S1 Guideline for Diagnostic Evaluation in Androgenetic Alopecia in Men, Women and Adolescents

U. Blume-Peytavi; A. Blumeyer; A. Tosti; A. Finner; V. Marmol; M. Trakatelli; P. Reygagne; A. Messenger


The British Journal of Dermatology. 2011;164(1):5-15. 

In This Article



AGA is an androgen-dependent trait, which leads to progressive miniaturization of the hair follicle in predisposed men.[10] It is thought that enhanced androgen effects at the genetically predisposed hair follicles are mediated by raised androgen receptor density and/or increased activity of 5-alpha-reductase type II.[2] Nearly all men afflicted with AGA have normal circulating androgen levels. The predisposition to AGA is predominately due to genetic factors. Twin studies show strong concordance rates of between 80% and 90% for monozygotic twins. Family analyses show a significantly increased risk for the development of AGA in men with a father suffering from AGA.[11,12] Conversely, the risk of AGA is significantly decreased in those men with a nonbalding father.

The current scientific data support the thesis that AGA has a polygenic trait. Significant associations have been reported with variant regions of the androgen receptor gene, which is located on the X-chromosome, using a candidate gene approach.[13,14] More recently, two independent genome-wide association studies have identified a susceptibility locus at chromosome 20p11.[15,16]


There are few studies on the genetic base of AGA in women. Smith and Wells[12] reported the frequency of female pattern hair loss with an incidence of 54% pattern hair loss in first-degree male relatives aged > 30 years and 21% in first-degree female relatives > 30 years. It is possible that early- and late-onset female AGA are genetically distinct entities. The role of androgens in female AGA is less certain than in men and other factors may be involved. For the purpose of this guideline the term 'androgenetic alopecia' is used, although the uncertainty of the role of androgens is recognized.

The European Consensus Group agreed not to differentiate between androgenic alopecia and AGA, but to define a subset of women with AGA and associated hormonal dysregulation.


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