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YOSHINOBU KOIDE, SATOSHI KIMURA, SETSUKO INOUE, MASAAKI IKEDA, KENZO UCHIDA, JUNKO ANDO, AKIHIKO SHIMIZU, KANZI ODA, MITSUO ITAKURA, IEHARU NABESHIMA, MASAYUKI MARUYAMA, KAMEJIRO YAMASHITA, KAORU ABE, Responsiveness of Hypophyseal-Adrenocortical Axis to Repetitive Administration of Synthetic Ovine Corticotropin-Releasing Hormone in Patients with Isolated Adrenocorticotropin Deficiency, The Journal of Clinical Endocrinology & Metabolism, Volume 63, Issue 2, 1 August 1986, Pages 329–335, https://doi.org/10.1210/jcem-63-2-329
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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.
