics of the patient (e.g.: previous abandon experience, personal
barriers to cessation).
The doctor should ask the patient to identify potential negative
consequences of tobacco use. He may suggest and clarify the ones that
seem more relevant to the patient. He should also stress that smoking low tar
or light nicotine cigarettes or using other forms of tobacco (e.g.: free smoke
tobacco, cigarillos, pipe) do not eliminate these risks.
Some risk examples:
• Acute risks: dyspnoea, asthma exacerbation, pregnancy hazard,
impotence, increase of carbon monoxide levels in serum;
• Long term risks: myocardial infarction, stroke, pulmonary neoplasias, other
neoplasias (larynx, oral cavity, pharynx, oesophagus, pancreas, bladder,
cervix uteri), chronic obstructive pulmonary diseases (chronic bronchitis and
emphysema) long term disability and need to continuous care;
• Environmental risks: higher risk to pulmonary neoplasia and cardiac disease
in the partner; higher rates of smokers amongst children of tobacco users;
higher risk of low birth weight, sudden infant death syndrome, asthma, disease
of the medium ear, and respiratory infections, in smokers’ children.
The doctor should ask the patient to identify potential benefits of suspending
tobacco use, and he can suggest and clarify the ones that seem more
relevant to the patient. Examples of benefits: better condition, all food tastes
better, improved sense of smell; reduction of expenses; feel better with one
self; the house, the car, clothes and breath have a better smell; you do not
have to worry about the cessation any more; it’s a good example to your
children; children are healthier; you feel in a better physical condition; better
performance in physical activities; delays skin ageing.
The doctor should ask the patient to identify barriers or obstacles to the
cessation
and
indicate
treatment
forms
(problem
resolution,
pharmacotherapy) addressed to their resolution. Examples of typical
difficulties: abstinence symptoms; fear of failing; weight gain; lack of support;
depression; having pleasure in tobacco.
The motivational intervention should be repeated each time a non motivated
patient comes to an appointment. Tobacco users who have failed in several
previous attempts should be informed that many people make repeated
attempts until attaining success.
Table adapted from Fiore MC, Bailey WC Cohen SJ, et al. Treating Tobacco USE and Dependence, Clinical
Practice Guideline. Rockville, MD: U.S. Department of Health and Human Services. Public Health Service.
June 2000, pp 32-33.
Page 86 of 106
31.2.5 Components of brief strategies to prevent tobacco use relapses
Minimal intervention
All ex-tobacco users should be congratulated for their achievement
and strongly encouraged to remain abstinent.
When faced with a recent ex-smoker, you should use open-ended
questions with the purpose of promoting the resolution of problems
by the patient himself (e.g.: in what manner was the suspension of
These interventions
tobacco use a benefit to you?).
should be part of all the
The doctor should encourage the active discussion by the patient of
appointments with a
the following topics:
patient who has recently
• the benefits, including potential health benefits, that the patient
abandoned the use of
my obtain from cessation
tobacco
• any success the patient might have had during the abandon
process (e.g.: abstinence duration, decrease of abstinence
symptoms)
• The problems found or predicable difficulties in keeping
abstinence(e.g.: depression, weight gain, alcohol, other tobacco
users at home)
Directed prevention of relapses
The components of the directed prevention of relapses are individualized according to the
problems experienced by the patients when trying to keep abstinence. These more intensive
interventions of relapse prevention may be applied during the scheduled follow-up
appointment (in person or by telephone). Below we present a list of some specific problems that
the patients may refer and some possible answers.
Problems
Responses
Programme follow-up appointments or telephone calls with the
patient.
Lack of support to
cessation
Help the patient to identify support sources in his environment.
Reference the patient to appropriate organizations that offer
counselling or support.
Negative humour or
If significant, give counselling, prescribe appropriate medication or
depression
reference the patient to a specialist.
If the patient refers craving or other abstinence symptoms, consider
Strong or prolonged
to prolong the use of pharmacotherapy or add / combine drugs to
abstinence symptoms
reduce strong abstinence symptoms.
Recommend initiating or increasing physical activity; discourage
strict diet. Stress the importance of a healthy diet.
Reassure the patient that some weight gain after abandon is
common and seems to be self-limited.
Weight gain
Keep the patient with a pharmacotherapy that delays weight gain
(e.g.: slow release bupoprion chloride and nicotine replacement
therapies, particularly nicotine chewing gums).
