L-10   FEMALE ANDROGENETIC ALOPECIA

R. Sinclair. University of Melbourne Department of Dermatology, St Vincent's Hospital, Australia.

We hypothesize that post- (or peri-) adolescent Australian women commonly experience psychologically distressing hair loss from the scalp; preferentially, but not exclusively from the crown; that may manifest clinically with either temporary or prolonged increased hair shedding or loss of hair volume from the crown or a combination of both; that is due in the main to the action of physiological levels of circulating androgens interacting with sensitive cellular androgen receptors in the hair follicles of the scalp; that is not caused by or associated with nutritional deficiency, metabolic disturbance or endocrinopathy; that is the female correlate of androgenetic alopecia; that can be reliably characterised histologically by an increase proportion of miniaturised hair follicles; that may be distinct aetiologically, histologically, in natural history and response to therapy from idiopathic chronic telogen effluvium; that long term oral antiandrogen therapy can safely prevent and partially reverse loss of hair volume on the crown (but not necessarily increased hair shedding); that is partially reversed but not prevented by topical minoxidil; and that may in the future benefit from novel therapeutic initiatives. To test this construct we examined: 1. the prevalence of androgenetic alopecia in the community 2. the relative prevalence of androgenetic alopecia in pre-menarchal, menstruating and post menopausal females among our cohort of female presenting with hair loss 3. the level of circulating androgens in women with AGA 4. the prevalence and significance of associated nutritional, metabolic and endocrinological abnormalities 5. the psychological morbidity associated with hair loss due to AGA in women 6. the reliability and reproducibility of histological diagnosis of androgenetic alopecia 7. the histological cut-points used to distinguish female androgenetic alopecia from chronic telogen effluvium 8. the clinical genetics of female AGA and the prevalence of male AGA in first degree relatives of probands 9. the presence of functional polymorphism's in the androgen receptor genes of women with AGA. 10. the natural history of chronic telogen effluvium 11. the response of female AGA to monotherapy with oral anti-androgens To test these hypotheses we were required to developed and/or validate the following instruments: 1. A clinical grading scale for female AGA that can also act as a reliable tool for women to self-assess the presence and severity of androgenetic alopecia 2. An instrument to assess the psychological morbidity associated with female AGA 3. An optimal histological specimen and method of examination 4. A objective method of assessing and grading response to therapy