OBJECTIVE: To present a case of thyrotoxic periodic paralysis (TPP) in a Hispanic man and to discuss the potential precipitating mechanisms. METHODS: We review the clinical and laboratory findings relative to the occurrence of TPP in a 34-year-old Hispanic man, who had been diagnosed as having Graves' disease. RESULTS: TPP is a rare complication of thyrotoxicosis. The two known triggers of TPP are high carbohydrate intake and rest after strenuous physical activity. Other precipitating factors include ingestion of alcohol, infection, trauma, emotional stress, and exposure to cold. Nonselective beta-adrenergic blocking agents are used as prophylaxis for the paralytic attacks. Glucocorticoids have been used to treat nonresponsive and recurrent episodes. Nevertheless, our patient, a 34-year-old Hispanic man, had received propranolol for 7 days and one single dose of prednisone 2 hours before the onset of the paralysis. In patients with TPP, the Na+/K+-adenosinetriphosphatase (ATPase) pump activity is considerably increased by excess thyroid hormones, resulting in an increased intracellular potassium shift. Insulin activates the Na+/K+-ATPase pump as well; thus, the precipitating effect of a high carbohydrate diet is explained. Glucocorticoids have been shown to increase the number of Na+/K+-ATPase molecules in skeletal muscle. They also increase insulin secretion in the basal state and the first-phase insulin release after a glucose load. CONCLUSION: In our patient with TPP, the onset of the attack was not prevented by the use of propranolol and was likely triggered by the administration of prednisone.
OBJECTIVE: To present a case of thyrotoxic periodic paralysis (TPP) in a Hispanic man and to discuss the potential precipitating mechanisms. METHODS: We review the clinical and laboratory findings relative to the occurrence of TPP in a 34-year-old Hispanic man, who had been diagnosed as having Graves' disease. RESULTS:TPP is a rare complication of thyrotoxicosis. The two known triggers of TPP are high carbohydrate intake and rest after strenuous physical activity. Other precipitating factors include ingestion of alcohol, infection, trauma, emotional stress, and exposure to cold. Nonselective beta-adrenergic blocking agents are used as prophylaxis for the paralytic attacks. Glucocorticoids have been used to treat nonresponsive and recurrent episodes. Nevertheless, our patient, a 34-year-old Hispanic man, had received propranolol for 7 days and one single dose of prednisone 2 hours before the onset of the paralysis. In patients with TPP, the Na+/K+-adenosinetriphosphatase (ATPase) pump activity is considerably increased by excess thyroid hormones, resulting in an increased intracellular potassium shift. Insulin activates the Na+/K+-ATPase pump as well; thus, the precipitating effect of a high carbohydrate diet is explained. Glucocorticoids have been shown to increase the number of Na+/K+-ATPase molecules in skeletal muscle. They also increase insulin secretion in the basal state and the first-phase insulin release after a glucose load. CONCLUSION: In our patient with TPP, the onset of the attack was not prevented by the use of propranolol and was likely triggered by the administration of prednisone.