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Introduction
Female alopecia, hirsutism, acne and polycystic ovary syndrome (PCOS) share a common thread: the endocrine abnormality of hyperandrogenism. Hirsutism and acne, and to a lesser extent, female alopecia, are all clinical signs of hyperandrogenization.[1] PCOS is considered primarily to be a syndrome of hyperandrogenism.[1] The majority of patients with hirsutism or unwanted hair growth (75-80%) have PCOS, and approximately 20-40% of patients with persistent acne only have PCOS;[1] approximately 10% of women with alopecia also only have PCOS.[1]
Female androgenetic alopecia, also known as female pattern baldness (FPB), is a common yet difficult-to-treat condition,[2] in which even mild cases can have a psychological impact on patients. FPB is characterized by the progressive miniaturization of hair follicles and a decrease in the percentage of anagen hair.[3,4] Usually there is a diffuse reduction in vertex hair density with retention of the front hairline.[2] It affects more than 50% of women over their lifetime, with a prevalence and severity that increases with age.[4] FPB is a more appropriate name for the disorder because the role of androgens in the etiology of the disorder is less certain than in men.[5] Although most patients with FPB show no signs of hyperandrogenism in laboratory testing, their condition improves after treatment with oral anti-androgens, confirming at least some involvement of androgens in the pathogenesis of this kind of alopecia.[6,7]
Hirsutism in women is excessive terminal hair appearing in a male (androgen-dependent) sexual pattern,[8] and is associated with psychological distress.[9] Approximately half of the cases of hirsutism in women are due to hyperandrogenism.[8] When hirsutism occurs in the absence of excess androgen it is termed 'idiopathic hirsutism'.[8] Hirsutism should be distinguished from hypertrichosis, which is an increase in body hair beyond the normal variation of the patient's reference group, may be congenital or acquired, and is associated with abnormal hair growth that is either localized or generalized.[10]
Another clear clinical signal of hyperandrogenism is acne.[11] Acne lesions (papules, pustules, nodules) form through the interaction of excess sebum production, sebaceous follicle obstruction and bacterium Propionibacterium acnes proliferation and subsequent inflammation.[12] There is a correlation between excess sebum production and androgen levels, but the sensitivity of the sebaceous glands to hormonal stimulation also contributes to the formation of acne,[9] as increased sensitivity results...