Elevated immunoreactive insulin concentration during spontaneous attacks in thyrotoxic periodic paralysis

Abstract

It has been well documented that administration of insulin or procedures that increase endogenous insulin secretion may provoke the attack of hypokalemic periodic paralysis. However, there have been no reports on the endogenous insulin levels before and during spontaneous attack of periodic paralysis. In the present investigation we measured concentration of blood glucose, serum immunoreactive insulin (IRI), human growth hormone (HGH), Na, and K during spontaneous attacks of periodic paralysis and also after an oral load of 100 g glucose in seven thyrotoxic patients with the history of periodic paralysis. Three attacks of paralysis were observed in two patients. In one patient basal level of IRI was abnormally high, and the postglucose IRI response was exaggerated. Preceding the attack, IRI increased to 500 μU/ml from the basal level of 75 μU/ml. In the other patient it increased to 105 μU/ml from the basal level of 7 μU/ml at the onset of paralysis. Those levels observed at the onset of paralysis were abnormally high when compared to those in patients in whom no attacks were observed. HGH, blood glucose, and Na had no correlation with paralysis, although K decreased during the attack. Thus, we demonstrated for the first time that the spontaneous attack of paralysis was preceded by an increased secretion of insulin. These results suggested the following two abnormalities in thyrotoxic periodic paralysis: abnormal increase in insulin in response to glucose or dietary load, and decrease in muscle membrane potential in response to elevated insulin.