OBJECTIVE: To characterize the course of therapy in a large cohort of Chinese patients with thyrotoxic periodic paralysis (TPP), a reversible electrolyte emergency fraught with therapeutic challenges. DESIGN AND METHODS: In this prospective interventional study, 78 patients with TPP (75 males and three females with an age range of 16-48 years) were consecutively enrolled over a 6-year period. Intravenous KCl at a rate of 10 mmol/h was administered until muscle strength recovered. Serum potassium (K(+)) and phosphorus concentrations were measured hourly during the paralytic attack and for 6 h after recovery. RESULTS: The serum potassium (K(+)) on attack was 2.1+/-0.2 mmol/l. The dose of KCl administered to restore muscle strength was 63+/-32 mmol, and peak serum K(+) concentration after recovery was 5.3+/-0.5 mmol/l. A paradoxical fall in serum K(+) concentration >0.1 mmol/l difference between presentation and treatment nadir was observed in approximately one-fourth of TPP patients (n=20). These patients had significantly higher serum-free thyroxine concentration, systolic blood pressure, and heart rate on presentation, as well as serum phosphate concentration on recovery. They not only needed much more KCl supplementation (104+/-34 vs 48+/-19 mmol, P<0.001), but also had significantly more severe rebound hyperkalemia (5.8+/-0.5 vs 5.1+/-0.4 mmol/l, P<0.001) on recovery than those who did not have paradoxical hypokalemia. There was a positive correlation between the dose of KCl administered and the difference between peak and nadir serum K(+) (Delta K(+)) (r=0.68, P<0.001). CONCLUSIONS: TPP patients who do not develop paradoxical hypokalemia need a smaller KCl dose to achieve recovery, whereas those who develop paradoxical hypokalemia have more severe hyperthyroidism and hyperadrenergic activity and may require blockage of intracellular K(+) shift to prevent rebound hyperkalemia.
OBJECTIVE: To characterize the course of therapy in a large cohort of Chinese patients with thyrotoxic periodic paralysis (TPP), a reversible electrolyte emergency fraught with therapeutic challenges. DESIGN AND METHODS: In this prospective interventional study, 78 patients with TPP (75 males and three females with an age range of 16-48 years) were consecutively enrolled over a 6-year period. Intravenous KCl at a rate of 10 mmol/h was administered until muscle strength recovered. Serum potassium (K(+)) and phosphorus concentrations were measured hourly during the paralytic attack and for 6 h after recovery. RESULTS: The serum potassium (K(+)) on attack was 2.1+/-0.2 mmol/l. The dose of KCl administered to restore muscle strength was 63+/-32 mmol, and peak serum K(+) concentration after recovery was 5.3+/-0.5 mmol/l. A paradoxical fall in serum K(+) concentration >0.1 mmol/l difference between presentation and treatment nadir was observed in approximately one-fourth of TPPpatients (n=20). These patients had significantly higher serum-free thyroxine concentration, systolic blood pressure, and heart rate on presentation, as well as serum phosphate concentration on recovery. They not only needed much more KCl supplementation (104+/-34 vs 48+/-19 mmol, P<0.001), but also had significantly more severe rebound hyperkalemia (5.8+/-0.5 vs 5.1+/-0.4 mmol/l, P<0.001) on recovery than those who did not have paradoxical hypokalemia. There was a positive correlation between the dose of KCl administered and the difference between peak and nadir serum K(+) (Delta K(+)) (r=0.68, P<0.001). CONCLUSIONS:TPPpatients who do not develop paradoxical hypokalemia need a smaller KCl dose to achieve recovery, whereas those who develop paradoxical hypokalemia have more severe hyperthyroidism and hyperadrenergic activity and may require blockage of intracellular K(+) shift to prevent rebound hyperkalemia.