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.
View Article and Find Full Text PDFHashimoto'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.
View Article and Find Full Text PDFParalysis due to hypokalemia results from an acute shift of potassium into cells or excessive potassium deficit. In the absence of potassium deficit, it is observed in Familial Hypokalemic Periodic Paralysis and in Thyrotoxic Hypokalemic Periodic Paralysis (TPP). This report describes the initial presentation of hyperthyroidism as sudden quadriplegia associated with hypokalemia.
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