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Hair Loss in the Dermatology Office: An Update on Alopecia Areata

May 2013 | Volume 12 | Issue 5 | Features | 588 | Copyright © May 2013



Hair Loss in the Dermatology Office: An Update on Alopecia Areata


Hair loss is a frequent clinical complaint encountered by dermatologists, and alopecia areata (AA)-induced hair loss is responsible for 0.7 to 3.8% of dermatology clinic visits.1 Alopecia areata is characterized by chronic yet reversible, non-scarring hair loss. It is postulated to be an autoimmune process that targets the hair follicle, although the pathogenesis is incompletely understood.1-3 This article summarizes the epidemiologic and clinical features of AA, outlines our current understanding of its pathogenesis, and reviews therapeutic options for this condition.


Alopecia areata affects patients of all ages and ethnicities with an equal sex distribution.1,2,4 Approximately 0.1-0.2% of the United States population is affected5; there is a lifetime risk of about 1.7%.6,7 Roughly 60% of patients present before age 20, and a family history of AA is seen in about 20% of patients.2

Clinical Presentation

Alopecia areata can affect any hair-bearing epidermal site, but involves the scalp in approximately 90%.1,2 Classic AA lesions are well-demarcated, ovoid patches with no overt epidermal change. Patients typically present with a spontaneous, asymptomatic hair loss in a solitary nummular patch. Alternate presentations include multiple alopecic patches or rapid progression to complete loss of scalp/facial hair (alopecia totalis) or body hair (alopecia universalis). Rarer hair loss variants include reticular, ophiasis, ophiasis inversus, and diffuse thinning over the entire scalp.1,8 Associated clinical findings that aid diagnosis include “exclamation mark” hairs, “cadaver” hairs, red lunulae, rows of nail pitting or trachyonychia, and the presence of other autoimmune disorders.1,8,9



Alopecia areata is considered a polygenic disorder with variable phenotypes in which several major genes dictate susceptibility to disease and numerous minor genes modulate phenotype.10 The latter may explain the variable disease severity seen in AA: some patients experience one patch of alopecia, and others demonstrate total body hair loss.10 The genetic component of alopecia areata is supported by several findings: there is a higher incidence of AA in genetically related individuals:7 up to 28% of patients report at least one affected family member,1 monozygotic twins have exhibited similar times of onset and patterns of hair loss,1,11,12 and several human leukocyte antigen (HLA) alleles are associated with AA.1,7 Finally, genes on chromosome 21 may be implicated in AA susceptibility because there is an association with both Down syndrome and Autoimmune polyendocrinopathy syndrome type 1, two conditions owing to genetic defects on this chromosome.7


The 42% - 55% concordance rate in monozygotic twins not only suggests a genetic etiology of AA, but it also implicates environmental influences in the pathogenesis of this condition.13,14 While the inheritance of specific alleles may provide innate susceptibility to developing AA, environmental factors likely trigger disease onset and modify the pattern and extent of hair loss, chronicity of disease, and resistance to treatment.1,7,10 Hormonal fluctuation,1 infection,15-17 vaccinations,18,19 and diet1,20 have all been cited as possible triggers for AA, though additional research is warranted to clarify these associations. The role that psychosocial stressors play on disease onset and relapse is largely uncharacterized. Life stressors may instigate AA onset and modify disease course, yet evidence is circumstantial and clinical studies are inconclusive: some studies found no correlation between the onset of hair loss and stressful life events,21-23 whereas others affirmed that stressful life events preceded disease onset and relapse.4,22,24,25,26


The normal hair cycle has four distinct phases: anagen, catagen, telogen and exogen (Figure 1). AA is characterized by abnormal hair cycling: T lymphocytes attack anagen hair follicles, which are subsequently maintained in a dystrophic state. Such dystrophy precludes hair production of appropriate integrity or size, and the shaft can no longer be firmly anchored in the hair canal, resulting in rapid hair shedding.1,8 Other perturbations in the hair cycle are seen: the follicle can be prematurely ushered into telogen and then proceed in a shortened cycle in which it is repeatedly arrested in early anagen.22 In chronic AA, follicles can persist in a prolonged telogen phase without cycling back to the anagen growth phase.1,2 Unlike scarring alopecias, the hair follicle stems cells are not destroyed in AA. Rather, the follicles are effectively switched off: they remain arrested in a hibernation-like state and can resume normal growth after a period of months to years.2,8
The pathophysiology of this process is not fully elucidated, but available evidence suggests a T cell-mediated autoimmune process directed at the hair follicle.1,8,10,15 Normally, the hair follicle creates a milieu of immunologic privilege, ie, it is protected from immune surveillance by autoreactive T cells. Failure of this immune privilege and development of autoantibodies against a hair follicle antigen is theorized in the pathogenesis of AA (Figure 2). However, the antigens responsible for initiating this autoimmune reaction remain unidentified.7,8,17