Alopecia Areata

Alopecia areata (AA) is a nonscarring autoimmune disorder characterizedby a T-cell-mediated attack on anagen hair follicles, resulting in abrupt hair loss without permanent follicular destruction. The lifetime risk is approximately 2%. Recent epidemiologic data demonstrate racial differences in disease prevalence, with the highest rates observed among Asian (414 per 100,000) and Black (226 per 100,000) individuals compared with White individuals (168 per 100,000). Although genetic susceptibility is a major contributor, viral infections, vaccinations, and physical or emotional stress have also been proposedas AA triggers that contribute to loss of immune privilege within the hair follicle.

Patients most commonly present with one or more well- demarcated patches of nonscarring alopecia with little to no erythema or scale. Several clinical patterns have been described, including patchy AA with circumscribed patches that may coalesce with disease progression; ophiasis, which affects the occipital and temporal scalp; sisaipho, the reverse pattern involving the frontal, temporal, and parietal scalp; and diffuse AA, which presents with fluctuating, generalized thinning rather than discrete patches. Facial terminal hair, including the beard, eyebrows, and eyelashes, may also be involved. Based on the extent of involvement, AA may progress to alopecia totalis, involving complete loss of scalp hair, or alopecia universalis, characterized by complete loss of scalp and body hair. Other uncommon clinical variants include reticular, annular, linear, and perinevoid AA. Nail involvement occurs in approximately 10% to 15% of patients and most commonly presents with pitting, trachyonychia, or onychorrhexis.

Diagnosis is usually clinical, although trichoscopy can provide additional diagnostic support. A positive hair pull test, in which gentle traction on 50–60 hairs near the scalp results in the extraction of >10% of hairs, indicates active disease. Classic trichoscopic findings include yellow and black dots, broken hairs, tapered hairs, exclamation mark hairs, short vellus hairs, and multiple yellow dots, i.e., craters of the moon sign—a marker of disease severity. In Black patients, these characteristic findings remain common. However, additional trichoscopic features have also been reported, including perifollicular hyperpigmentation, perifollicular scale, and a prominent honeycomb pigment pattern. Recognition of these findings may improve diagnostic confidence when evaluating patients with richly pigmented skin.

Treatment depends on the patient’s age and disease severity. Therapeutic options include topical therapies (corticosteroids, minoxidil, anthralin, topical immunotherapy, and calcineurin inhibitors) and intralesional corticosteroids for mild, localized disease. For moderate-to-severe AA, historical systemic treatments have included corticosteroids and conventional immunosuppressants (methotrexate, cyclosporine, azathioprine, and mycophenolate mofetil), with recent US Food and Drug Administration (FDA) approval of three oral JAK inhibitors , offering impressive disease stabilization and regrowth potential, albeit at significant cost. Adjunctive therapies include intralesional platelet- rich plasma, cosmetic camouflage, hair prostheses, and psychological support.

1.Strazzulla LC, Wang EHC, Avila L, et al. Alopecia areata: Disease characteristics, clinical evaluation, and new perspectives on pathogenesis. J Am Acad Dermatol. 2018;78(1):1–12. https://doi.org/10.1016/j.jaad.2017.04.1141

2.Pyles J, Palmer V, Balding E, et al. Alopecia areata in skin of color: trichoscopic analysis in Black/African American patients. J Drugs Dermatol. 2025;24(7):708–712. https://doi. org/10.36849/JDD.9139

3.Sangha AM. Alopecia areata in skin of color. J Clin Aesthet Dermatol. 2025;18(11–12 Suppl 1):S30–S31. https://pubmed.ncbi.nlm.nih.gov/41647049/

4.National Alopecia Areata Foundation. New research: prevalence of alopecia areata across races and ethnicities. Published July 31, 2023. Accessed July 27, 2026. https://www.naaf.