OBJECTIVE: To describe a rare case of thyrotoxic hypokalemic periodic paralysis in a half Native American and half African American person. METHODS: We present a case of a man of Native American descent with thyrotoxic periodic paralysis and review the pertinent literature. RESULTS: In a 53-year-old man with untreated hyperthyroidism, bilateral lower extremity weakness developed as a result of hypokalemia. Two months before admission, the patient had thyroid function test results that were consistent with hyperthyroidism. He also had undergone a thyroid radioiodine uptake study and scan, which demonstrated a diffuse 60% uptake in the thyroid at 24 hours. His symptoms resolved promptly after treatment with potassium, a 3-adrenergic blocking agent, and propylthiouracil. The pathophysiologic features of this disorder have not been entirely elucidated but most likely involve a sudden increase in intracellular shift of potassium and progressive depolarization of the resting membrane potential. Therapy consists of replacing the potassium and treating the cause. CONCLUSION: Thyrotoxic hypokalemic periodic paralysis, although rare in the Native American and African American population, should be considered in the differential diagnosis of hypokalemia and flaccid paralysis. Timely recognition and prompt treatment can reduce the risk of severe morbidity.
OBJECTIVE: To describe a rare case of thyrotoxic hypokalemic periodic paralysis in a half Native American and half African American person. METHODS: We present a case of a man of Native American descent with thyrotoxic periodic paralysis and review the pertinent literature. RESULTS: In a 53-year-old man with untreated hyperthyroidism, bilateral lower extremity weakness developed as a result of hypokalemia. Two months before admission, the patient had thyroid function test results that were consistent with hyperthyroidism. He also had undergone a thyroid radioiodine uptake study and scan, which demonstrated a diffuse 60% uptake in the thyroid at 24 hours. His symptoms resolved promptly after treatment with potassium, a 3-adrenergic blocking agent, and propylthiouracil. The pathophysiologic features of this disorder have not been entirely elucidated but most likely involve a sudden increase in intracellular shift of potassium and progressive depolarization of the resting membrane potential. Therapy consists of replacing the potassium and treating the cause. CONCLUSION:Thyrotoxic hypokalemic periodic paralysis, although rare in the Native American and African American population, should be considered in the differential diagnosis of hypokalemia and flaccid paralysis. Timely recognition and prompt treatment can reduce the risk of severe morbidity.