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Therapeutic analysis in Chinese patients with thyrotoxic periodic paralysis over 6 years

Division of Nephrology, Department of Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan, ROC¹ Division of Nephrology² Division of Endocrinology and Metabolism, Department of Medicine³ Department of Emergency Medicine, National Defense Medical Center, Tri-Service General Hospital, No 325, Section 2, Cheng-Kung Road, Neihu 114 Taipei, Taiwan, ROC

(Correspondence should be addressed to S-H Lin; Email: shihhualin{at}yahoo.com)

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⁺ ( 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.