SAT-365 A Rare Presentation of Hyperthyroidism: Thyrotoxicosis Periodic Paralysis

Abstract Disclosure: J.E. Villarreal Del Moral: None. M. Azevedo Jales Brandao: None. Thyrotoxicosis periodic paralysis (TPP) is a rare and potentially lethal complication of hyperthyroidism characterized by muscle paralysis and hypokalemia. We present a case of a Hispanic patient with an unknown history of hyperthyroidism who developed TPP. A 31-year-old healthy male presented to the emergency department with acute generalized weakness and myalgia, unable to move his arms and legs. He reported recurrent episodes of thigh numbness and weakness for twelve months before the current presentation. Physical examination revealed 4/5 strength in distal extremities and proximal weakness in all four limbs, with intact sensation. Laboratory results were significant for severe hypokalemia (2.1 mmol/L), and hypomagnesemia (1.6 mmol/L), with normal kidney function (creatinine 0.44 mg/dL and BUN 15 mg/dL) . Thyroid studies revealed suppressed TSH (<0.01mIU/ml) and elevated T4 (3.6 ng/dL) and T3 (19.5 pg/dL). Thyroid ultrasound showed an enlarged, hypervascular thyroid, and serology confirmed positive thyroid peroxidase and thyroglobulin antibodies, consistent with Graves' disease. The patient did not present any overt hyperthyroid symptoms. He was started on methimazole and potassium and electrolytes were repleted with quick improvement of symptoms. The patient was discharged on methimazole and advised to follow a high-potassium diet. Symptoms of TPP typically range from recurrent, transient episodes of muscle weakness to complete paralysis. Notably, only about 10% of patients report other symptoms of thyrotoxicosis during an event (1). Our case highlights the importance of recognizing thyrotoxicosis periodic paralysis as a rare but serious complication of hyperthyroidism, even in the absence of overt thyrotoxicosis symptoms. The hallmark feature of TPP is hypokalemia, primarily attributed to increased activity of the Na+/K+-ATPase pump. However, increased activity is also observed in other conditions, including thyrotoxicosis, without consistently resulting in hypokalemia (1). In TPP, hypokalemia is associated with impaired outward potassium flux, linked to mutated Kir (inward rectifier potassium) channels (2). Environmental factors such as hyperinsulinemia, alcohol consumption, or strenuous physical activity further inhibit Kir channel function, leading to intracellular potassium sequestration within skeletal muscle cells (2). Thus, the pathophysiology in TPP includes a genetic predisposition, thyrotoxicosis, and environmental influences (3). TPP has traditionally been recognized as a prevalent complication of thyrotoxicosis in Asian populations but has been underdiagnosed in Caucasians. Emerging evidence indicates that TPP is increasingly observed across diverse populations (1), as highlighted by the present case. Presentation: Saturday, July 12, 2025