[Polycystic ovarian dystrophies. Diagnostic criteria and treatment]

Polycystic ovary syndrome (PCOS) is an association of oligomenorrhoea, anovulation, hyperandrogenism, obesity and enlarged polycystic ovaries. It provides a model of loss of cyclic ovarian function. It is classical to distinguish between type I and type II PCOS. In type I, the primary mechanism seems to be hypothalamic dysfunction, which causes an increase in the frequency and amplitude of LH pulses, with diminished FSH release. LH hypersecretion stimulates ovarian stroma hyperplasia while FSH insufficiency results in the failure of folliculare maturation and hence anovulation. Aromatization of androgens to oestrogens is responsible for permanent oestrogen overproduction, which favours LH hypersecretion. Type II PCOS is more frequent and may have multiple causes (local, endocrine, systemic, iatrogenic) that interfere with the gonadotropic axis and alter the FSH/LH ratio. The most efficient treatment of hirsutism is cyproterone acetate which alone has both antiandrogenic and antigonadotropic properties. Clomifene citrate remains the "first choice" treatment of infertility associated with anovulation.