Abstract

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women in reproductive age. Depending on the diagnostic criteria used, the prevalence varies between 8% and 13% [1–4]. This syndrome was initially defined as a reproductive disease characterized by the presence of hyperandrogenism (HA), ovulatory dysfunction, and polycystic ovaries. However, growing data have shown the strong association with metabolic dysfunction. Although PCOS has been recognized clinically for more than 80 years, there has been an evolving set of diagnostic criteria and definition of PCOS phenotypes. In 1990, the National Institutes of Health (NIH) criteria defined PCOS diagnosis based on the presence of clinical or biochemical HA and chronic oligo-anovulation (OA) [1]. Subsequently, Rotterdam Consensus Criteria (2003) established a new diagnostic definition, including HA, OA, and polycystic ovarian morphology (PCOM) diagnosed by transvaginal ultrasound. This consensus introduced two new phenotypes: hyperandrogenic ovulatory (HA + PCOM) or non-hyperandrogenic anovulatory phenotypes (OA + PCOM), not previously considered [2]. The Androgens Excess and PCOS Society (2006) proposed an amendment to Rotterdam Consensus criteria: clinical or biochemical androgen excess was compulsory, including oligo-anovulation and polycystic ovarian morphology as secondary criteria [3]. Finally, new modifications were introduced by International PCOS Network (2018) about PCOM definition [4]. These different criteria have amplified the PCOS phenotype spectrum in a 30-year period of time.