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Rapid Reversal of Acute Psychosis in the Cushing Syndrome with the Cortisol-Receptor Antagonist Mifepristone (RU 486)

Aart-Jan van der Lely, MD; Karin Foeken, MD; Roos C. van der Mast, MD; and Steven W. J. Lamberts, MD
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Requests for Reprints: A. J. van der Lely, MD, Department of Medicine, University Hospital Dijkzigt, 40 Dr. Molewaterplein, 3015 GD Rotterdam, the Netherlands.

Current Author Addresses: Drs. van der Lely, Foeken, van der Mast, and Lamberts: University Hospital Dijkzigt, 40 Dr. Molewaterplein, 3015 GD Rotterdam, The Netherlands.

Ann Intern Med. 1991;114(2):143-144. doi:10.7326/0003-4819-114-2-143
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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


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