Results of biliopancreatic diversion in two patients with Prader-Willi syndrome.

Prader-Willi Syndrome (PWS) is a genetic disorder characterized by hypotonia, mental retardation or learning disability, hyperphagia and compulsive eating due to hypothalamic dysfunction. Obesity is a major cause of increased morbidity and mortality among patients with PWS. Gastric restrictive surgery has been associated with partial breakdown of the staple-line in PWS. We report two patients with PWS associated with morbid obesity and obstructive sleep apnea who underwent biliopancreatic diversion (BPD). A 27-year-old male with BMI 52 kg/m(2) and a 20 year-old female with BMI 64 kg/m(2) underwent BPD. No perioperative complications were observed. After BPD, the male's BMI was 36.7 kg/m(2) at 12 months and the female's BMI was 48.4 kg/m(2) at 28 months, with excess weight loss 58% and 48%, respectively. They developed loose stools associated with eating. These patients have shown a considerable improvement in hypersomnia and respiratory difficulties. BPD proved to be an effective approach to weight loss in PWS, resulting in improvement of sleep apnea, behavior problems and quality of life.

Prevalence of subclinical hypothyroidism in a morbidly obese population and improvement after weight loss induced by Roux-en-Y gastric bypass.

BACKGROUND: There are many studies concerning thyroid function in obesity, and some of them describe higher TSH levels in obese subjects. Few studies evaluated long-term changes in thyroid function caused by weight loss after bariatric surgery. Our aims were to evaluate the prevalence of subclinical hypothyroidism (SH) in a morbidly obese population and to analyze the effect of weight loss induced by Roux-en-Y gastric bypass (RYGBP) on TSH and thyroid hormone (TH) levels. METHODS: TSH, free thyroxine (fT4) and total triiodothyronine (T3) levels were analyzed before and 12 months after RYGBP in patients with grade III or grade II obesity with co-morbidities. Subjects taking TH and/or with positive antithyroid antibodies and/or with overt hypothyroidism were excluded. RESULTS: 72 subjects (62F/10M), with mean age 39.6+/-9.8 years and mean BMI 53.0+/-10.4 kg/m2 were studied. The prevalence of SH before RYGBP was 25% (n=18). There was a significant post-surgical decrease in BMI in the whole population, as well as in SH patients. In the SH group and normal TSH group, there was a decrease in TSH and T3, but not in fT4. TSH was not correlated with initial BMI or percent change in BMI. TSH concentrations reached normal values in all SH patients after RYGBP. CONCLUSION: Our data confirm that severe obesity is associated with increased TSH. The decrease in TSH was independent of BMI, but occurred in all SH patients. A putative effect of weight reduction on the improvement of SH in all patients may be an additional benefit of bariatric surgery.

Lipid peroxidation in bariatric candidates with nonalcoholic fatty liver disease (NAFLD) -- preliminary findings.

BACKGROUND: Pathogenesis of nonalcoholic fatty liver disease (NAFLD) remains incompletely known, and oxidative stress is one of the mechanisms incriminated. The aim of this study was to evaluate the role of liver oxidative stress in NAFLD affecting morbidly obese patients. METHODS: 39 consecutive patients with BMI >40 kg/m2 submitted to Roux-en-Y gastric bypass were enrolled, and wedge liver biopsy was obtained during operation. Oxidative stress was measured by concentration of hydroperoxides (CEOOH) in liver tissue. RESULTS: Female gender was dominant (89.7%) and median age was 43.6 +/- 11.1 years. Histology showed fatty liver in 92.3%, including 43.6% with nonalcoholic steatohepatitis (NASH), 48.7% with isolated steatosis and just 7.7% with normal liver. Liver cirrhosis was present in 11.7% of those with nonalcoholic steatohepatitis. Concentration of CEOOH was increased in the liver of patients with NASH when compared to isolated steatosis and normal liver (0.26+/- 0.17, 0.20+/- 0.01 and 0.14+/- 0.00 nmol/mg protein, respectively) (P < 0.01). Liver biochemical variables were normal in 92.3% of all cases, and no difference between NASH and isolated steatosis could be demonstrated. CONCLUSIONS: 1) Nonalcoholic steatosis, steatohepatitis and cirrhosis were identified in substantial numbers of morbidly obese patients; 2) Concentration of hydroperoxides was increased in steatohepatitis, consistent with a pathogenetic role for oxidative stress in this condition.

