RESUMO
We report a case of a 39 year-old Asian man in whom profound lower limb paralysis, along with severe hypokalemia and electrocardiographic changes, were the presenting features of Graves' disease (GD)-related thyrotoxicosis. Rapid recognition and management of the disorder were the key factors to avoid fatal hypokalemia-induced cardiac arrhythmias and promptly restore patient's capacity to ambulate.
Assuntos
Doença de Graves/complicações , Paralisia Periódica Hipopotassêmica/etiologia , Tireotoxicose/etiologia , Antagonistas Adrenérgicos beta/uso terapêutico , Adulto , Antitireóideos/uso terapêutico , Eletrocardiografia , Emergências , Doença de Graves/diagnóstico , Doença de Graves/tratamento farmacológico , Hong Kong/etnologia , Humanos , Paralisia Periódica Hipopotassêmica/sangue , Paralisia Periódica Hipopotassêmica/tratamento farmacológico , Paralisia Periódica Hipopotassêmica/etnologia , Transporte de Íons , Masculino , Metimazol/uso terapêutico , Exame Neurológico , Potássio/metabolismo , Cloreto de Potássio/uso terapêutico , Propranolol/uso terapêutico , ATPase Trocadora de Sódio-Potássio/metabolismo , Estresse Psicológico/complicações , Tireotoxicose/tratamento farmacológicoRESUMO
Hashimoto's thyroiditis (HT) and Graves' disease (GD) are two opposite poles in the spectrum of autoimmune thyroid disease. On one extreme, HT or Chronic Lymphocytic thyroiditis (CLT) courses, as its name implies, with lymphocytic infiltrates replacing thyroid follicles, resulting in a loss of hormone-producing cells and, thus, primary hypothyroidism. On the other extreme, GD is characterized by primary hyperthyroidism due to stimulating autoantibodies against thyroid-stimulating hormone receptors (TSHRs) localized on thyrocytes' membranes of intact thyroid follicles. The presence of HT after GD or the concomitant combination of these two autoimmune entities ending in HT-depending hypothyroid state is well known. However, occurrence of GD after primary hypothyroidism due to CLT is very rare since thyrocytes with their TSHRs are promptly lost. We report a case in which hyperthyroidism occurred seven months after presentation of primary hypothyroidism and discuss potential mechanisms involved.