title: Common pathophysiological mechanisms involved in luteal phase deficiency and polycystic ovary syndrome. Impact on fertility.
abstract: Luteal phase deficiency (LPD) is a consequence of the corpus luteum (CL) inability to produce and preserve adequate levels of progesterone. This is clinically manifested by short menstrual cycles and infertility. Abnormal follicular development, defects in neo-angiogenesis or inadequate steroidogenesis in the lutein cells of the CL have been implicated in CL dysfunction and LPD. LPD and polycystic ovary syndrome (PCOS) are independent disorders sharing common pathophysiological profiles. Factors such as hyperinsulinemia, AMH excess, and defects in angiogenesis of CL are at the origin of both LPD and PCOS. In PCOS ovulatory cycles, infertility could result from dysfunctional CL. The aim of this review was to investigate common mechanisms of infertility in CL dysfunction and PCOS.
authors.affiliation: Division of Endocrinology, First Department of Internal Medicine, Laiko General Hospital, Medical School, University of Athens, Aghiou Thoma 17 Street Goudi, Athens, Greece. gboutzios@gmail.com
authors.forename: Georgios
authors.initials: G
authors.lastname: Boutzios
authors.forename: Maria
authors.initials: M
authors.lastname: Karalaki
authors.forename: Evangelia
authors.initials: E
authors.lastname: Zapanti
mesh_terms: D054304:Anti-Mullerian Hormone / Q000502:physiology; D003338:Corpus Luteum / Q000378:metabolism*; D005260:Female; D006801:Humans; D006946:Hyperinsulinism / Q000503:physiopathology; D007247:Infertility, Female / Q000378:metabolism / Q000503:physiopathology*; D008183:Luteal Phase / Q000502:physiology*; D018919:Neovascularization, Physiologic / Q000502:physiology; D011085:Polycystic Ovary Syndrome / Q000378:metabolism / Q000503:physiopathology*; D011374:Progesterone / Q000172:deficiency*
chemical_list: D011374:Progesterone; D054304:Anti-Mullerian Hormone