Hyperinsulinaemia and Na+, K(+)-ATPase activity in thyrotoxic periodic paralysis

Thyrotoxic periodic paralysis (TPP) usually follows a heavy carbohydrate meal and this may be explained by hyperinsulinaemia stimulating Na+, K(+)-ATPase activity. To clarify this the effect of glucose load on serum insulin concentration and platelet Na+, K(+)-ATPase activity in thyrotoxic periodic paralysis (TPP) was examined.

In all subjects a standard 75-g glucose tolerance test was done and blood samples were taken at 0, 1 and 2 hours.

Twenty-five healthy controls (8 M and 17 F), 17 uncomplicated thyrotoxic patients (7 M and 10 F), 15 TPP patients who presented with paralysis and 4 TPP patients after treatment with antithyroid drugs.

Plasma glucose was measured by the glucose oxidase method, serum insulin by radioimmunoassay and platelet Na+, K(+)-ATPase by the release of phosphate from ATP.

TPP patients showed glucose intolerance (area under the curve (AUC) 16.5 +/- 4.4 (mean +/- SD) in TPP compared to 12.9 +/- 4.5 in controls (P < 0.01)) and hyperinsulinaemia (AUC 189.6 +/- 100.6 vs 98.5 +/- 53.4, P < 0.001). In uncomplicated thyrotoxicosis the results were similar to that in healthy controls. Platelet Na+, K(+)-ATPase were significantly higher in thyrotoxic patients compared to controls and in TPP patients were even higher. Ingestion of glucose increased platelet Na+, K(+)-ATPase in all groups. AUC for platelet Na+, K(+)-ATPase in TPP patients were significantly higher than in uncomplicated thyrotoxicosis (601 +/- 99.3 vs 482 +/- 109.4, P < 0.01) or healthy controls (320 +/- 107.3). In the 4 TPP patients studied after antithyroid treatment the results were similar to healthy controls.

Patients with thyrotoxic periodic paralysis have hyperinsulinaemia and this is accompanied by higher Na+, K(+)-ATPase activity.