Reference the patient to a specialist or specialized programme.
Reassure the patient that these feelings are common.
Recommend compensating activities.
Fall of motivation/feeling
Investigate to be sure that the patient does not use tobacco
of loss
periodically, since that consumption increases the smoking stimulus,
making the abandon more difficult.
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June 2000, pp 34-35
Page 88 of 106
31.2.6 Components of an intensive intervention to abandon the habit of smoking
Component
Evaluation
Programme professionals
Programme intensity
Programme format
Types of counselling and
behavioural therapies
Pharmacotherapy
Population
Implementation strategy
The evaluation should assure that the tobacco users wish to
make an abandon attempt using an intensive treatment
programme. Other evaluations may supply useful information to
counselling (e.g.: stress level, co morbidity presence)
Multiple types of professionals are effective and should be used.
A counselling strategy would be to place a doctor providing
messages on risks and benefits to health and prescribing
pharmacotherapy, and non-clinical professionals supplying
additional psychosocial or behavioural interventions.
Due to the evidence of a strong dose-response relation, the
programme should consist of 4 or more sessions, being the
longest session over 10 minutes (Total contact time= 30 minutes)
Individual or group counselling can be used.
Pro-active telephone counselling is also effective.
The use of adjuvant self-help material is optional.
Intervention processes should be used in follow-up evaluations.
Counselling and behavioural therapies should include practical
counselling (problems resolution / performance training) and
social support intra and extra-treatment.
All
smokers
should
be
encouraged
to
use
the
pharmacotherapies mentioned in the present CPG, except in
special circumstances.
In selected populations (e.g.: pregnant women, teenagers) the
use of pharmacotherapy should be subject to special
considerations.
The doctor should explain the patient the way these drugs
increase the success rate of smoking cessation and reduce
abstinence symptoms.
The intensive intervention programmes can be used with all
tobacco users who wish to participate
June 2000, p. 39.
31.3 The Agree Instrument
PLEASE SEE ATTACHED FILE
31.4 The GLIA Instrument
PLEASE SEE ATTACHED FILE
31.5 Glossary
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This glossary aims to standardize – as far as possible – the methodological and
scientific concepts applied to the base studies of any CPG. If was initially
published in Revista Portuguesa de Cardiologia (2001;20:99-103 and
2001;20:203-210) to whom we thank permission to publish.
31.5.1 TERMS USED IN THE DIAGNOSIS
Result of the diagnosis
test
•
•
•
•
•
•
•
•
•
•
Positive test
a+b
c+d
Negative test
Results of the reference test
Existing disease
Non existing disease
a+c
b+d
True positive
False positive
A
b
C
d
False negative
True negative
Sensitivity (a/a+c): proportion of patients with the target disease presenting
a positive test.
Specificity (d/b+d): proportion of patients without the target disease
presenting a negative test.
Positive predictive value (a/a+b): proportion of patients with a positive test
with the target disease.
Negative predictive value (d/c+d): proportion of patients with a negative
test without the target disease.
Precision (a+d)/(a+b+c+d): proportion of patients correctly classified
through the test (true positive + true negative).
Pre-test probability (prevalence) (a+c)/(a+b+c+d): proportion of patients
who have the target disease, determined before the use of the diagnostic
test.
Pre-test odds: likelihood of the patient having the target disease before the
use of diagnostic test. Calculation: prevalence/1- prevalence.
Post-test odds: likelihood of the disease after the application of the
diagnostic test. Calculation: pre-test odds x likelihood ratio.
Post-test probability (post-test odds/1 + post-test odds): proportion of
patients with a given result presenting the target disease.
Likelihood ratio (LR): relationship between the probability of a given
outcome in the population with the target disease and the likelihood of that
outcome amongst non-patients. The LR can be a positive result (sensitivity/1 specificity) or a negative result (1 – sensitivity / specificity).
Calculation:
LR+ = [a/(a+c)] / [b/(b+d)]
LR- = [c/(a+c)] / [d/(b+d)]
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31.5.2 TERMS USED IN THERAPY
Control group
Experimental group
•
•
•
Event / final outcome
Yes
No
a
b
c
d
Total
a+b
c+d
Event rate: is the proportion of subjects on which an event is observed. For
example: if in 100 patients the event is observed 35 times, the event rate is
0.35.
Control Event Rate: CER = a/a + b.
