Female Androgenetic Alopecia: An Update on Diagnosis and Management

Michela Starace; Gloria Orlando; Aurora Alessandrini; Bianca Maria Piraccini


Am J Clin Dermatol. 2020;21(1):69-84. 

In This Article


Sex hormonal milieu is the main pathogenetic mechanism studied in FAGA. Even though the relationship between dihydrotestosterone (DHT) and male AGA has been confirmed,[15] the role of androgens is not clearly defined in FAGA. Indeed, only one-third of women with FAGA show abnormal androgens levels.[16]

An increased peripheral sensitivity to androgens has been postulated to explain cases with normal levels of androgens.[17] However, FAGA has also been described in patients lacking androgen receptors, suggesting that an androgen-independent mechanism could be involved.[18]

Estrogen could have a protective role on human hair growth, suggested by the increased prevalence of FAGA following menopause, the prolongation of anagen during pregnancy,[19] the hair loss in women taking tamoxifen or aromatase inhibitors for treatment of breast cancer[20] and the documented complete hair regrowth in transsexual individuals with AGA on estrogen.[21,22]

Recently, sequence variations in the androgen receptor gene (AR) and estrogen receptor 2 gene (ESR2) have been associated with susceptibility to FAGA.[8] However, the association between FAGA and the aromatase gene (CYP19A1) has not been confirmed.[8] No definitive family inheritance has been identified.

Moreover, several data suggest that chronic inflammation in the scalp may promote hair loss.[23] Histologically, the miniaturization process is associated with microinflammatory lymphocytic infiltrate in the periinfundibular region; and prostaglandin D2 (PG-D2), which can inhibit hair growth in explanted human hair follicles and in mice, is elevated in bald scalps, but this study is confirmed only in men.[24]