TY - JOUR
T1 - Corticotropin-releasing hormone (CRH) stimulation in nelson’s Syndrome
T2 - Response of adrenocorticotropin secretion to pulse injection and continuous infusion of CRH
AU - Oldfield, Edward H.
AU - Schulte, Heinrich M.
AU - Chrousos, George P.
AU - Gold, Philip W.
AU - Benker, Georg
AU - Peterson, Ralph E.
AU - Cutler, Gordon B.
AU - Loriaux, D. Lynn
PY - 1986/5
Y1 - 1986/5
N2 - 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 µg/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.
AB - 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 µg/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.
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U2 - 10.1210/jcem-62-5-1020
DO - 10.1210/jcem-62-5-1020
M3 - Article
C2 - 3007552
AN - SCOPUS:0022647653
SN - 0021-972X
VL - 62
SP - 1020
EP - 1026
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 5
ER -