Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • br Acknowledgments This work was

    2022-03-12


    Acknowledgments This work was supported by the National Institutes of Health (R01 A1084898) to M.V. Williams and M.E. Ariza.
    Introduction Female pattern hair loss (FPHL) has emerged as the preferred term for androgenetic alopecia (AGA) in women due to the uncertain relationship between androgens and this entity (Olsen, 2001). FPHL is the most common hair loss disorder in women. Initial symptoms may develop during the teenage years and lead to progressive hair loss with a characteristic pattern distribution (Vujovic and Del Marmol, 2014). FPHL is characterized as a nonscarring diffuse alopecia that evolves from the progressive miniaturization of hair follicles and subsequent reduction in the number of hairs, especially in the central, frontal, and parietal scalp regions (Olsen, 2002; Fig. 1). FPHL has three main clinical manifestations. The first manifestation is the diffuse thinning of the upper biparietal and vertex regions and preservation of the anterior hair Human Angiopoietin 4 / ANG4 / ANGPT4 Protein (His Tag) line. There are several hair loss scales that attempt to categorize FPHL and each has advantages and disadvantages (Ludwig, 1977, Ramos and Miot, 2015, Savin, 1994, Yip and Sinclair, 2006; Fig. 2, Fig. 3). A wide discussion of each scale is not the primary scope of the paper. Another manifestation is the thinning of the upper bitemporal region and vertex with frontal accentuation that configures as a triangular or Christmas tree form with hair loss in a triangular shape in the frontal-vertical area (Olsen, 1999; Fig. 4). A third manifestation is a deep recession of the frontal-temporal hairline and true vertex balding, which is typically seen in men but occasionally occurs in women although uncommon (Redler et al., 2017).
    Epidemiology The frequency of FPHL varies among population groups and ordinarily increases with age. However, a comparison of prevalence between different studies is hampered by the lack of universally accepted criteria for the disease (Ramos and Miot, 2015). Among healthy women, approximately 6% to 38% experience some degree of frontal and/or frontal-parietal hair loss (Birch et al., 2001). The age of onset for FPHL is during the reproductive years, which is later than in men. Twelve percent of women first develop clinically detectable FPHL by age 29 years, 25% by age 49 years, 41% by 69 years, and >50% have some element of FPHL by 79 years (Birch et al., 2002). More severe cases of the disease during puberty are more rarely described. Nevertheless, there is a greater demand for treatment among patients ages 25 to 40 years (Tosti and Piraccini, 2006). In the United Kingdom, 6% of women younger than age 30 years have FPHL for women older than 70 years, FPHL reaches a rate of 42% (Birch et al., 2002). Only 43% of women age >80 years show no evidence of FPHL (Sinclair and Dawber, 2001).
    Pathophysiology FPHL and male AGA share a final common pathway that causes follicular regression but current knowledge suggests that the etiology is not necessarily the same in both sexes. Although the role of androgens in the pathogenesis of male hair loss has been clearly established, the role of androgens in FPHL is less clear. In fact, FPHL may develop even in the absence of androgens (Herskovitz and Tosti, 2013). However, it is likely that other nonandrogenic factors that are currently unidentified may play a role in the pathogenesis of FPHL (Redler et al., 2017). Therefore, the involvement of these genes in the etiopathogenesis of FPHL cannot be completely excluded. In women with FPHL who do not have elevated androgen levels, a genetic predisposition may be involved. This genetic disposition permits normal levels of circulating androgen to act on follicular target cells, which are specially sensitized by binding to specific intracellular androgen receptors. In other cases, an androgen-independent mechanism may be involved in the development of FPHL (Orme et al., 1999). Two recent studies by Heilmann-Heimbach et al. (2017) and Pickrell et al. (2016) have substantially found an increased number of gene loci (>60) associated with male AGA.