Experimental Event Rate: EER = c/c + d
31.5.2.1 When the experimental treatment reduces the risk of an unfavourable
event
•
•
•
Relative Risk Reduction - RRR: proportional reduction in the rates of adverse
events among patients in the therapeutic / experimental group (EER) and
the ones in the control group (CER) in a clinical trial calculated using the
formula (EER–CER/CER) with a confidence interval of 95%.
Absolute Risk Reduction - ARR: absolute arithmetic difference between the
rates in experimental and control groups (EER-CER).
Number Needed to Treat - NNT: number of patients who need to be treated
to achieve a favourable additional outcome; is the reverse of the ARR
(1/ARR) and is rounded to the next whole number, with a confidence
interval of 95%.
31.5.2.2 When the experimental treatment increases the likelihood of a
favourable event
•
•
•
Relative Benefit Increase –RBI: increase the rate of favourable events
comparing the patients of the experimental group and the control group in
a clinical trial (EER-CER/CER).
Absolute Benefit Increase – ABI: absolute arithmetic difference between the
event rates (EER-CER).
Number Needed to Treat - NNT: number of patients who need to be treated
to achieve a favourable additional outcome comparing to the control
group; is the reverse of ABI (1/ABI) and is rounded to the next whole number,
with a confidence interval of 95%.
31.5.2.3 When the experimental treatment increases the likelihood of an
unfavourable event (iatrogeny)
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•
•
•
Relative Risk Increase - RRI: proportional increase in the rates of adverse
events among patients in the therapeutic / experimental group (EER) and
the patients in the control group (CER) in a clinical trial, calculated in a
manner similar to the RBI (EER–CER/CER) with a confidence interval of 95%. It
is also used in the evaluation of the effect of risk factors.
Absolute Risk Increase - ARI: absolute arithmetic difference between the
adverse events rates in the experimental and the control groups, whenever
the treatment has more harmful effects. It is estimated in a manner similar to
the ABI (EER-CER).
Number Needed to Harm - NNH: number of patients that, if received the
experimental treatment, would lead to an additional lesion in an
experimental individual compared with the patients in the control group. It is
the reverse of ARI (1/ARI) and is rounded to the next whole number, with a
confidence interval of 95%.
31.5.3 TERMS USED IN RISK/IATROGENIA
Adverse results
Present
a+c
Exposure
•
•
•
•
Yes
a+b
c+d
No
a
c
Absent
b+d
b
d
In a randomized or prospective trial: Relative Risk = RR = [a/(a+b)]/[c/(c+d)]
In a retrospective trial: Relative Odds = RO = ad/bc
Patient Expected Event Rate – PEER = susceptibility of the emergence of an
adverse event in a given patient who does not receive treatment
(experimental or conventional).
To calculate the Number Needed to Harm - NNH – to a certain odds ratio
and PEER:
NNH = [PEER (OR – 1) + 1]/[ PEER (OR – 1) x (1 – PEER)]
31.5.4 TERMS USED IN DIFFERENT CONTEXTS
•
Odds Ratio: odd is a relationship between the probability of the occurrence
with the non-occurrence of a particular event, that is, a relationship
between the probability that something is really something and the
probability that it may be nothing. For example, in 100 smokers, 80 develop
chronic coughing and 20 do not, the odd of cough onset of this group is
80:20, that is, 4; in contrast, the probability that these smokers have to
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develop chronic cough is 80/100, that is, 0,8 (80%). The odds ratio is the ration
between the two odds thus described. Another example: if the odds (O) of
the occurrence of an event (for example, a determined side effect) after
the exposure to a drug A is called Oa, and if the odds of the occurrence of
the same events after exposure to drug B is called Ob, the odds ratio is
OR=Oa/Ob. If, hypothetically, the OR=6 then the probability of a patient
presenting the side effect (event) with the drug A is six times higher than the
probability that the event occurs with the drug B. Calculations (relating to
the above table):
Event odds in the control group –
EOC = a/b
Event odds in the experimental group –
EOE = c/d
•
•
•
•
•
•
•
Odds Ratio) –
OR: (c/d) / (a/b)
Relative Risk –
RR: EER/CER
Confidence intervals (CI): is the range within which it is hoped that the real
value of a statistical measure is situated, is generally accompanied by a
percentage (usually 95%), which defines the level of the respective
confidence: in 95% of cases the value is within the limits defined.
