Polycystic ovary syndrome (PCOS) is a common disorder often emerging post-menarche, and hallmarked by androgen excess and a low ovulation rate. Less consistently, PCOS is characterized by hyperinsulinemic insulin resistance, dyslipidemia, increased abdominal adiposity, low-grade inflammation, and the presence of polycystic ovaries (PCO) on ultrasound.
At least two developmental pathways seem to lead to PCOS. One begins with a normal prenatal growth and continues, via simple obesity, to an absolute fat excess; the other begins with fetal growth restraint, continues in infancy with rapid catch-up of weight into the upper-normal range, and leads to relative adiposity at age 4 year, and to visceral fat excess at age 6 year. In late childhood and puberty, both pathways may converge to conform pre-PCOS, a state characterized by hyperinsulinemia, adiposity, low-grade inflammation (as reflected by an increased neutrophile-to-lymphocyte ratio and decreased concentrations of total and high molecular weight adiponectin), amplified adrenarche (with or without precocious pubarche), and early-normal puberty and menarche, which may result in a decreased final stature. Finally, the two pathways diverge again, the postnatal-overweight pathway rather leading to PCOS-with-PCO, while the prenatal-underweight pathway is more often linked to an adult PCOS phenotype with glucose intolerance and without PCO.
In conclusion, markers have been identified along two pathways to PCOS. These markers allow for timely recognition of pre-PCOS and for intervention, with overweight-control and/or insulin sensitization. The early origins of PCOS may thus be pivotal in the development of the adult phenotype, and partly determine the heterogenity in the clinical presentation.
03 - 07 May 2008
European Society of Endocrinology