Changes in Plasma ACTH, Cortisol and Aldosterone in Thyrotoxic Periodic Paralysis

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  • TAKEDA Ryoyu
    The Second Department of Internal Medicine, School of Medicine, University of Kanazawa
  • MORIMOTO Shinpei
    The Second Department of Internal Medicine, School of Medicine, University of Kanazawa
  • SAITO Zenzo
    The Second Department of Internal Medicine, School of Medicine, University of Kanazawa
  • UCHIDA Kenzo
    The Second Department of Internal Medicine, School of Medicine, University of Kanazawa
  • UEDA Misao
    The Second Department of Internal Medicine, School of Medicine, University of Kanazawa
  • YAMAMOTO Ikuo
    The Second Department of Internal Medicine, School of Medicine, University of Kanazawa
  • MIYAMORI Isamu
    The Second Department of Internal Medicine, School of Medicine, University of Kanazawa

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  • Changes in plasma ACTH cortisol and ald
  • With presentation of a typical case of an induced attack

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Changes in plasma ACTH, plasma cortisol (PC) and plasma aldosterone (PA) were serially investigated in a thyrotoxic patient (K. T.) with a paralytic attack induced by glucose and insulin infusion (GI). Also, changes in PC and PA in five patients with an induced complete quadriplegia were compared to those in four patients in whoman infusion produced slight or no paralysis of the legs or arms. In patient K.T., basal levels of plasma ACTH, PC and PA were within normal. Induction of a paralytic attack was not associated with any changes in PC and PA. Plasma ACTH before the onset of attack also was normal. During the development of complete quadriplegia, plasma ACTH rapidly increased in parallel with somewhat delayed increases in PC and PA. In five patients with an induced complete quadriplegia, the mean values of PC and PA were normal in baseline and did not show any significant changes either 15min before or after the onset of attack. At the stage of complete quadriplegia, PC significantly increased in parallel with an increase in PA. On the other hand, in four patients with a slight or no paralysis of the legs or arms, changes in PC and PA were insignificant during observation period of 180 min. These results demonstrate that an induction of paralytic attack can be produced without endogenous ACTH excess. However, during the development of complete quadriplegia ACTH might partly contribute to an augmented secretion of aldosterone, because the simultaneous rises of PC and PA were noted at the stage of complete quadriplegia.

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