title: [Polycystic ovary syndrome: A model of follicular excess].
abstract: Polycystic ovary syndrome (PCOS) is the most common etiology of menstrual disorders and hyperandrogenism. It is characterized by an excess of ovarian follicles. The mechanisms that underlie folliculogenesis disorder in PCOS appear to arise from primitive ovarian hyperandrogenism. This can be modulated by hormonal factors, such as LH or insulin. Ovarian hyperandrogenism results from a real theca cells dysfunction, whose origin is still poorly understood. It seems that complex genetic factors may be involved, but these have not yet been clearly identified. PCOS also results from granulosa cells dysfunction. For example, intra-ovarian factors, such as anti-mullerian hormone, are possibly involved in ovulation's disorders by blocking the physiological process of follicular recruitment. In turn, the oocyte could also be one of the actors possibly involved in the follicular excess in PCOS.
authors.affiliation: hôpital Jeanne-de-Flandre, CHRU de Lille, France. Geoffroy.robin@chru-lille.fr
authors.forename: G
authors.initials: G
authors.lastname: Robin
authors.forename: S
authors.initials: S
authors.lastname: Catteau-Jonard
authors.forename: D
authors.initials: D
authors.lastname: Dewailly
authors.forename: C
authors.initials: C
authors.lastname: Decanter
mesh_terms: D005260:Female; D006107:Granulosa Cells / Q000502:physiology; D006801:Humans; D017588:Hyperandrogenism / Q000209:etiology; D009865:Oocytes / Q000502:physiology; D006080:Ovarian Follicle / Q000503:physiopathology; D010053:Ovary / Q000503:physiopathology; D011085:Polycystic Ovary Syndrome / Q000150:complications / Q000235:genetics / Q000503:physiopathology; D013799:Theca Cells / Q000502:physiology