Clinical communicationPotassium Chloride Supplementation Alone May Not Improve Hypokalemia in Thyrotoxic Hypokalemic Periodic Paralysis
Introduction
Thyrotoxic periodic paralysis (TPP) is a hyperthyroidism-related hypokalemic muscle weakness resulting from an acute shift of potassium (K+) into cells. Failure to recognize TPP may lead to improper management. Thyroid hyperfunction per se can impair glucose tolerance and stimulate insulin secretion (1, 2). Thus, hyperinsulinemia with glucose intolerance is one of the characteristics of TPP (3). Previous reports have claimed that first-line therapy with potassium chloride (KCl) supplementation for TPP may promote rapid recovery of muscle strength (4). However, it is not clear that this is the case. In this situation, administration of a low dose non-selective β-blocker may result in a more rapid recovery from muscle weakness. For definitive management, control of the hyperthyroidism will prevent future attacks of TPP.
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Case Report
A 29-year-old man was admitted to the medical ward from the Emergency Department (ED) because of sudden onset of bilateral lower extremity weakness and inability to ambulate. Before the attack, he claimed to have ingested a high carbohydrate meal and 300 mL of beer (Taiwan beer, 4.5% alcohol).
This patient was relatively healthy before this admission, played basketball frequently, and denied history of previous episodes. His medical history was non-contributory. Blood pressure on admission was
Discussion
Thyrotoxic periodic paralysis (TPP) is an endocrine disorder most prevalent among individuals of Asian descent. It usually presents as proximal muscle weakness with hypokalemia and signs of hyperthyroidism. Paralysis usually occurs after ingestion of a heavy carbohydrate meal, heavy exercise, or both (5).
Although the pathophysiology of TPP has not yet been entirely explained, episodes of hypokalemic paralysis most likely begin with increased intracellular shift of K+. Active K+ flux into the
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Clinical Communications (Adults) is coordinated by Thomas O. Stair, md, of Harvard Medical School, Boston, Massachusetts