Propranolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxic periodic paralysis.
Hypokalemia and hypophosphatemia are commonly encountered during paralysis in patients with thyrotoxic periodic paralysis (TPP) and may contribute to neuromuscular manifestations. Potassium and phosphate supplements have been recommended to hasten recovery and prevent cardiopulmonary complications. However, this recommendation has not yet proven efficacious. Hyperadrenergic activity has been implicated in the pathogenesis of TPP. We tested whether nonselective beta-blockers could terminate neuromuscular symptoms rapidly while reducing an intracellular shift of potassium and phosphate. We describe two patients who had an acute attack of TPP with characteristic hypokalemia and hypophosphatemia associated with low urinary potassium and phosphate excretion. After oral propranolol, 3 mg/kg, serum potassium and phosphate concentrations increased promptly in 2 hours in both patients, and there was complete amelioration of paralysis. No rebound hyperkalemia or hyperphosphatemia was detected. Given their efficacy in this pilot study, they should be considered as a first-line therapy for TPP.
Department of Medicine, Division of Nephrology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC. l521116@ndmc1.ndmctsgh.edu.tw
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D000284:Administration, Oral; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000328:Adult; D006801:Humans; D020514:Hypokalemic Periodic Paralysis / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D017674:Hypophosphatemia / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D010865:Pilot Projects; D011433:Propranolol / Q000627:therapeutic use*; D013971:Thyrotoxicosis / Q000150:complications*
D000319:Adrenergic beta-Antagonists; D011433:Propranolol