Severe thiamine deficiency following bariatric surgery

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Severe thiamine deficiency following bariatric surgery – Case report
José Henrique da Silva1, Bruno Monteiro de Carvalho2; Caroline Richene Oeiras2,
Eduardo Fernandes da Silva Junior2, Elysson Oliveira Abinader4, Henri Horstmann4.
Isolda Prado de Negreiros Nogueira Maduro5
Estágio em Clínica Médica, Disciplina de Nutrologia do Curso de Medicina das
Universidade do Estado do Amazonas, Manaus, AM.
1
Physician, Discipline of Nutrology, Hospital das Clinicas, Ribeirão Preto School of
Medicine, São Paulo University
2
Graduate student, Medical School from Amazonas State University
3
Resident physician, General Surgery, University Hospital Getúlio Vargas /UFAM.
4
Intensive care physician, University Hospital, pela AMIB, University Hospital Getúlio
Vargas /UFAM.
5
Médica PhD, Professor of Nutrology, Medical School from Amazonas State University,
coordinator of the nutrition support team of University Hospital Getúlio Vargas /UFAM.
Correspondence to:
Dr Isolda Prado de Negreiros Nogueira Maduro
Universidade do Estado do Amazonas, Escola Superior de Ciências da Saude.
Av. Carvalho Leal, 1777 Edifício Adriano Jorge, Faculdade de Medicina, Internato.
Cachoeirinha
69065-001 - Manaus, AM – Brasil Tel: (92) 36334372 E-mail: [email protected]
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Abstract: Thiamine deficiency has 4 clinical forms: dry beriberi, wet (chronic and acute),
Wernicke encephalopathy and Korsakoff syndrome. It can be related to intake reduction,
impaired absorption or increased consumption conditions. The present report shows the
case of an obese patient who underwent bariatric surgery, and after 3 months presented
with severe vitamin deficiency and evident beriberi symptoms and Wernicke, with
significant improvement after nutrient replenishment.
Keywords: bariatric surgery, thiamine deficiency, beriberi, Wernicke encephalopathy,
Korsakoff syndrome
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Introduction
Vitamins are indispensable to metabolic functions and their deficiency may lead to
peculiar clinical manifestations. B1 vitamin – thiamine – deficiency displays four classical
forms:
sensory-motor
and
symmetrical
peripheral
reflex
painful
or
non-painful
polineuropathy, affecting mostly distal limbs; peripheral vasodilation, sodium and water
retention, resulting in high cardiac output, edema and bilateral ventricular dysfunction
(chronic wet beriberi); acute wet beriberi associated with myocardial injury and circulatory
shock (Shoshin beriberi) and Wernicke encephalopathy, characterized by the triad: ocular
motor dysfunctions, ataxia, mental confusion, associated to amnestic syndrome, learning
impairment and confabulation (Korsakoff)1.
Description of the case
A 44-year-old female, class III obesity, with type II diabetes, hypertension,
underwent gastroplasty, Fobi-Capella technique, in January 2008, weighing then 150kg with
body mass index (BMI) of 56,45kg/m2. At 3 months post-surgery, she presented with daily
vomiting for over a month, upper and lower limbs paresis and paresthesia, drawling with
sensation of heavy tongue, mental confusion, hyporexia and moderate efforts dyspnea. She
also mentioned an approximate 30kg weight loss since surgery (20% reduction of
preoperative weight), constipation for about 7 days and dysuria. On physical examination,
she was in a regular state of health, afebrile, dehydrated, pale (++/4+), moderate efforts
dyspnea, slow response to verbal commands, mental confusion, horizontal and vertical
nystagmus, bilateral leg and ankle edema. No palpable adenopathy. Grade IV muscle
strength in all limbs. Heart rate 92bpm, blood pressure ranging between 140-160 (systolic)
and 70-110 (diastolic), respiratory rate 22 per minute. On auscultation, bibasilar diminished
vesicular murmur, S1S2 hypophonesis, no rhythm abnormalities or murmurs. On the first
day of admission, at the surgical, treatment for urinary tract infection (UTI) was started with
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ciprofloxacin based on the pyuria found on urine sample. However, on the fifth day of
admission, the patient had worsening of symptoms with mild effort dyspnea, grade III
muscle strength and ascending flaccid paralysis of lower limbs. The neurology specialists
suggested Guillain-Barré’s Syndrome. However, a posterior nutrology evaluation suggested
a vitamin B complex severe deficiency, especially thiamine, presenting as beriberi and
Wernicke. Thus, vitamin B complex supplement was started (Beplexoran®) 14 ampoules in
1.000ml of normal saline 0,9% infused for 24 hours; cyanocobalamin 1.000mcg
intramuscular and posteriorly 5.000mcg 3 times a week, and also ferrous sulfate and folic
acid. Before this intervention, the patient had been in use of O2 with macronebulizer
evolving to respiratory failure. After two days of vitamin replenishment she was sitting on the
bed, referring improvement of the paresthesia and dyspnea (respiratory rate 18 in ambient
air). On the ninth day after admission, she had grade IV muscle strength in all limbs and
almost imperceptible nystagmus. Skull and lumbosacral CT were performed. It revealed
only osteophytes on vertebral bodies and annulus fibrosus calcification. Another chest CT
scan showed a slight increase in the cardiac area (Figure 1), which can be explained by the
wet beriberi.
