ROLE OF GNRH DRIVE IN THE PATHOPHYSIOLOGY OF POLYCYSTIC-OVARY-SYNDROME

Citation
Mp. Leondires et Sl. Berga, ROLE OF GNRH DRIVE IN THE PATHOPHYSIOLOGY OF POLYCYSTIC-OVARY-SYNDROME, Journal of endocrinological investigation, 21(7), 1998, pp. 476-485
Citations number
77
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
03914097
Volume
21
Issue
7
Year of publication
1998
Pages
476 - 485
Database
ISI
SICI code
0391-4097(1998)21:7<476:ROGDIT>2.0.ZU;2-3
Abstract
Polycystic ovary syndrome may result from multiple mechanisms, but ful l expression of the PCO syndrome with hyperandrogenic anovulation depe nds upon sustained LH drive and relative FSH deficiency. We have descr ibed possible intrinsic and extrinsic factors capable of modifying the hypothalamic-pituitary-ovarian axis. Available evidence suggests the presence of an intrinsic alteration in GnRH-LH drive. The long-term na tural history of HAA is variable and depends on several factors includ ing obesity, aberrations in insulin action, intrinsic ovarian function , and end-organ responsiveness to androgens. Figure 1 presents a conce ptualization of the pathogenesis of PCOS diagramming the multiple modu lators of its expression. Long-term suppression of androgens when fert ility is not desired should modify the full expression of the PCO synd rome. It is important to appreciate that therapy with oral contracepti ve agents has few drawbacks and many immediate and potential long-term benefits for women with HAA. This therapy may be of greatest benefit when started in adolescence prior to the progression of obesity, hirsu tism, and thecal-stromal hyperplasia. Women with HAA represent a large subgroup of patients who require individualization of their health ca re with sensitivity to issues surrounding anovulation, obesity, hirsut ism, and infertility. (J. Endocrinol. Invest. 21: 476-485, 1998) (C) 1 998, Editrice Kurtis.