Cost-benefit analysis: evaluates whether the cost of an intervention is
justified by the benefit obtained, using identical units of measuring the costs
and benefits (usually monetary).
Cost-effectiveness analysis: measures the real cost of a service and its
outcomes – which are reported in the same unit of measure.
Cost-utility analysis: converts the effects of an intervention in personal
preferences of the patients (also known s utilities), indicating the cost of any
additional quality (e.g. cost per QALY – quality-adjusted life year).
Decision analysis: support technique for the clinical decision, used especially
when it is accompanied by a high degree of uncertainty; includes the
systematic description of all relevant information, quantifying the degree of
uncertainty. The graphical form is a tree of decision.
Tests of N-1: in this type of testing patients are tested in pairs of consecutive
and alternate periods, in which in one of them is used an experimental
treatment and in the other is used the usual treatment (or placebo); ideally,
the details are concealed from patients and doctors in monitoring
outcomes; this process is repeated the number of times necessary to
establish the efficacy (or inefficacy) of the treatment in that individual
patient.
Effectiveness: measure of the effect of an intervention in normal clinical
practice conditions. Tests for evaluating effectiveness are called
management trials.
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•
•
•
•
•
•
•
•
•
Efficacy: measure of the effect of an intervention in ideal conditions – usually
in randomized and controlled trials. Tests for evaluating efficacy are called
explanatory trials.
Incidence: number of new cases of a certain disease in a population, during
a given period of time.
Prevalence: number of cases of the disease existent in a population in a
given point in time.
Phase I trials: testing of a drug in normal volunteers (healthy), without the
existence of a control group.
Phase II trials: testing of a drug in normal volunteers (healthy), but sometimes
as RCTs.
Phase III trials: testing of a drug in patients usually compared to the standard
therapy and as RCTs.
Phase IV trials: post marketing pharmacovigilance.
Point estimate: are the results of a sample of a study, to be used as the
estimate closer to reality on the population from which it was selected; the
confidence interval of a point estimate is a measure of the uncertainty (due
to chance) associated with that estimate.
Sensitivity analysis: is a process which re-estimates the results of a trial,
changing certain parameters or perspectives, in order to investigate if the
initial conclusions remain unchanged.
31.5.5 GENERAL TERMS FOR CLINICAL TRIALS
•
Evaluation of a study design: in lactu sensus, the design is one of the most
important characteristics of a trial, because it has a crucial importance in
determining causality. A causal factor is defined as “… a factor which
operation increases the frequency of an event…”, this implies that: a)
people affected by the causal factor present a higher frequency of a
certain event or outcome; to test this hypothesis, we have to compare two
groups, only one exposed to the putative factor – it is a cohort trial; and b)
the individuals presenting a determined event or outcome, have had, in the
past, a higher exposure to the causal factor than the individuals without
that(those); to test this hypothesis, we have to compare two groups, one
with the study event and the other without it – a case-control trial. In global
terms, there are four main trial groups, which try to respond to different issues:
interventional trials (…”what is the effect of this intervention?”…), surveys
(…”is this condition/disease common?”… and … “is there some associations
between certain conditions / diseases and certain exposures?”…), cohort
trials (…”which are the effects cause by a certain exposure?”…) and casecontrol trials (…” What are the causes of this condition / disease?”…).
Adverse event
Present (case)
Absent
Totals
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(control)
Exposure to
Yes (cohort)
a
b
a+b
treatment
No (cohort)
c
d
c+d
Totals
a+c
b+d
a+b+c+d
• Randomized and controlled trials – RCTs: start with a + b + c + d and randomize to (a + b)
and (c + d)
• Prospective (or cohort) trial: select (a + b) and (c + d)
• Crossed / analytical sectional trial: select a + b + c + d
• Case-control trial: select (a + c) and (b + d)
• In a RCT or cohort trial, the Relative Risk (RR) = [a/(a+b)]/[c/(c+d)]
• In a case-control trial, the Odds Ratio (OR) = ad/bc
•
•
•
•
Clinical trial (clinical trial, therapeutic trial, intervention study): is a trial that
seeks to text the efficacy and safety of a drug, or an intervention. Clinical
trials can be randomized and controlled or only controlled.
