This chapter discusses the issues around the diagnosis and management of polycystic ovary syndrome (PCOS) through puberty and adolescence. The diagnosis of PCOS may be made incidentally in girls undergoing investigation for severe obesity or prospectively in young women being investigated for irregular periods, acne or hirsutism. There may be a family history of PCOS or infertility and, although the classic biochemical features and ovarian ultrasound appearances may be not being evident immediately, diagnosis unravels over time. Symptomatic treatment focused on the restoration of regular menses is the most common starting point and the oral contraceptive pills (OCPs) are the mainstay of pharmacological therapy for PCOS for many decades. The effects of metformin administration in adolescent girls with PCOS have been assessed in both obese and non-obese populations. Irregular periods are treated with OCPs with or without the inclusion of cyproterone acetate depending on the extent of hirsutism and acne.

Hyperandrogenism is the most common endocrinopathy seen in women and may result from ovarian or adrenal overproduction of androgens, altered peripheral metabolism and/or end-organ hypersensitivity. The clinical manifestions of hyperandrogenism in polycystic ovary syndrome (PCOS) are frequently very visible and, as a result, produce significant psychological morbidity. The three main naturally occurring steroids responsible for androgen activity are testosterone and the weak androgens dehydroepiandrosterone (DHEA) and androstenedione. Managing the dermatological signs of hyperandrogenism, which generally present as acne, seborrhoea, hirsutism and female-pattern hair loss in PCOS, is achieved by reducing the circulating levels and effects of androgens. Potential mechanisms by which this may occur include: direct suppression of androgen production, change in androgen binding to sex hormone-binding globulin (SHBG), impairing the peripheral conversion of free testosterone to dihydrotestosterone by inhibiting 5 alpha-reductase type I and inhibiting androgens acting at the site of target tissue.