Aart-Jan van der Lely, MD; Karin Foeken, MD; Roos C. van der Mast, MD; Steven W. J. Lamberts, MD
The progesterone-receptor antagonist, RU 486 (mifepristone), is also, at higher concentrations, an effective antagonist of glucocorticoid action in vitro and in vivo (1-3). In normal humans, RU 486 blocks glucocorticoid negative feedback at the hypothalamic-pituitary level, inducing a compensatory increase in plasma adrenocorticotropin (ACTH) and cortisol levels (4, 5). In previous studies, patients with the Cushing syndrome caused by ectopic ACTH secretion or by adrenocortical carcinomas who received therapy with RU 486 (5 to 22 mg/kg body weight per day) showed clinical improvement, and no compensatory increases in plasma ACTH or cortisol levels were noted, probably because of ongoing hypothalamic
van der Lely A, Foeken K, van der Mast RC, Lamberts SWJ. Rapid Reversal of Acute Psychosis in the Cushing Syndrome with the Cortisol-Receptor Antagonist Mifepristone (RU 486). Ann Intern Med. 1991;114:143–144. doi: 10.7326/0003-4819-114-2-143
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Published: Ann Intern Med. 1991;114(2):143-144.
Adrenal Disorders, Endocrine and Metabolism.
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