Randomized clinical trial – RCT: a randomized and controlled clinical trial is
an epidemiological experience in which the subject in study (sample)
selected through explicit methods from a larger group (population), are
randomly distributed between two groups: the experimental one, over which
the treatment will occur (or preventive measure, or intervention) and the
control group. The results are rigorously evaluated, comparing in both groups
the disease, recovery, mortality, morbidity rates or any other outcome
considered interesting. One can inclusively adapt a cross-over design in
which patients and controls, after receiving treatment (or placebo, e.g.) are
changed to the other group, that is, the initial experimental group changes
to control group and vice-versa. The RCT design is considered the most valid
to the testing of an intervention, so we consider it the gold-standard to the
determination of the efficacy of a drug. Advantages: blinding of the
distribution for treatment (blinding is easier), equal distribution of
confounding factors and larger representativeness of statistical analysis.
Disadvantages: expensive activity, possible volunteer bias (see below) and,
sometimes, ethically problematic.
Controlled clinical trial: trial that compares one or more experimental groups
with one or more control groups. It can be non randomized (but all
randomized trials are by definition controlled ones).
Prospective (or cohort) trial: is a trial where the subjects are recruited and
followed to that point in time forward, during a certain period. It is a
particularly used design to the definition of risk and prognostic: for example,
a group of health volunteers (cohort) can be recruited, subject to a risk
factor (No. of cigarettes/day) to a certain disease (lung carcinoma), and
follow the group for a certain period of time (years). The comparison, in the
end of the follow-up period, of the disease incidence in certain subgroups
(<10, 11-20, >20 cigarettes/day, e.g.) allows the establishment of the relation
power between the risk factor and the respective disease. Advantages:
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•
•
•
•
•
•
ethically safe, possibility of mating the subjects and establishing the
temporality and direction of events, standardization of eligibility criteria and
the evaluation of outcomes, easy to execute and nor very expensive.
Disadvantages: difficult to identify controls, eventual impossibility to mate the
subjects, difficulty in blinding, inexistence of randomization, need for large
dimension samples to study rare diseases and highly expensive.
Cross-sectional study: also known as prevalence trial, is a trial whose aim is to
observe a certain population in a specific point (or interval) of time,
determining the exposure and outcome simultaneously. Advantages:
ethically safe and with limited costs; Disadvantages: it only establishes
association (not causality), susceptible to recall bias (see below), possibility
of unequal distribution of confounding factors and possibility of unequal
distribution of the groups dimension.
Retrospective (or case control) trial: is a trial whose design permits to test the
disease aetiology. This type of trial is based upon a concept which agrees
that the clarification of the relationship between exposure to factors that
may be a source of a particular disease (putative / causal factors), and the
disease, can be achieved through data related to the individual
characteristics of the study subjects, as well as the identification of events
experienced by those in the past. The essential point is that some study
subjects present the disease (or other interesting result) and others do not,
therefore allowing comparing both groups in terms of past events.
Advantages: ideal to rare diseases, need for few study subjects, quick and
nor very expensive; Disadvantages: need to recur to remembrances of the
subject or written processes, existence of confounding factors, difficulty in
selecting the control group, potential remembrance and selection bias (see
below).
Case Series: an observational trial, non controlled, involving an intervention
and a result in more than one patient.
Observational trial: a trial with no intervention from the investigator, that is,
he only collects data without influencing the course of the disease.
Sequential trial: it is a trial in which the data are permanently analyzed
according to the outcomes which are available for each individual patient.
This process is kept until a clear benefit is detected in one of the
experimental groups or it is verified that there will be no benefit; these trials
are shorter and should only be used in situation where the outcome is shown
relatively early.
Statistical power: is the probability that the null hypothesis is rejected when in
fact it is false; in a clinical trial, for example, it is the dimension of the
certainty of the non existence of a false negative result (the drug is not
effective when in fact it reveals efficacy); the statistical power of a trial
depends on: 1) its dimension (No. of participants); 2) number of events in the
Page 96 of 106
•
•
•
trial (e.g. acute myocardial infarctions); 3) the variation degree of a
continuous outcome (e.g. weight); 4) which dimension of the effect
between control and experimental groups is deemed important; and 5)
which is the certainty we want to assure to avoid a false-positive result (the
definition point of statistical significance).
