Hirsutism and virilisation.

Hirsutism by definition describes the quality of body hair, implying coarseness, but common usage has extended the meaning to denote an excess of hair-locally or generalised. Body hair is of two types: fine, non-pigmented vellus hair-for example, facial "down"-and coarser pigmented terminal hair as in the scalp and axillas. The visual impression of hairiness is produced by the coarser type. Hirsutism reflects the response of hair follicles to androgenic stimulation, and is therefore a symptom and a clinical sign but not a specific disease entity. Both genetic and hormonal factors affect hair growth, and in different parts of the world cultural factors determine what is socially acceptable in respect of quality, quantity, and distribution of body hair. Thus hirsutism that is quite acceptable in one community may cause severe embarrassment or even psychological disturbance to a woman in another. Yet around 30V0 of women between the ages of 15 and 44 normally have hair on the upper lip, 90' on the chin, and 60o on the sides of the face.' In virilisation progressive hirsutism is complicated by deepening of the voice, clitoromegaly, temporal hair recession, breast atrophy, and an increase in muscle bulk. The appearance of any of these additional signs is an indication for full investigation. Aetiology of hirsutism The main factors responsible for the development of hirsutism are a rise in the concentration of free androgens, resulting from increased androgen secretion and a reduction in sex-hormone-binding globulin (SHBG) concentration. Individual skin sensitivity and an increase in local androgen conversion in the skin may also be important, particularly in certain ethnic groups. The three most important androgens are androstenedione, testosterone, and dihydrotestosterone. Androstenedione is the least and dihydrotestosterone the most potent, but as andro-stenedione can be directly converted to dihydrotestosterone in the skin its potential androgenic importance may be considerable .' Secretion of both androstenedione and testosterone from the adrenals and ovaries increases in hirsute women.3-5 There is also evidence in some hirsute women that increased conversion of androstenedione to dihydrotestosterone may occur locally in the skin2 but whether other androgens, such as de-hydroepiandrosterone or androstenediol, influence the development of hirsutism is not known.