Polycystic Ovary Syndrome Endocrine and Cardio-Metabolic Abnormalities: how to Manage?

Abstract

Polycystic ovary syndrome (PCOS), the main cause of androgen excess in women of reproductive age, is a multifaceted, dynamic and clinically heterogenic disorder. Rotterdam 2003 ESHRE/ASRM definition criteria were recently reinforced at the NIH Consensus Meeting 2012. Concomitant identification of the clinical phenotypes of the syndrome is mandatory in medical care and clinical studies, as these are strongly related to reproductive, cardiovascular and metabolic outcomes. Documentation of polycystic ovarian morphology (PCOM) is challenging, with the AE/PCOS Task Force 2014 suggesting a threshold of ≥25 follicles/ovary in 1835 years old women when using high-frequency transducers. Elevated levels of total testosterone and/or free testosterone and/or low sex hormone-binding globulin (SHBG) stand for androgen excess in women, as stated by the ESE Position Statement 2014. Despite evidence of increased metabolic and cardiovascular risk, increased prevalence of cardiovascular events linked to PCOS status per se is still insufficient documented, mainly because of the clinical heterogeneity of studies populations and lack of prospective data. First-line therapy in the medical management of PCOS is metformin, at least 1.5 g/d, in all patients with documented insulin resistance and hyperinsulinemia. According to Endocrine Society Guidelines 2013, other insulin-sensitizers (e.g. thiazolidinediones) raise safety concerns on the long-term, whereas statins need further evaluation to demonstrate their benefits in the treatment of PCOS, however, are indicated in dyslipidemic patients. Anti-androgens and combined oral contraceptives (COC) are targeting androgen excess, particularly in non-insulin resistant patients, with an overall benefit to risk ratio in PCOS favoring benefits.