ABSTRACT
Introduction 265 Insulin resistance in polycystic ovarian syndrome and its
role in reproductive abnormalities 265 Insulin resistance and metabolic features in women
with polycystic ovarian syndrome 266 Mechanisms to reduce diabetes and vascular risk in
women with polycystic ovarian syndrome 272
Future research questions in relation to long-term diabetes and vascular risk in polycystic ovarian syndrome 275
Conclusion 275 References 276
Polycystic ovary syndrome (PCOS) is a common disorder of chronically abnormal ovarian function and hyperandrogenism affecting 5-10 percent of the female population of reproductive age.1 The primary etiology remains unclear, and historically there has been no consensus on absolute defining features of the phenotype. At the National Institutes of Health conference in 1990, three key features of PCOS were generally agreed as oligomenorrhea, hyperandrogenism (clinical or laboratory evidence), and the absence of other endocrine disorders (congenital adrenal hyperplasia, hyperprolactinemia, thyroid dysfunction, and androgen-secreting tumors).2 The presence of polycystic ovaries, determined by ultrasound evaluation, was not included at that stage as a definitive requirement. A more recent consensus statement (European Society of Human Reproduction and Embryology)3 has revised the criteria for diagnosis of PCOS to include two from three of the following: oligomenorrhea/anovulation; clinical or biochemical evidence of hyperandrogenism; and polycystic ovaries. The inclusion of polycystic ovaries has been promoted by improvements in ultrasound technology and more robust criteria for diagnosis. Women with PCOS tend to present at clinics complain-
without acne. They are therefore seen by gynecologists, primary care physicians, endocrinologists, and dermatologists. It is noteworthy that it has been accepted for some years now that abnormal insulin metabolism is a major underlying feature of PCOS, but no aspect of it is included in the most recent definition.3
