L-09   CURRENT UNDERSTANDING OF ANDROGENETIC ALOPECIA

AG Messenger, MP Birch. Department of Dermatology, Royal Hallamshire Hospital, Sheffield, UK.

Like other common human traits the predisposition to male androgenetic alopecia (AGA) is probably multifactorial. There is a high level of concordance in monozygotic twins indicating that these factors are predominantly genetic but our knowledge of the genes involved is very limited. An association between early onset AGA and a polymorphism in the androgen receptor gene has been reported but, on its own, this does not explain the strong paternal influence on AGA. Understanding the genetics of AGA in men is complicated by doubts over the identity of female AGA (female pattern hair loss, FPHL). Nevertheless, the frequency of male AGA is increased when brothers, but not fathers, have AGA, suggesting that the genetic predisposition may be inherited from either parent. In recent years there has been controversy over the role of androgens in FPHL. Hair loss is undoubtedly a feature of hyperandrogenism but many women with FPHL do not have clinical or biochemical evidence of androgen excess. Clinical trials suggest that women with FPHL showing features of hyperandrogenism may respond to treatment with finasteride or cyproterone acetate but those without these signs do not. It seems likely, therefore, that FPHL is a complex trait. Androgen responses contribute to hair loss in some women but other factors, as yet undetermined, are also involved. Whatever the aetiology the hair follicle changes in male AGA and FPHL appear identical in that both show follicular miniaturisation and a reduction in the duration of anagen. A more productive approach to understanding the aetiology of hair loss in both sexes may be to concentrate on the mechanisms involved in a final common pathway of follicular regression.