Effect of dexamethasone and ACTH on the secretion pattern of fractionated 17-ketosteroids in hirsutism.

Urinary steroid fractionations of 17-ketosteroids were carried out in 3 normally-ovulating young women and in 2 women with hirsutism. Dehydroepiandrosterone, aetiocholanolone, androsterone, 11 beta-hydroxyaetiocholanolone, 11 beta-hydroxyandrosterone, 11-oxoaetiocholanolone and 11-oxondrosterone were determined quantitatively by paper chromatography. Both patients had decreased levels of 11-deoxy and 11-oxy-17-ketosteroids compared with the normals. The ready suppression of 11-oxy-17-ketosteroids and the poor suppression of 11-deoxy-17-ketosteroids by dexamethasone in both patients suggests an ovarian origin of 11-deoxy-17-ketosteroids. Supporting evidence for an ovarian origin in Case 1 was furnished by the poor suppression of testosterone by dexamethasone and lack of response to ACTH stimulation of the adrenal glands. The presented data emphasize that the precursor of 11-deoxy-17-ketosteroids of ovarian origin, possibly testosterone, may well be the cause of hirsutism in both patients.