Polycystic ovary syndrome and insulin-resistant hyperinsulinemia

Abstract

In a broad sense, polycystic ovary syndrome (PCOS) may be considered to be synonymous with chronic unexplained hyperandrogenemia, which accounts for approximately 95% of hyperandrogenism in women. PCOS comprises a mosaic of classic and nonclassic forms, which may ultimately prove to have distinct genetic determinants. The hyperandrogenism appears to arise from generalized abnormal regulation (dysregulation) of steroidogenesis. This dysregulation seems to result from imbalance among the various extrinsic and intrinsic factors involved in the modulation of trophic hormone action. Hyperinsulinemia seems to be an important extrinsic factor in many cases of PCOS; it results from resistance to the effects of insulin on glucose metabolism. The elevation in insulin levels may precipitate hyperandrogenemia in genetically vulnerable individuals by unmasking latent abnormalities in the regulation of steroidogenesis. One of these may be a polycystic ovary gene that is expressed in the male as pattern baldness. Insulin also seems to be one of many factors that interact with androgen to regulate pilosebaceous unit development. Treatment of PCOS with antidiabetic insulin-lowering agents may improve ovarian function and androgen levels; it remains to be determined whether it will benefit the pilosebaceous unit manifestations of the disorder. (J Am Acad Dermatol 2001;45:S95-104.)