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Responsiveness of Hypophyseal-Adrenocortical Axis to Repetitive Administration of Synthetic Ovine Corticotropin-Releasing Hormone in Patients with Isolated Adrenocorticotropin Deficiency

Responsiveness of Hypophyseal-Adrenocortical Axis to Repetitive Administration of Synthetic Ovine... Abstract The primary lesion site in isolated ACTH deficiency was studied in three patients by examining the responses of immunoreactive ACTH to insulin-induced hypoglycemia, lysine vasopressin, and synthetic ovine corticotropin-releasing hormone (CRH). In all patients, no significant changes in im-munoreactive ACTH followed insulin-induced hypoglycemia or lysine vasopressin. Fifty micrograms (≥1 µg/kg BW) of CRH administered as an iv bolus dose daily for 6 consecutive days elicited no significant increase in plasma immunoreactive ACTH, β-lipotropin, or cortisol levels in all patients. Eight iv bolus injections of 0.63 µg/kg BW CRH at 4-h intervals also failed to induce a significant response of immunoreactive ACTH to an iv bolus dose of 1 µg/kg CRH at 36 h in one patient. In contrast, a single bolus dose of 50 µg CRH induced a response of plasma immunoreactive ACTH in a patient with Cushing’s disease and a patient with Addison’s disease. The present results suggest that the primary lesion of isolated ACTH deficiency is not the hypothalamus, but, rather, is located in pituitary ACTH-secreting cells. This content is only available as a PDF. Author notes * This work was supported in part by a Research Grant for the Intractable Diseases from the Ministry of Health and Welfare, Japan. Copyright © 1986 by The Endocrine Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Clinical Endocrinology and Metabolism Oxford University Press

Responsiveness of Hypophyseal-Adrenocortical Axis to Repetitive Administration of Synthetic Ovine Corticotropin-Releasing Hormone in Patients with Isolated Adrenocorticotropin Deficiency

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References (27)

Publisher
Oxford University Press
Copyright
Copyright © 1986 by The Endocrine Society
ISSN
0021-972X
eISSN
1945-7197
DOI
10.1210/jcem-63-2-329
Publisher site
See Article on Publisher Site

Abstract

Abstract The primary lesion site in isolated ACTH deficiency was studied in three patients by examining the responses of immunoreactive ACTH to insulin-induced hypoglycemia, lysine vasopressin, and synthetic ovine corticotropin-releasing hormone (CRH). In all patients, no significant changes in im-munoreactive ACTH followed insulin-induced hypoglycemia or lysine vasopressin. Fifty micrograms (≥1 µg/kg BW) of CRH administered as an iv bolus dose daily for 6 consecutive days elicited no significant increase in plasma immunoreactive ACTH, β-lipotropin, or cortisol levels in all patients. Eight iv bolus injections of 0.63 µg/kg BW CRH at 4-h intervals also failed to induce a significant response of immunoreactive ACTH to an iv bolus dose of 1 µg/kg CRH at 36 h in one patient. In contrast, a single bolus dose of 50 µg CRH induced a response of plasma immunoreactive ACTH in a patient with Cushing’s disease and a patient with Addison’s disease. The present results suggest that the primary lesion of isolated ACTH deficiency is not the hypothalamus, but, rather, is located in pituitary ACTH-secreting cells. This content is only available as a PDF. Author notes * This work was supported in part by a Research Grant for the Intractable Diseases from the Ministry of Health and Welfare, Japan. Copyright © 1986 by The Endocrine Society

Journal

Journal of Clinical Endocrinology and Metabolism – Oxford University Press

Published: Aug 1, 1986

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