MON-352 - When Hypokalemia Signals Thyrotoxicosis: Recognizing Thyrotoxic Periodic Paralysis in Hispanic Patients

Introduction:
Thyrotoxic periodic paralysis (TPP) is a rare, potentially life-threatening complication of thyrotoxicosis characterized by recurrent episodes of acute muscle weakness with hypokalemia in the setting of biochemical hyperthyroidism. The hypokalemia results from transcellular potassium shift caused by increased Na⁺/K⁺-ATPase activity, rather than true potassium depletion. TPP affects predominantly young men, originally described in East Asian populations, although growing reports in Hispanic patients indicate broader ethnic susceptibility. Episodes are often triggered by high-carbohydrate meals, alcohol, or strenuous exercise. Misdiagnosis is frequent,as it may mimic neurologic disorders or isolated hypokalemia, leading to delayed recognition and inappropriate management.

Case Presentation
We describe three Hispanic men aged 24 to 33 years with no significant medical history who presented with acute muscle weakness. Two patients had bilateral lower extremity involvement and one had both upper and lower extremity weakness. All reported myalgias, and one noted numbness. Each had preceding symptoms of thyrotoxicosis including tremor, palpitations, diarrhea, and weight loss. One patient had a prior similar episode treated with potassium alone without thyroid evaluation.
All episodes occurred at night or early morning; two followed large high-carbohydrate meals and one followed alcohol intake. Initial serum potassium ranged from 2.0 to 2.8 mEq/L, with normal glucose, calcium, and magnesium. Thyroid studies showed undetectable TSH and elevated free T4 (2.7–4.05 ng/dL), and thyroid-stimulating immunoglobulin was positive in all cases, confirming Graves disease. Sinus tachycardia was observed in two patients.
All patients received low-dose potassium (40–60 mEq/24 h) and nonselective beta-blockade, with full resolution of weakness and normalization of potassium levels within 24 hours. One developed rebound hyperkalemia (5.3 mEq/L). All were discharged on methimazole and propranolol; one had recurrence after self-discontinuation of antithyroid therapy.
Discussion and Conclusion
This case series highlights TPP in Hispanic men, emphasizing the need for broader clinical awareness beyond traditionally recognized populations. A key teaching point is the risk of rebound hyperkalemia after potassium repletion, reflecting reversal of an intracellular potassium shift rather than true potassium depletion. This explains why low-dose potassium with early nonselective beta-blockade is the preferred initial therapy.Long-term management relies on definitive control of thyrotoxicosis, achieving and maintaining euthyroidism to prevent reoccurance. Early recognition and appropriate treatment reduce morbidity and prevent life-threatening arrhythmias from both hypokalemia and rebound hyperkalemia.

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