Clinical manifestations and diagnosis of alopecia areata
- Andrew G Messenger, MD, FRCP
Andrew G Messenger, MD, FRCP
- Professor of Dermatology
- University of Sheffield
- Section Editors
- Robert P Dellavalle, MD, PhD, MSPH
Robert P Dellavalle, MD, PhD, MSPH
- Section Editor — General Dermatology
- Professor of Dermatology and Public Health
- University of Colorado School of Medicine
- Colorado School of Public Health
- Chief, Dermatology Service
- US Department of Veterans Affairs
- Eastern Colorado Health Care System
- Maria Hordinsky, MD
Maria Hordinsky, MD
- Section Editor — Hair and Scalp Disease
- Chair and Professor - Department of Dermatology
- University of Minnesota Medical School
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 . 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 . 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'.)To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- Disruption of the hair cycle
- Genetic background
- CLINICAL FEATURES
- Nail abnormalities
- Associated diseases
- Course of disease
- Laboratory studies
- DIFFERENTIAL DIAGNOSIS
- Tinea capitis
- Nervous hair pulling (trichotillomania)
- Cicatricial alopecia
- Androgenetic alopecia
- Secondary syphilis
- Telogen effluvium
- Triangular alopecia
- INFORMATION FOR PATIENTS
- SUMMARY AND RECOMMENDATIONS