Ovarian suppression with triptorelin and adrenal stimulation with adrenocorticotropin in functional hyperadrogenism: role of adrenal and ovarian cytochrome P450c17 alpha

• Published in: Fertility and sterility Vol. 62; no. 3; p. 521
• Main Authors: Escobar-Morreale, H, Pazos, F, Potau, N, García-Robles, R, Sancho, J M, Varela, C
• Format: Journal Article
• Language: English
• Published: United States 01-09-1994
• Subjects: Adenoma - etiology; Adolescent; Adrenal Gland Neoplasms - etiology; Adrenal Glands - diagnostic imaging; Adrenal Glands - drug effects; Adrenal Glands - physiopathology; Adrenocorticotropic Hormone - pharmacology; Adult; Female; Humans; Hyperandrogenism - complications; Hyperandrogenism - diagnosis; Hyperandrogenism - physiopathology; Ovary - diagnostic imaging; Ovary - drug effects; Ovary - physiopathology; Polycystic Ovary Syndrome - etiology; Steroid 17-alpha-Hydroxylase - physiology; Testosterone - blood; Triptorelin Pamoate - pharmacology; Ultrasonography
• ISSN: 0015-0282
• DOI: 10.1016/S0015-0282(16)56940-4

To validate combined ovarian suppression with triptorelin and adrenal stimulation with ACTH in the diagnosis of female hyperandrogenism and to provide new insights into the adrenal-ovarian relationship present in this disorder.
Comparison of sexual steroids and basal and ACTH-stimulated steroid levels before and after ovarian suppression induced by triptorelin.
Department of Endocrinology, Hospital Ramón y Cajal, Madrid, Spain.
Thirty-nine nonselected women with hyperandrogenism.
Serum levels of T, 17-hydroxyprogesterone (17-OHP), 17-hydroxy-pregnenolone, DHEA and DHEAS, androstenedione (delta 4-A), 11-deoxycortisol, and cortisol.
Elevated T independent of ovarian suppression pointed to an adrenal disorder in six patients (one with an androgen-producing adenoma, two with late-onset 21-hydroxylase deficiency, three with functional adrenal hyperandrogenism). Nineteen patients had functional ovarian hyperandrogenism as elevated T normalized after ovarian suppression and were subdivided into ovDHEAS+ (n = 7) and ovDHEAS = (n = 12) subgroups depending on the presence of DHEAS hypersecretion. Finally, 14 patients had idiopathic hirsutism according to normal T before and after ovarian suppression. Comparisons of initial hormonal values between groups and with reference values obtained from normal women (n = 11) disclosed in functional adrenal hyperandrogenism an elevation of T and basal and stimulated DHEAS, delta 4-A, and 17-OHP with respect to normal women. These abnormalities were also present in ovDHEAS+ except for basal delta 4-A, which was normal, whereas only T and stimulated 17-OHP were elevated in ovDHEAS =. In the idiopathic group all steroids were normal with the exception of a mild elevation in stimulated DHEAS.
These results show a continuum of abnormalities in hyperandrogenic women, suggesting an enhanced cytochrome P450c17 alpha activity in the adrenal and the ovary as the shared mechanism between functional adrenal hyperandrogenism and functional ovarian hyperandrogenism.