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Dermatol Ther. 2011 Mar-Apr;24(2):296-300. doi: 10.1111/j.1529-8019.2011.01407.x.

Therapeutic hotline. Genetic variations in the androgen receptor gene and finasteride response in women with androgenetic alopecia mediated by epigenetics.

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DermaGenoma Inc., 17682 Mitchell N., Irvine, CA 92614, USA.


When studies of postmenopausal women with hair loss failed to reveal a response to the 5 alpha reductase inhibitor, finasteride, researchers began to question the existence of androgenetic alopecia in women and renamed the clinical entity female pattern hair loss. However, recently published reports of finasteride response in some women with hair loss suggest that an androgenic mechanism is mediating response in this group. Variant repeat nucleotide sequences in exon 1 of the androgen receptor (AR) gene have been shown to determine androgen sensitivity in a variety of androgenic conditions in men and women. In an effort to identify whether this AR variant may help determine which women are likely to respond to finasteride therapy, a pilot study was undertaken. In our 6-month pilot of 13 patients, women with greater androgen sensitivity (<24 cytosine, adenine, and guanine (CAG) repeats) were likely to have a significant response to finasteride 1 mg/day compared with patients treated with placebo, and compared with patients with normal androgen sensitivity (≥24 CAG repeats) based on epigenetic weighted evaluation of the CAG alleles. Results of the present pilot study support the hypothesis that AR-CAG repeats, in conjunction with epigenetic factors, can help determine which women with hair loss will respond to finasteride therapy.

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