Epidemiology of Alopecia Areata

Alopecia areata (AA) is a frequent autoimmune disease with a lifetime risk of about 1.7% in the general population, including males and females across all ethnic groups. The prevalence of AA is 0.1% to 0.2% worldwide, as well as in the United States, and is responsible for 0.7% to 3.0% of patients seen by dermatologists. The peak incidence of AA seems to occur among 15- to 29-year-old individuals, with as many as 44% of people having onset of the disease before their 20s and less than 30% of patients having onset after their 40s. The clinical course of AA is highly unpredictable, and it can occur at any age from birth to the late decades of life.

Clinical Findings and Cause

AA is a nonscarring type of hair loss that usually manifests suddenly as 1 or more well-defined circumscribed areas that can occur anywhere in the body, although they are most frequently seen on the scalp (90% of cases). The disease can then remit spontaneously or, alternatively, the initial patches can coalesce and progress to cover the scalp (alopecia totalis) or even the entire body surface (alopecia universalis). The clinical heterogeneity and unpredictable course of AA is a major source of distress for affected individuals.

Epidemiologic studies in AA have demonstrated that a history of autoimmune disease increases the risk of AA. Specific reported associations include AA with thyroid disease, celiac disease (CeD), rheumatoid arthritis (RA), vitiligo, and type 1 diabetes (T1D). Although the exact pathophysiology of AA is not clear, AA is a T-lymphocyte mediated autoimmune condition that occurs in genetically susceptible individuals. Histopathologic findings have revealed inflammatory perifollicular infiltrates of T cells around anagen (growth phase) hair follicles (“swarm of bees”), which consist of both CD4+ and CD8+ T cells. The focus of the attack by the infiltrating lymphocytes is the base of the hair follicle, such that the stem cell compartment, is spared from destruction and, therefore, hair regrowth remains possible. Increased levels of autoantibodies, cytokine abnormalities, and increased prevalence of autoimmune comorbidities have been described in patients with AA. An acute onset of disease has been documented in affected individuals at times of profound stress, grief, or fear, indicating that besides the autoimmune and genetic components, environmental (nongenetic) factors may contribute to the manifestation of this disease, thus supporting the multifactorial cause of AA.

Lack of Cure or Preventive Treatment of AA

AA can cause tremendous emotional and psychosocial distress in affected individuals and their families. Patients can experience profound feelings and frustrations, such as loneliness, isolation, anger, depression, and embarrassment, among many others. However, despite the high prevalence and extreme psychosocial burden of AA, there are no evidence-based treatments as yet, and treatment of AA is symptomatic and directed toward halting disease activity. A comprehensive Cochrane analysis assessment of 17 randomized control trials (RCTs) involving a total of 540 participants found no proven treatment of AA. These trials included 6 to 85 individuals each; treatments included topical and oral corticosteroids, topical cyclosporine, photodynamic therapy, and topical minoxidil. Even though topical corticosteroids and minoxidil have been widely used to reduce inflammation and/or stimulate hair growth, respectively, and seem to be safe, there is no convincing evidence that they are beneficial in the long term. Most trials have been poorly reported and/or are small and underpowered, resulting in inconclusive results. No RCTs were found on the use of other drugs that are also commonly used for the treatment of AA, such as diphencyprone, dinitrochlorobenzene, dithranol, or intralesional corticosteroids.

Because of this lack of evidence-based treatment of AA and because of the high rate of spontaneous remission, particularly in individuals with a recent onset and small patches of hair loss, the initial approach typically includes topical or intralesional steroids or observation. However, approximately 20% to 30% of cases fail to resolve using these strategies, and only one-third of all cases achieve complete recovery for about 10 to 15 years.