[Polycystic ovary syndrome: physiopathology review]

Polycystic ovary syndrome (PCOS), the most common gynecological endocrinopathy in women of reproductive age, is characterized by hyperandrogenism, chronic anovulation and /or polycystic ovaries. Although the cause of PCOS is still unknown, there are several hypotheses attempting to explain the primary defect; the most commonly accepted is insulin resistance. Due to its high prevalence, the patients have increased risk of developing metabolic and cardiovascular alterations. The compensatory hyperinsulinemia contributes to hyperandrogenism in different ways: by stimulating ovarian androgen synthesis and inhibiting hepatic production of sex hormone binding globulin. From the study of the intrauterine environment in recent years it has been suggested that PCOS may have an origin in utero associated with prenatal exposure to androgens. The aim of this paper is to review the main mechanisms proposed to cause the syndrome.