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Clinical manifestations and diagnosis of alopecia areata

Andrew G Messenger, MD, FRCP
Section Editors
Robert P Dellavalle, MD, PhD, MSPH
Maria Hordinsky, MD
Deputy Editor
Abena O Ofori, MD


Alopecia areata is a chronic immune-mediated disorder that targets anagen hair follicles and causes nonscarring hair loss. The condition most commonly presents with discrete patches of alopecia on the scalp. Other hair-bearing areas may also be affected. In severe cases, patients may experience loss of all scalp or body hair.

The clinical manifestations and diagnosis of alopecia areata will be discussed here. The therapeutic management of alopecia areata and information on other types of nonscarring hair loss are reviewed separately. (See "Management of alopecia areata" and "Evaluation and diagnosis of hair loss", section on 'Nonscarring alopecia'.)


The estimated prevalence of alopecia areata is approximately 1 in 1000 people, with a lifetime risk of approximately 2 percent [1,2]. For most patients the onset is before age 30; however, the disorder may occur at any age [2]. Men and women are equally affected.


T-cell mediated peribulbar inflammation leading to disruption of the normal hair cycle has been implicated in the pathogenesis of alopecia areata [3]. Unlike cicatricial alopecias (eg, lichen planopilaris or discoid lupus), the inflammatory process in alopecia areata does not lead to scarring and destruction of the hair follicle. (See 'Cicatricial alopecia' below.)

Disruption of the hair cycle — Hair follicles in normal skin cycle through periods of active hair growth (anagen), follicular involution (catagen), and follicular rest (telogen) (figure 1). In alopecia areata, peribulbar inflammation is associated with dystrophic changes in anagen follicles and stimulates premature transition of anagen follicles to the nonproliferative catagen and telogen phases [3-5]. (See "Evaluation and diagnosis of hair loss", section on 'Hair cycle'.)


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Literature review current through: Sep 2016. | This topic last updated: Jan 16, 2015.
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