Surrogate end-points: measurements /factors related to the outcomes and
that, although not practical relevant, are believed to reflect important
aspects of the outcomes. The surrogate end-points are usually biochemical
or physiological markers, that can be easily measured and may be used as
predictive factors for important outcomes; for example, a determined
cardiac biochemical value (troponin) can be a marker of the existence of
coronary disease (AMY). The characteristics which a surrogate end-point
should have are: 1) be reliable, reproducible, easy to measure and to obtain
and present a relationship level / disease (i.e. the higher, the greatest
possibility of disease); 2) it should be a real predictor of the disease (or its risk)
and its relation to the disease should have a biological plausible
explanation; 3) it should be sensitive (a positive result should detect most
patients) and specific (a negative result should exclude most healthy
individuals), and have a good predictive positive value (an abnormal value
identifies patients at risk) and negative (a normal value identifies healthy
individuals); 4) it should have a clear definition of what a normal value is; 5)
the standardization of changes values should imply a response to therapy.
Importance of a trial: it is a valorisation inference in terms of the outcomes
impact of a trial / study in biomedical, epidemiological or research
knowledge.
Bias of a clinical trial: a bias is defined as a systematic deviation of the true
value of a variable, factor or characteristic. A bias exists when the findings of
a study are systematically away from the truth, due to problems with the
collection, analysis, interpretation, publication or review of their data. There
are several ways to introduce bias in a study: 1) systematic error in the
measurement of data; 2) systematic error in the statistical calculations
(medium, rates, measures of association, etc.); 3) methodological
weaknesses of the study (in the collection, analysis, interpretation,
publication or review of the data); 4) wrong analytical techniques
applicable to the constituent factors of a test / clinical study; and 5)
deviations caused by prejudices of the researchers. There are many bias
described: 1) publication bias: it is a trend that the editors of medical journals
have to publish more frequently studies that show "positive" results (especially
if they are considered "news"), as opposed to studies with "negative" non
significant results (especially if they confirm data already known in the
literature). A major consequence of this bias is the potential to decrease the
perception of the existence of an association between two factors (for
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•
example a tumour marker with the original tumour) or the therapeutic
efficacy of a new molecule (which seems more effective than in fact it is). A
second major consequence is to be a source of problems in meta-analyses;
2) volunteer bias: the fact that the patients (or controls) that volunteer to
participate in a clinical trial may have different characteristics, or respond to
treatment differently from other groups selected at random; for example,
there is evidence that patients who volunteer to studies on preventive
measures may have, at the outset, a healthier lifestyle than most patients
randomly selected from a non volunteer database; 3) recall bias: errors due
to lack of sufficient information on retrospective studies, by difficulties of the
subjects, when asked, to be able to remember precisely the relevant facts,
for example, when questioned about the use of a particular drug, a patient
experiencing a side effect with a particular drug, tends to recall more
accurately that drug than a patient who never experienced a similar
episode; 4) selection bias: errors due to the existence of systematic
differences in the characteristics of the subjects selected for a study, versus
those not selected; for example, volunteers selected as being in a certain
place at a certain time (the emergency services during the night), forgetting
the other potential candidates (patients going to the doctor during the
day); 5) ascertainment bias: it is the systematic non inclusion of all potential
classes or subgroups of patients supposedly representative in the formation
of a sample; for example, select the population to study from hospital
patients when the primary care are also important; 6) detection bias:
systematic error in the verification, diagnosis and follow-up of patients in a
trial; for example, to require analytical tests in patients in the hospital and
forget the patients studied in clinic; 7) bias of interpretation: error from
inferences and speculation (not considering all possible interpretations
consistent for the facts, or ignoring the cases of exception); 8) sampling bias:
systematic error in the study of a non-randomized sample of the population;
9) attrition bias: error in the comparison of results of patients in both groups of
a RCT by differences in drop-outs or exclusion of those - for example due to
side effects of the experimental drug.
Sample size: the determination of the size of the sample is the mathematical
process in which the decision is based, before the start of the trial, of how
many patients will be studied. This decision is based on several factors: 1)
incidence or prevalence of the condition that you want to study; 2) the
strength of the relationship (real or putative) among the variables included in
the trial; 3) the power that want the trial to have, that is, the ability to
demonstrate a causal association (if any); 4) the extent permitted that the
study may have in relation to the type I error (rejection of the null hypothesis
when it is true, that is, saying that a treatment is effective when in fact it is
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•
•
•
•
not); 5) the level of significance; 6) the existing confounding factors; 7) errors
in the classification.
