Polycystic ovary syndrome (PCOS) was first described by Stein and Leventhal (1935), although the overweight, hirsuit, amenorrheic phenotype they originally described, we now realize, probably reflects the severe end of the spectrum of the syndrome. Diagnosis is made primarily by ultrasound and endocrine changes, although there remains some controversy about the significance of ultrasound-only diagnosed PCOS when the clinical phenotype and endocrine pattern are normal (Polson et al. 1988, Abdel Gadir et al. 1992). The ultrasound features of PCOS are enlarged ovaries, thickened ovarian stroma, multiple peripheral cysts (2 –10 mm diameter), and an increased intraovarian stromal blood flow (Adams et al. 1986, Zaidi et al. 1995, Buckett et al. 1999). The endocrine pattern is characterized by raised serum luteinizing hormone (LH) levels in the early follicular phase or raised ratio of LH to follicle stimulating hormone (FSH) and raised levels of testosterone and androstenedione, often associated with reduced levels of sex hormone binding globulin (SHBG) (Hull 1987, DeVane et al. 1975). However, not all these features are present in every case of PCOS and it is clear that the syndrome, primarily anovulation associated with hyperandrogenemia, is an end-point of multiple causes and this is reflected in the unknown etiology of the syndrome.
This heterogeneity has spawned many avenues for treatment of PCOS such as weight loss and lifestyle management, ovulation induction with varieties of agents, the treatment of hyperinsulinemia, the treatment of hyperandrogenemia, and the surgical treatment of PCOS. All these are described elsewhere in this volume.