• K P Ober.
• Department of Internal Medicine, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157-1047.
• Medicine (Baltimore). 1992 May 1; 71 (3): 109-20.

AbstractAlthough hypokalemic periodic paralysis is a common complication of hyperthyroidism among Asian populations, it is an uncommon problem in the United States. The recent experience in an American medical center with 7 patients with thyrotoxic periodic paralysis (TPP) is reviewed. Compared to most descriptions of this disorder, which tend to reflect the international experience with this disease, patients with TPP in the United States reflect the ethnic makeup of the local population: the predisposition of patients of Asian origin is very evident, but whites are more frequently affected than most previous reports have recognized. Hispanics and American Indians also appear to be at increased risk, and blacks have also been affected. Except for the fact that hyperthyroidism is an absolute requirement for expression of the disease, TPP is identical to familial periodic paralysis (FPP) in its clinical presentation. TPP affects predominantly males (to an even greater degree than FPP), is rarely associated with a positive family history, and has a later onset of presentation than FPP (reflecting the need for hyperthyroidism to occur before the disorder can be expressed). Graves disease is the most common cause of hyperthyroidism in affected patients, but any cause of thyrotoxicosis (including administration of excessive amounts of exogenous thyroid hormone) can trigger attacks of TPP in susceptible subjects. Clinical features of thyroid disease may be very subtle or virtually nonexistent; as a result, thyroid function tests should be routinely monitored in patients with features of hypokalemic paralysis. The pathophysiology of the disorder is not well understood. Definitive treatment of hyperthyroidism leads to cessation of periodic hypokalemic paralysis, but symptoms can return with recurrence of the hyperthyroid condition. Potassium administration during an acute attack will shorten the duration of the episode, and treatment with propranolol, potassium supplementation, or spironolactone may prevent attacks in some patients.

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