Criteria for inclusion and exclusion: are the characteristics to be satisfied by
the subjects to be included (criteria for inclusion) or excluded (criteria for
exclusion) in a trial; these criteria are defined in advance and are crucial in
defining the samples, and especially important in the implementation of the
results of a clinical trial to the individual patient in the day-to-day (external
validity). The transposition of the scientific evidence of a RCT to a
therapeutic gesture involves a judgment on the applicability of that in the
individual patient, and can be achieved by answering the following
questions: 1) is my patient so different from the ones participating in the trial
that its results can not be applied? 2) In the context in which we are, will the
treatment be feasible? 3) What will be the benefits (and dangers) of
treatment? 4) Will the values (moral, practical) of my patient influence the
final decision?
Randomization: is a method used for generation of a sequence of the
random distribution of the participants in a RCT; usually, a correct
randomization is achieved by using a table of random numbers or
generated by computer, in which each subject is sequentially assigned a
code that defines in what group he will be included. There are more
sophisticated techniques of randomization for special cases: 1) stratification,
where the groups are formed by having in common a confounding factor;
2) matching, in which the subjects of comparison are selected for their
similarity – relating to confounding specific factors - with the studied subjects
(which, in a retrospective study, present for example a given risk); and 3)
techniques of multivariate regression, in which the analysis of a trial defines
the outcome as the dependent variable of the equation, including in the
latter the putative causal factor and the confounding factors.
Blinding or masking: maintaining secrecy about which group the
participants of a RCT were included in the initial randomization, the blinding
can be simple (when patients do not know to which group they were
distributed - experimental or control), double (besides the patient, also the
investigator does not know what kind of treatment the patient is doing) and
triple (the patient, the investigator and the statistician / investigator who
analyzes the results do not know the groups in the study).
Concealment of allocation: it is a process used to prevent the knowledge of
the distribution of the subjects by the trial groups; is different from blinding
and can be done, for example, by making the process of randomization to
be done by an investigator who is not involved in recruitment of participants
in the trial, or when the envelopes with the codes of randomization are
opaque to light so that we can not know to which particular group will be
assigned a certain patient.
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•
•
•
Overall validity of the results of a trial: is the degree of confidence that the
results of a clinical trial - especially when you want to generalize them
beyond the study population - transmit to whoever analyses them, based on
the methodological analysis of the study, the representativeness of the
sample and in the nature of the population from which this comes. There are
two types of validity: 1) internal validity: the two studied groups experimental and control - are selected and compared in such a way that
any differences found in the variables can only be attributed to the effect
under study (or possible sampling error) 2) external validity (generalizability,
applicability): the results are applicable to other populations (not to the
studied one).
Intention to treat analysis: is the one that analysis all participants in a trial
according to the intervention for which they had been randomized in the
beginning, whether they have received it or not, for example, a patient in
the experimental group will be analyzed at the end as having being treated,
even if he has left the trial.
Factorial Design of a Test: the participants of a trial with 2X2 factorial design
are distributed to four groups: experimental I (with a particular treatment),
experimental II (with a second different treatment), experimental III (both)
and experimental IV (none). For example, in the prevention of an embolic
stroke in patients with non-rheumatic arterial fibrillation, we could test a
platelet anti-aggregant (aspirin), an anticoagulant (varfarin), both and
none.
31.5.6 GENERAL TERMS FOR SYSTEMATIC REVIEWS AND META-ANALYSIS
•
Systematic review: is a scientific literature review on a particular theme,
executed so that the biases are reduced to a minimum. A key feature of a
systematic review is the clear and not ambiguous explanation of the criteria
used for the selection, critical evaluation and the inclusion of scientific
evidence. Thus, a systematic review presents formal and precise objectives
and criteria for inclusion (and exclusion) of the trials thoroughly explained.