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Discussion
Vitamin B1, thiamine, was the first to be discovered from the vitamin B complex,
and is involved in many metabolic processes such as of carbohydrates and branched-chain
amino acids, as well as in nerve conduction. It acts on the decarboxylation of alpha-keto
acids, as the pyruvate-alpha-ketoglutarate and branched-chain amino acids, playing an
important role in energetic metabolism1. Thiamine pyrophosphate, a metabolite, acts as a
coenzyme for the formation of transketolase, which converts hexose and pentose. In
elevated doses, it is passively absorbed in the digestive tube, being in small doses carriermediated transported, and phosphorylated in this process1. Once absorbed, it is transported
along with plasma proteins (mainly albumin) and erythrocytes. It is stored mainly in skeletal
muscle, but also in the heart, liver, kidneys and brain1. The total organic reserve of vitamin
B1, mainly as thiamine pyrophosphate, is approximately 30mg, with a half-life of 9-18 days.
The daily quota is 1,2mg for men and 1,1mg for women, being greater in men because of
greater energy expenditure. Thiamine needs increase in 10% with pregnancy and
breastfeeding. The primary sources of this vitamin are pork, beef, vegetables, all grains and
nuts1-6. It is important to remember that vitamin B1 is photosensitive, denatured by heat and
destructed at pH>8. Tea, coffee, raw fish, seafood contain thiaminases which can destroy
the vitamin, thus a large intake of these foods may reduce the organic reserve of this
nutrient. Thiamine and its metabolites excretion is essentially through urine1-3.
Thiamine deficiency is mostly caused by low intake. In western countries the
commonest primary causes are alcoholism and chronic diseases such as cancer. Alcohol
interferes directly in the absorption of vitamin B1 and in the formation of thiamine
pyrophosphate, thus it must always be supplemented during refeeding of alcoholic patients,
since the replenishment of carbohydrates without vitamin B1 may precipitate its acute
deficiency with severe symptomatology and its complications. Patients with alcoholic liver
disease have even higher risks of presenting this deficiency1-3.
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Thiamine deficiency is a commonly ignored cause of lactic acidosis. In this case we
see a patient with acute thiamine deficiency presenting with neurological (Wernicke) and
cardiovascular (beriberi) disorders, secondary to bariatric surgery complications. Bariatric
surgery can be exclusively restrictive (e.g. gastric band), exclusively disabsortive (e.g.
biliopancreatic diversion) or restrictive-disabsortive (e.g. Roux-en-Y or Capella gastric
bypass)4. In gastric bypass (our patient’s surgery), the rate of nutritional and electrolyte
disturbances is 17% and mortality ranges between 0,3 and 1,9%. It is estimated that
thiamine and/or vitamin B12 deficiency may correspond to 40% of neuropathy cases after
bariatric surgery4. In these patients, thiamine deficiency is often found among those with
frequent vomiting3.
In its initial stage, thiamine deficiency induces anorexia, irritability, apathy and
generalized weakness. As it continues, it leads to beriberi, classically divided in dry and wet,
showing in both forms pain and paresthesia. Wet beriberi presents as a cardiovascular
syndrome due to the disturbance in myocardial energy metabolism and autonomic
dysfunction, occurring as late as 3 months after the onset of an insufficient vitamin B1 diet.
The patients present with cardiomegaly, tachycardia, congestive heart failure with high
cardiac output, peripheral edema and neuritis. Patients with dry beriberi present with
symmetrical peripheral sensory-motor neuropathy and hyporeflexia, mainly in the lower
limbs1-3.
Wernicke encephalopathy, described as a severe neurological manifestation in
vitamin B1 deficiency in alcoholics, consists of a syndrome with ophthalmoplegia (due to
ophthalmoparesis of one or more extraocular muscles), horizontal nystagmus, cerebellar
ataxia and mental deterioration. When there is memory loss and associated confabulatory
psychosis, it is named Wernicke-Korsakoff syndrome, which despite being described in
alcoholics, could be associated with a genetic predisposition involving a variant
transketolase isozyme1-6.
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The diagnosis of this deficiency can be performed through functional enzyme assay of
transketolase activity, measured before and after addition of thiamine pyrophosphate. A
stimulation value greater than 25% after addition of the pyrophosphate (activity coefficient of
1,25) is considered normal2.
The treatment of wet beriberi thiamine deficiency consists of parenteral
administration of thiamine in the dose of 50 to 100mg, to reestablish the cellular and hepatic
deposits, and reversal of symptomatology often occurs after 24 hours. In the WernickeKorsakoff syndrome, literature data suggest an intravenous administration of 100mg of
thiamine, followed by intramuscular 100mg daily for 5 days, plus permanent thiamine
supplementation. There are still reports that some patients may not respond to this
supplementation due to magnesium deficiency. Magnesium acts as a transketolase cofactor
via pentose phosphate pathway, making it necessary to supplement it as well so there can
be a response5-7.
It is important to note that thiamine deficiency must be thought of not only in situations with
absorption and deficiency disturbances, but also in those in which basal needs are
increased like strenuous physical exercises, fever, hypercatabolism, parenteral nutrition,
use of loop diuretics in heart failure and dialysis in chronic kidney disease. These conditions
may be present in many pathologies, which can be aggravated by the concomitant thiamine
deficiency2-7.
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Figure 1: Axial chest CT scan slice showing enlargement of the heart