Estudo clínico, molecular e terapêutico de um caso de adenoma hipofisário produtor de TSH / Clinical, molecular and therapeuthic of a case of pituitary adenoma

O adenoma produtor de TSH é o mais rato dos adenomas hipofisários (<1 por cento) e deve ser suspeitado em todo paciente com quadro clínico de hipertireoidismo e nível sangüíneo de TSH detectável, dosado por ensaios ultrassensíveis. Descrevemos a história clínica de um homem de 38 anos, tratado por hipertireoidismo com drogas antitireoideanas durante três anos, antes de se estabelecer o diagnóstico de macroadenoma hipofisário secretor de tireotrofina. Apresentava níveis elevados de T3 (380mcg/dl). T4 (18,6mcg/dl) e TSH (19,8uU/ml), este último interpretado, inicialmente, como erro laboraotrial. A TC e RNM de hipófise evidenciaram um macroadenoma com expansäo para e supra-selar. Após compensaçäo do hipertireoidismo com antitiroideanos, o paciente foi submetido à adenomectomia transesfenoidal. A análise dos exons 8 e 9 pGS e dos exons 5 e 6 da pGi em DNA extraído do tecido hipofisário, mostrou migraçäo normal no gel em gradiente de denaturaçao, afastando presença de mutaçao ativadora no gene da proteína G na etiologia do tumor. A administraçäo aguda de octreotídeo promoveu queda significativa dos níveis de TSH. Seis dias após a cirurgia, os níveis e T3, T4 e TSH estavam normais. Após dois meses, entretanto, constatou-se recorrência clínica e bioquímica do hipertireoidismo, caracterizada por níveis elevados de T3 e T4 na presença de níveis sangüíneos inapropriadamente detectáveis de TSH. Segundo nosso conhecimento bibliográfico, este foi o primeiro caso relatado no Brasil.

Envolvimento do polimorfismo do gene do transportador de serotonina em pacientes com transtorno disfórico do pré-menstrual / Involvement of serotonin transporter gene polymorphism in premenstrual dysforic disorder

O objetivo do estudo foi avaliar o polimorfismo da proteína transportadora de serotonina (PSERT) no transtorno disfórico do pré-menstrual. Foram tratadas 51 pacientes com placebo e 20 mg de fluoxetina, num estudo duplo-cego. Houve resposta terapêutica com fluoxetina em 86,3 por cento das pacientes e com placebo em 19,6 por cento. Quanto à prevalência do PSERT, a distribuição genotípica foi de 25,5 por cento para o alelo longo/longo (LL), 64,7 por cento para o longo/curto(LC) e 9,8 por cento para o curto/curto(CC). A melhora nas pacientes LL foi de 83,3 por cento, nas LC de 74,9 por cento, enquanto nas CC foi de 50,4 por cento (P=0,03). Concluímos que a presença do alelo longo confere melhor resposta ao uso da fluoxetina em transtorno disfórico do pré-menstrual / The purpose of this study was to investigate the involvement of serotonin transporter (SERT) gene polymorphism in premenstrual dysphoric disorder. 51 women were randomized to double-blind study with fluoxetine 20 mg/day or placebo treatment. Among the patients, 86.3 per cent were responsive to fluoxetine and 19,6 per cent to placebo. The genotype distribution was 25.5 per cent for long/long, 64.7 per cent for long/short and 9.8 per cent for short/short allele. Homozygous (83.3 per cent) and heterozygous (74.9 per cent) long allele carriers were responsive to fluoxetine treatment, whereas only 50.4 per cent for short carriers (P=0.03). We concluded that the presence of long allele of SERT was found to be associated with better response to fluoxetine in premenstrual dysphoria...