Introduction

Polycystic ovary syndrome (PCOS) is a common endocrinopathy affecting 6–10% of reproductive-age women (Azziz et al. 2004). The definition has evolved over time. The National Institute of Health diagnostic criteria, released in 1990 (Table 6.1) (Zawadzki and Dunaif 1992), highlighted the clinical features of PCOS including ovarian dysfunction (anovulation, irregular cycles, infertility) and hyperandrogenism (hirsutism and acne). The recent and more controversial Rotterdam criteria broaden the condition to include ovarian ultrasound features (Table 6.1) (Zawadski and Dunaif 1992, Group TREAC 2004).

Despite recognition of the important role that insulin resistance plays in PCOS, diagnostic criteria for PCOS do not currently encompass insulin resistance. The difficulties surrounding the diagnosis of PCOS are likely to reflect multiple factors. These include the lack of clarity on the etiology of PCOS, the lack of simple, accurate methods to measure insulin resistance, and the heterogeneity of clinical syndrome that is PCOS today. With greater understanding of PCOS, sub-categories are likely to emerge in what is essentially a heterogeneous syndrome (Norman et al. 1995). This is important to consider when evaluating results of clinical trials, as effects of therapy may vary across the heterogeneous spectrum that is labeled as PCOS today.

The pathogenesis of PCOS is not well understood. A combination of genetic and environmental factors contributes, with potential etiological factors including insulin resistance, ovarian dysfunction, hyperandrogenism, and hypothalamic pituitary abnormalities. Increasingly it is recognized that in the majority of women with PCOS, insulin resistance leading to hyperinsulinemia plays a central role (Dunaif 1997).