Ovarian influence on adrenal androgen secretion in polycystic ovary syndrome

To determine whether the ovary influences adrenal androgen secretion in polycystic ovary syndrome (PCOS). The adrenal androgen secretion was evaluated before and during ovarian suppression with a long-acting GnRH agonist. Department of Obstetrics and Gynecology, Pisa, Italy. Women with PCOS and high...

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Published inFertility and sterility Vol. 63; no. 4; pp. 734 - 741
Main Authors Fruzzetti, Franca, De Lorenzo, Daniele, Ricci, Cabiria, Teti, Giancarlo
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.04.1995
Elsevier Science
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ISSN0015-0282
1556-5653
DOI10.1016/S0015-0282(16)57474-3

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Summary:To determine whether the ovary influences adrenal androgen secretion in polycystic ovary syndrome (PCOS). The adrenal androgen secretion was evaluated before and during ovarian suppression with a long-acting GnRH agonist. Department of Obstetrics and Gynecology, Pisa, Italy. Women with PCOS and high (10 subjects) and normal (12 subjects) DHEAS levels and 6 normal women. After 1 mg dexamethasone, an ACTH-(1-24) stimulation test was performed in the early follicular phase of the menstrual cycle. The test was repeated after two injections of a long-acting GnRH analogue (GnRH-a). Basal plasma levels of gonadotropins, E2, T, androstenedione (A), 17α-hydroxyprogesterone (17-OHP), DHEAS, and Cortisol (F) were evaluated before the evening administration of dexamethasone. Serum A, T, 17-OHP, DHEAS, and F were measured 9 hours after dexamethasone and in samples collected 60 and 120 minutes after ACTH IV injection. In the high DHEAS group the maximum increases in T, A, 17-OHP, and DHEAS in response to ACTH were significantly higher than in normal DHEAS PCOS women and in normal women. The GnRH-a modified the A and T responses to ACTH in the high DHEAS group. Ovarian steroids, or other extra-ovarian factors, seem to be responsible for the increased A and T responses to the corticotropin stimulation demonstrated in some PCOS women.
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ISSN:0015-0282
1556-5653
DOI:10.1016/S0015-0282(16)57474-3