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Clinical Features of Frontal Fibrosing Alopecia ( N = 29 )

Frontal fibrosing alopecia (FFA) is a form of scarring alopecia whose diagnosis is increasing globally. Although its etiology is unknown, FFA is thought to be a clinical subset of lichen planopilaris (LPP) that primarily affects postmenopausal women. Patients diagnosed with FFA between January 2006 and December 2013 at clinics of the Washington University Division of Dermatology (St. Louis, Missouri) were studied using patient surveys and chart notes to assess demographics, clinical features, medical history, and treatment. Twenty-nine patients were enrolled in the study, including 28 women and 1 man. The average age of disease onset was 55.4 years (range, 29–75 years). Many patients (55%) had a history of autoimmune diseases, including hypothyroidism (35%), mucocutaneous lichen planus (28%), psoriasis (7%), vitiligo (3%), systemic lupus erythematosus (3%), iritis (3%), Sjögren syndrome (3%), and ulcerative colitis (3%). Patients often identified a stressful inciting event prior to onset of hair loss. Patients tried an average of 3 different treatments for hair loss, with topical and intralesional steroids, hydroxychloroquine, topical calcineurin inhibitors, and excimer laser therapy being the most efficacious at limiting hair loss. Cutis. 2019;103:E16-E22. F rontal fibrosing alopecia (FFA) is a form of lymphocytic cicatricial alopecia that presents as frontotemporal hairline recession, typically in postmenopausal women.1 The condition is considered to be a variant of lichen planopilaris (LPP) due to its similar histologic appearance.2 Loss of eyebrow1-11 and body5-11 hair also is commonly present in FFA, and histologic findings are identical to those for hair loss on the scalp,8,9 suggesting that FFA may be a form of generalized alopecia. The pathogenesis of FFA is unknown, but several etiologies have been postulated. Some suggest that as a variant of LPP, FFA is a hair-specific autoimmune disorder characterized by a T cell–mediated immune reaction against epithelial hair follicle stem cells, leading to fibrosis and depletion of hair regeneration potential.12 In support of this theory, FFA has been associated with other autoimmune diseases including hypothyroidism,6,8,13-16 mucocutaneous lichen planus,8,15,17 vitiligo,15,18 Sjögren syndrome,19 and lichen sclerosus et atrophicus.15,20 Another hypothesis suggests that the proandrogenic state in postmenopausal women may be related to the disease process.1 This hypothesis is supported by the reported success of antiandrogen therapy with 5α-reductase inhibitors (5α-RIs) in stabilizing FFA.3-5,7 Finally, genetic16,21 and environmental factors related to smoking and socioeconomic status5 also have been postulated to be risk factors for FFA. A variety of treatments have shown varying success, including topical and intralesional corticosteroids, hydroxychloroquine, immunomodulators, antibiotics, and 5α-RIs.1,3-6,8,15,17,22 However, FFA is considered to be relatively difficult to treat and commonly progresses regardless of treatment before spontaneously stabilizing.2-4,6,8,10 Frontal Fibrosing Alopecia Demographics: A Survey of 29 Patients