Horm Metab Res 1985; 17(6): 301-305
DOI: 10.1055/s-2007-1013524
Clinical

© Georg Thieme Verlag, Stuttgart · New York

Transient Glucose Intolerance during Attacks of Thyrotoxic Periodic Paralysis

N. Hamada, T. Ishii, M. Hasegawa2 , N. Ishikawa2 , T. Tabata, Y. Okuno, K. Ito2 , S. Matsuura1 , H. Morii, M. Wada
  • Second Department of Internal Medicine, Osaka City University, Osaka, Japan
  • 1First Department of Physiology, Osaka City University, Osaka, Japan
  • 2Ito Thyroid Clinic and Hospital, Tokyo, Japan
Further Information

Publication History

1983

1985

Publication Date:
14 March 2008 (online)

Summary

In a 19-year-old Japanese male (case 1) with thyrotoxic periodic paralysis (TPP), an increase of plasma glucose concentration together with abnormally high levels of serum immunoreactive insulin (IRI) was observed preceding a spontaneous attack of paralysis. Therefore, the plasma glucose, glucagon, epinephrine, norepinephrine, serum IRI, growth hormone and cortisol levels, and the erythrocyte insulin receptors were measured in case 1 and a 40-year-old Japanese male (case 2) with TPP during attacks of paralysis induced by prolonged glucose loading. In case 1, the serum IRI concentration was elevated to the extraordinarily high level of 655.0 μU/ml at the beginning of paralysis, and at that time, the plasma glucose concentration was 147 mg/dl. However, when paralysis was not induced by a similar glucose loading during methimazole treatment, the serum IRI and plasma glucose levels at the corresponding time after glucose loading were 20.9 μU/ml and 87 mg/dl, respectively. Furthermore, the affinity of the erythrocyte insulin receptors was decreased during the attack. In case 2, plasma glucose and serum IRI concentrations were increased in accordance with the initiation of paralysis although the blood levels of hormones counteracting insulin were not significantly changed. These findings suggest that there is something interacting with the normal action of the insulin in the early phase of paralysis.