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Corticotropin-Releasing Hormone (CRH) Stimulation in Nelson''s Syndrome: Response of Adrenocorticotropin Secretion to Pulse Injection and Continuous Infusion of CRH^*

Clinical Neurosurgery Section, Surgical Neurology Branch, National Institute of Neurological and Communicative Disorders and Stroke
The Developmental Endocrinology Branch, National Institute of Child Health and Development
Biological Psychiatry Branch, National Institute of Mental Health
National Institutes of Health Bethesda, Maryland 20205
Medizinische Klinik, Universitat Essen, Abt. fur Endok'rinologie Essen, Federal Republic of Germany
New York Hospital, Cornell Medical Center New York, New York 10021

Address requests for reprints to: Edward H. Oldfield, M.D., National Institutes of Health, 9000 Rockville Pike, 10-5N240, Bethesda, Maryland20892.

Nelson's syndrome develops in 10–15% of patients with Cushing's disease who undergo bilateral adrenalectomy. Whether the pituitary tumors of Nelson's syndrome are autonomous or are regulated by hypothalamic signals or glucocorticoids is controversial. We, therefore, compared the plasma ACTH responses to synthetic ovine corticotropin-releasing hormone (CRH) in l i patients with Nelson's syndrome, 1 patient with Cushing's disease who had had bilateral adrenalectomy and did not have Nelson's syndrome, 14 patients with Cushing's disease, and 27 normal subjects. The plasma ACTH response to CRH in 10 patients with Nelson's syndrome was markedly increased and prolonged compared to the responses of normal subjects or patients with Cushing's disease. In 4 patients with Nelson's syndrome, plasma ACTH and cortisol concentrations also were determined at frequent intervals for 10–24 h during continuous infusions of 0.15 M saline or CRH (1 g/kg-h). There was no desensitization of ACTH secretion during short term continuous infusion of CRH. Exogenous cortisol inhibited CRHstimulated ACTH secretion.

These findings suggest that the ACTH response to CRH of patients with ACTH-secreting tumors of Nelson's syndrome differs from the response of those who have the microadenomas of Cushing's disease in two ways: the magnitude is greater, and the response is prolonged. These differences can be explained by the greater size of the tumor and the reduced glucocorticoid feedback in adrenalectomized patients with Nelson's syndrome.

^* Presented in part at the 14th Acta Endocrinologica Conference, June 1983, and at a Combined Conference of the Clinical Staff, "The Clinical Applications of Corticotropin Releasing Factor," at the NIH, January 1984.

Received July 10, 1985.

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