In vivo and in vitro sodium pump activity in subjects with thyrotoxic periodic paralysis

Abstract

Objective: To examine whether sodium pump activity plays a part in the pathogenesis of thyrotoxic periodic paralysis. Design: Measurement of platelet sodium-potassium ATPase and in vivo sodium pump activities in healthy subjects and thyrotoxic subjects with and without paralysis. Setting: University hospital in Hong Kong. Subjects: 21 healthy subjects, 23 untreated thyrotoxic subjects, 13 untreated men with periodic paralysis, seven treated thyrotoxic subjects, and six treated men with periodic paralysis. Main outcome measures: Platelet Na+, K+-ATPase activity and plasma rubidium concentration after oral loading. Results: Median (range) platelet Na+, K+-ATPase activity in thyrotoxic subjects was 253 (169-821) μmol inorganic phosphate/h/g protein-significantly higher than that in healthy subjects (134 (81-180) μmol/h/g protein; p < 0.001). Na+, K+-ATPase activity in those with periodic paralysis was 374 (195-1196) μmol/h/g protein, again significantly higher than that in healthy subjects (p < 0.001) and that in other thyrotoxic subjects (p < 0.01) despite similar degrees of hyperthyroidism. Activities in treated thyrotoxic subjects with and without periodic paralysis were 148 (110-234) and 131 (86-173) μmol/h/g protein respectively. Mean (95% confidence interval) plasma rubidium concentration have hours after oral administration in thyrotoxic subjects (7.0 (6.6 to 7.5) μmol/l) was significantly lower than in healthy subjects (10.2 (9.5 to 10.9) μmol/l; p < 0.001) and higher than in those with periodic paralysis (6.0 (5.7 to 6.3) μmol/l; p < 0.01). Conclusions: Sodium pump activity in untreated subjects with periodic paralysis is higher than in other thyrotoxic subjects, and this may be responsible for the hypokalaemia.