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RESUMOIntrodução: A toxicidade da vitamina D é rara e potencialmente grave. As características clínicas da hipervitaminose D são decorrentes, principalmente, da hipercalcemia. Relato de caso: Feminina, 50 anos, em acompanhamento no serviço de endocrinologia e metabologia do HC-UFPR devido bócio multinodular (BMN) tóxico, sendo iniciado tratamento com tapazol. Encaminhada para tireoidectomia total pelo serviço de cirurgia de cabeça e pescoço do HC-UFPR. Evoluiu, no pós operatório, com hipoparatireoidismo e hipocalcemia grave sintomática, necessitando reposição de gluconato de cálcio endovenoso. Recebeu alta hospitalar com cálcio total de 8,2mg/dl e prescrição de calcitriol 0,25mcg 6 comprimidos (cp) ao dia, carbonato de cálcio (CaCO3) 500mg 8 cp ao dia e vitamina D3 15.000U/semana e retorno ambulatorial em 2 semanas. No retorno, três meses após, queixa de náuseas, vômitos, hiporexia e perda de 5,8kg em dois meses, apresentando sinais de desidratação ao exame físico. Cálcio total no retorno de 11,4mg/dl, PTH < 5,00pg/ml, fósforo (Pi) 3,5mg/dl, albumina (alb) 3,9g/dl, creatinina (Cr) 1,5mg/dl. Suspenso CaCO3 e vitamina D, reduzida dose de calcitriol para 2 cp ao dia e orientada hidratação via oral. Após 1 semana, melhora dos sintomas, com cálcio total de 8,1mg/dl, Pi 3,9mg/dl, alb 3,8g/dl, PTH 10,70pg/ml, 25-OH-vitamina D 43ng/ml, Cr 1,1mg/dl. Mantida dose de calcitriol e reiniciado CaCO3 na dose de 1g/dia. Novo retorno em um mês, assintomática, com cálcio total de 8,3mg/dl, PTH 20pg/ml e 25-OH-vitamina D 41ng/ml, Cr 0,8mg/dl, compatível com hipoparatireoidismo transitório e intoxicação por calcitriol resolvida. Conclusão: Diante de um quadro de vômitos persistentes e hipercalcemia, na presença de hormônio da paratireódide normal ou baixo, o diagnóstico de intoxicação por vitamina D deve ser suspeitado e, a normalização de seus níveis alivia os sintomas e pode prevenir lesão renal aguda.Descritores: intoxicação, calcitriol, hipercalcemia ABSTRACT Introduction: Vitamin D toxicity is rare and potentially serious. The clinical features of hypervitaminosis D are due mainly to the hypercalcemia. Case report: Female, 50, followed at endocrinology and metabology HC-UFPR due multinodular goiter toxic, and treatment with tapazol. Forwarded to total thyroidectomy by the head and neck surgery department of the HC-UFPR. It evolved in the postoperative with hypoparathyroidism and symptomatic severe hypocalcemia, requiring calcium gluconate intravenous replacement. He was discharged with total calcium of 8,2mg/dl and calcitriol prescription 0,25mcg 6 tablets per day, calcium carbonate (CaCO3) 500mg 8 tablets per day and vitamin D3 15.000U/week and outpatient in two weeks. Three months later, complaining of nausea, vomiting, appetite loss and loss of 5.8 kg in two months, showing signs of dehydration on physical examination. Total calcium in the return 11,4mg/dl, PTH <5,00pg/ml, phosphorus (P) 3.5 mg/dL albumin (alb) 3.9g/dL creatinine (Cr) 1.5 mg/dl. Suspended CaCO3 and vitamin D, reduced dose of calcitriol for 2 tablets daily a...

25 hydroxyvitamin D [25(OH)D] is the major metabolite for ascertaining vitamin D status, which circulates bound to a speci c carrier (vitamin D-binding protein -VDBP). A portion that circulates unbound vary according to the VDBP genotype. This study evaluates the behavior of different forms of 25(OH)D, before and after supplementation with 14,000 IU of vitamin D3, weekly for 12 weeks, in individuals with primary hyperparathyroidism and controls. Fifty-six patients with active primary hyperparathyroidism (PHPT) and 64 paired controls (CTRL), not taking vitamin D3 for the last three months, were enrolled. The genetic isotypes of VDBP were determined to calculate bioavailable and free 25(OH)D. A p<0.05 was considered signi cant.There were no statistical differences in free, bioavailable, and total 25(OH)D levels between PHPT and CTRL groups at baseline. The distribution of VDBP haplotypes 1s/1s, 1f/1f, 1s/1f, 2/2, 1s/2, and 1f/2 was similar between groups. After supplementation, all three forms of 25(OH)D proportionally increased within each group, although the percentage increment was lower in the PHPT group (p<0.05).Total 25(OH)D is better correlated with PTH in the PHPT group than bioavailable and free 25(OH)D (r=-0.41; p<0.05).The concentrations of total, free, and bioavailable 25(OH)D were similar in both PHPT and CTRL groups, and all forms increased proportionally after supplementation, although this increment percentage was higher in the CTRL group, with a subsequent reduction of PTH and AP. Total 25(OH)D correlated better with PTH than other forms, suggesting no advantages in measuring free or bioavailable 25(OH)D in these situations.

RESUMOIntrodução: A ascite causada por hipotireoidismo é uma condição rara e sua causa ainda não está bem definida. Quando causas comuns de ascite forem excluídas, a possibilidade de ascite mixedematosa deve ser considerada e a função tireoidiana deve ser avaliada. Objetivo: relatar um caso de ascite mixedematosa. Relato de caso: Paciente feminina, 57 anos, encaminhada para abordagem cirúrgica de prolapso retal e uterino. No internamento, observada ascite volumosa e iniciada investigação etiológica. Constatado GASA de 2 e descartadas outras causas de ascite por exames complementares, foram solicitados exames laboratoriais para avaliação da função tireoidiana, cujos resultados foram compatíveis com hipotireoidismo (TSH >100 Ui/ml e T4L <0.4 ng/dl). Foi iniciado tratamento com levotiroxina e a paciente recebeu alta com normalização da função tireoidiana e evidente melhora da ascite. Conclusão: Em caso de ascite mixedematosa, haverá uma resposta importante após o tratamento do hipotireoidismo somente. A resposta ao uso de levotiroxina confirma a etiologia da ascite secundária ao hipotireoidismo.Descritores: hipotireoidismo, ascite e ascite mixedematosa ABSTRACT Introduction: Ascites caused by hypothyroidism is a rare condition and its cause is not well defined. When common causes of ascites are excluded, the possibility of myxedema ascites should be considered and thyroid function should be assessed. Objective: To report a case of myxedema ascites. Case report: A female patient, 57 years old, was referred for surgical treatment of rectal and uterine prolapse. In the hospital, we observed large ascites and started etiological investigation. A SAAG of 2 was observed, and common causes of ascites had been ruled out through complimentary exams. Laboratory tests were requested to evaluate thyroid function and the results were consistent with hypothyroidism (TSH >100 UI/ml and fT4 <0.4 ng/dl). Treatment was started with levothyroxine and the patient was discharged with normalization of thyroid function and great improvement of ascites. Conclusion: In case of myxedema ascites, there will be an important improvement after adequate treatment. The impressive response to the use of levothyroxine confirms the etiology of ascites secondary to hypothyroidism.

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