The systematic review is different from the usual reviews (also designated as
narrative reviews):
Differences between systematic and narrative reviews
Narrative review
Systematic review
Issue/theme
Usually broad and
Usually focused and precise
comprehensive
Non specified (and therefore
Sources comprehensive and
subject to bias)
complete; explicit research
Sources and research
strategy
Non specified (and therefore
Selection based in pre-defined
subject to bias)
criteria, uniformly applied
Selection
Evaluation
Variable
Rigorous and critical
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Synthesis
Inferences and
recommendations
•
•
•
•
•
•
Qualitative summary
Sometimes based on
scientific evidence
Quantitative summary (if it
includes statistical synthesis, it is a
meta-analysis)
Always based on scientific
evidence
Meta-analysis: is a statistical technique that allows the combination of results
of different clinical trials (usually RCTs) from a systematic review. The rationale
of this approach is justified by the fact that most trials do not have enough
power per si to respond effectively to the posed question. The meta-analyses
have two kinds of structural components: 1) qualitative, with application of
pre-defined methodological criteria of quality (absence of bias, degree of
availability of data, e.g.) and 2) quantitative, which consist on the
integration of numerical information. Usually, the meta-analyses have a
typical graphic representation. A meta-analysis can be considered a
systematic review with formal statistical information.
Heterogeneity of the trials for inclusion in a meta-analysis: the heterogeneity
of the trials can be detected up into three fields: the non-uniform effects of
the treatment under analysis (statistical heterogeneity), the differences in the
design of the studies (methodological heterogeneity) and in the groups of
patients included in the trials (clinical heterogeneity); these differences
should be systematically analyzed before the inclusion of clinical trials in
meta-analysis, especially in situations where there are numerous clinical
differences but only a small number of trials available for analysis.
Cumulative meta-analysis: the trials are added one at a time by a particular
order (publication date, e.g.), but the results are summarized with each new
trial that is added.
Funnel plot: is a graphical representation comparing the size of the samples
with the size of the therapeutic effect, in clinical trials included in a metaanalysis; in certain circumstances, it can provide clues for determining the
absence of trials.
Patient Expected Event Rate - PEER: is the probability that the patient will
demonstrate a particular event (e.g. sudden death) for a specific period of
time. It is produced through prognostic studies, databases or personal
experience.
The importance of the results of a systematic review is based on the
determination of NNTs, using odds ratios (OR) - especially when the results
are binary - and the patient expected event rates (PEER); these calculations
are different as the ORs are superior or inferior than 1 (see equation below).
In the calculation of NNTs we may also use the following tables (which are
based on the mentioned equations):
Page 101 of 106
For an OR <1: NNT = 1 - [PEER x (1 - OR)] / (1 - PEER) x PEER x (1 - OR). The
numbers of the table are the NNTs for the corresponding ORs in the expected
level of events to the specific patient (PEER). This table applies whenever an
adverse event is avoided by the therapy.
0.05
0.10
0.20
0.30
0.40
0.90
209
110
61
46
40
0.80
104
54
30
22
19
Odds Ratios
0.70
69
36
20
14
12
0.60
52
27
14
10
9
0.50
41
21
11
8
7
0.50
38
18
11
8
6
0.70
44
20
13
9
0.90
101
46
27
18
Note: for a given OR the NNT is the lowest when PEER = 0.50
6
12
Patient
PEER
For an OR> 1: NNT = 1 + [PEER x (OR - 1)] / (1 - PEER) x PEER x (OR - 1). The
numbers of the table are the NNTs for the corresponding ORs in the expected
level of events to the specific patient (PEER). This table applies whenever a
beneficial event is increased by therapy and when a side effect is caused by
this.
0.05
0.10
0.20
0.30
0.40
1.1
212
112
64
49
43
1.2
106
57
33
25
23
Odds Ratios
1.3
71
38
22
17
16
1.4
54
29
17
13
12
1.5
43
23
14
11
10
0.50‡
42
22
15
12
10
0.70
51
27
19
15
0.90
121
66
24
38
Note: for a given OR the NNT is the lowest when PEER = 0.50
13
32
Patient
PEER
The calculation of a NNT from the Relative Risk (RR) varies according to this
being greater or less than 1:
For a RR <1: NNT = 1 / (1-RR) x PEER
For a RR> 1: NNT = 1 / (RR-1) x PEER
Page 102 of 106
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Protecting Children and Families from Tobacco: Leadership Training
Additional Resources for Portugal
World Health Organization
http://www.who.int/countries/prt/en/
http://www.euro.who.int/en/where-we-work/member-states/portugal
http://www.euro.who.int/en/what-we-do/health-topics/disease-prevention/tobacco
Tobacco Control Laws
http://www.tobaccocontrollaws.org/legislation/country/portugal
Ministry of Health
http://www.min-saude.pt/portal
http://www.min-saude.pt/portal/conteudos/informacoes+uteis/deixar+de+fumar/deixardefumar.htm

Portugal - AAP.org

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