A51-03 Recurrent Thyrotoxic Periodic Paralysis in a Young Male: A Reversible Cause of Acute Hypokalemic Weakness

Abstract Introduction Hypokalemic periodic paralysis is a rare channelopathy characterized by episodic flaccid weakness due to intracellular potassium shifts. While most cases are familial, acquired forms occur in the setting of thyrotoxicosis, where beta-adrenergic stimulation and enhanced Na+/K+ ATPase activity drive potassium into skeletal muscle, precipitating profound hypokalemia. Case Presentation A 25-year-old man with recently diagnosed Graves’ disease presented with acute bilateral lower extremity weakness resulting in a fall. His diagnosis had been established a few months earlier after laboratory evaluation revealed undetectable thyroid-stimulating hormone (TSH), elevated triiodothyronine (T3) and thyroxine (T4) levels, and positive thyroid autoantibodies. Thyroid ultrasound demonstrated diffuse hypervascularity consistent with thyroiditis. He had been initiated on methimazole and propranolol but was noncompliant with his medications. On admission, serum potassium was 2.1 mEq/L, magnesium 1.7 mEq/L, with undetectable TSH, T3 of 383 ng/dL, and free T4 of 3.96 ng/dL. He was admitted for aggressive potassium replacement and reinitiation of methimazole and propranolol. Neuromuscular strength improved within 24 hours, and serum potassium normalized to 4.0 mEq/L by the second hospital day. One month later, he re-presented with recurrent weakness after a week of medication nonadherence. Repeat evaluation again demonstrated severe hypokalemia and uncontrolled hyperthyroidism. He responded rapidly to potassium supplementation and resumption of antithyroid therapy, with full recovery of motor strength. Discussion This case highlights an acquired and reversible cause of hypokalemic periodic paralysis triggered by uncontrolled thyrotoxicosis. The reproducible pattern of symptom recurrence following withdrawal of methimazole and propranolol, and rapid recovery upon their resumption, reinforces the causal relationship between thyroid hormone excess and episodic paralysis. Clinicians should maintain a high index of suspicion for thyrotoxic periodic paralysis in young patients presenting with acute, profound muscle weakness and severe hypokalemia, particularly in emergency or critical care settings. Timely potassium repletion combined with restoration of euthyroidism typically results in rapid and complete resolution of symptoms. This abstract is funded by: None