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Pituitary-Adrenal Response to the Antiglucocorticoid Action of RU 486 in Cushing's Syndrome^*

Centre de Recherches Endocrinologiqu.es Hopital Cochin, Institut Roussel-Uclaf Paris 75014;
Laboratoire d'Explorations Fonctionnelles Hopital Trousseau, HÔopital Trousseau Paris 75007;

Address requests for reprints to: Prof. J. P. Luton, Endocrinology, Hopital Cochin, 27 rue du Faubourg St Jacques, Paris 75014, France.

RU 486 [17β-hydroxy-l1β-(4-dimethylaminophenyl) 17ª-(prop-l-ynyl)estra-4,9-dien-3-one[ is a steroid analog which antagonizes glucocorticoid action at the receptor level. The pituitary-adrenal response to RU 486 was evaluated in patients with Cushing's syndrome. The acute administration of 400 mg RU 486 at 0800 h in five patients with Cushing’s disease induced no significant change in plasma cortisol during the next 10 h compared with the administration of placebo. However, prolonged administration (400 mg daily for 3 days) caused activation of the pituitary-adrenal axis; urinary cortisol increased the most from 727 to 5720, 830 to 8200, 610 to 1020, 110 to 570, and 300 to 990 µg/day. Plasma cortisol and lipotropins increased to a lesser extent. Hormone changes appeared on the second day of drug administration and lasted up to 3–4 days after the drug was discontinued. In two patients with nonpituitary-dependent ushing's syndrome, RU 486 induced no significant change in steroid secretion. We conclude that RU 486 induced a delayed and prolonged pituitary-adrenal response in Cushing's disease; whether theresulting cortisol overproduction will overcome the peripheral effect of RU 486 remains to be determined. {J Clin ndocrinol Metab 63: 639, 1986)

^* This work was supported by INSERM Grant CRE 834002.

Received March 18, 1986.

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