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Journal of Clinical Endocrinology & Metabolism, Vol 57, 963-968, Copyright © 1983 by Endocrine Society
ARTICLES |
M Nakahara, T Shibasaki, K Shizume, Y Kiyosawa, E Odagiri, T Suda, H Yamaguchi, T Tsushima, H Demura and T Maeda
Corticotropin-releasing factor (CRF) tests were performed in normal subjects and patients with hypothalamic-pituitary-adrenal disorders. In normal subjects, after iv administration of 500 micrograms synthetic ovine CRF, plasma ACTH rose significantly to approximately 3.6 times the basal level at 30-60 min and cortisol reached a peak of 2.3 times the basal level at 60-90 min, whereas aldosterone peaked at 1.6 times the basal level at 60 min. Injection of 100 micrograms CRF in normal subjects also caused a significant increase in plasma ACTH and cortisol levels but only a slight increase in aldosterone. However, the total hormone released and their peak levels were lower than those elicited by the 500-microgram dosage. In patients with Cushing's disease, although the basal and peak levels of plasma ACTH and cortisol induced by administration of CRF were variable, the ratios of increase for the two hormones elicited by CRF were lower than those in normal subjects, especially for cortisol. In patients with Cushing's syndrome due to an adrenal adenoma, basal levels of ACTH were markedly suppressed and plasma ACTH and cortisol did not rise after CRF. In patients with isolated ACTH deficiency or Sheehan's syndrome the basal level of plasma ACTH was less than 5 pg/ml and no change in plasma ACTH occurred after injection of CRF. In patients with Nelson's syndrome or Addison's disease the basal levels of ACTH were extremely elevated but infusion of CRF increased plasma ACTH to even higher levels.
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