Abstract
Thyrotoxic periodic paralysis (TPP), a disorder most commonly seen in Asian men, is characterized by abrupt onset of hypokalemia and paralysis. The condition primarily affects the lower extremities and is secondary to thyrotoxicosis. The underlying hyperthyroidism is often subtle causing difficulty in early diagnosis. Factors like high-carbohydrate meal exercise, steroid, and stress can precipitate an attack of TPP. Evidence is building up showing role of genetic mutations in Kir2.6 channel in the pathogenesis of TPP. Loss of function of Kir2.6 together with increased activity of Na+/K+ ATPase may trigger a positive feed-forward cycle of hypokalemia. Biochemical hyperthyroidism with normal urinary potassium excretion and ECG changes are characteristic of TPP. Treatment with low-dose potassium supplements and nonselective beta-blockers should be initiated upon diagnosis, and the serum potassium level should be frequently monitored to prevent rebound hyperkalemia.
Highlights
Association of periodic paralysis and thyrotoxicosis had been documented by Rosenfeld as early as 1902 [1]
The etiology of hypokalemic paralysis can be generally classified into two groups: hypokalemic periodic paralysis, due to shift of potassium into the intracellular space without a total potassium deficit; and nonhypokalemic periodic paralysis, due to a large potassium deficit via gastrointestinal or renal loss
Thyrotoxic periodic paralysis (TPP) must be differentiated from other causes of hypokalemic periodic paralysis. (Table 2) Workup for other causes of hypokalemia include urinary potassium excretion (>30 mEq indicates urinary loss), arterial blood gas for acidosis, urinary potassium to creatinine ratio which is
Summary
Association of periodic paralysis and thyrotoxicosis had been documented by Rosenfeld as early as 1902 [1]. Thyrotoxic periodic paralysis (TPP) is more commonly reported in oriental Asians [2]. It has been reported from the western countries as a result of migration of different ethnic populations [3]. TPP is characterized by acute onset of severe hypokalemia and profound proximal muscle weakness in patients with thyrotoxicosis [4]. TPP is commonly misdiagnosed in Western countries because of its similarities to familial periodic paralysis. The neuromuscular presentations of both are identical and physicians need to look for subtle features of hyperthyroidism in the presence of hypokalemic periodic paralysis. Diagnosis aids in definitive management with nonselective beta-blockers and correction of hyperthyroidism, and prevents the risk of rebound hyperkalemia due to excessive potassium replacement
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