Polycystic ovarian disease (PCO) is the most common primary reproductive abnormality associated with impaired fertility in young women. This syndrome is hallmarked by hypersecretion of luteinizing hormone (LH), ovarian theca-cell hypertrophy, hyperandrogenemia, oligo- or anovulation, amenorrhea, hyperinsulinism, dyslipidermia and increased cardiovascular risk. Within this constellation, cardinal pathophysiological features are hyperinsulinism and excessive LH secretion. At least four categories of insulin-depleting regimens are able to improve or normalize various facets of reproductive impairment in PCO. However, the mechanistic bases of LH hypersecretion and insulin resistance, and the manner (if any) whereby the foregoing major pathophysiologies are causally interlinked are unknown.
|Translated title of the contribution||Highlights on the neuroendocrine adaptation in polycistic ovarian syndrome|
|Number of pages||12|
|Journal||Cuadernos de Medicina Reproductiva|
|State||Published - Jan 1 2003|
ASJC Scopus subject areas
- Obstetrics and Gynecology