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.