TY - JOUR
TI - Common pathophysiological mechanisms involved in luteal phase deficiency and polycystic ovary syndrome. Impact on fertility
AU - Boutzios, G.
AU - Karalaki, M.
AU - Zapanti, E.
JO - Endocrine Development
PY - 2013
VL - 43
TODO - 2
SP - 314-317
PB - Humana Press Inc.
SN - null
TODO - 10.1007/s12020-012-9778-9
TODO - androgen;  follitropin;  insulin;  luteinizing hormone;  Muellerian inhibiting factor;  progesterone;  vasculotropin, angiogenesis;  corpus luteum function;  disease association;  female fertility;  hormonal regulation;  hormone action;  hormone blood level;  hormone release;  human;  hyperinsulinemia;  insulin resistance;  luteal insufficiency;  luteal phase;  menstrual cycle;  nonhuman;  ovary polycystic disease;  pathophysiology;  priority journal;  protein expression;  protein function;  review
TODO - 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. © 2012 Springer Science+Business Media, LLC.
ER -