Guidelines for the Management of Alopecia Areata

S.P. MacDonald Hull; M.L. Wood; P.E. Hutchinson; M. Sladden; A.G. Messenger

Disclosures

The British Journal of Dermatology. 2003;149(4) 

In This Article

Summary and Introduction

These guidelines for management of alopecia areata have been prepared for dermatologists on behalf of the British Association of Dermatologists. They present evidence-based guidance for treatment, with identification of the strength of evidence available at the time of preparation of the guidelines, and a brief overview of epidemiological aspects, diagnosis and investigation.

Alopecia areata is a chronic inflammatory disease which affects the hair follicles and sometimes the nails. The onset may be at any age and there is no known race or sex preponderance. Alopecia areata usually presents as patches of hair loss on the scalp but any hair-bearing skin can be involved. The affected skin may be slightly reddened but otherwise appears normal. Short broken hairs (exclamation mark hairs) are frequently seen around the margins of expanding patches of alopecia areata. The nails are involved in about 10% of patients referred for specialist advice. Data from secondary and tertiary referral centres indicate that 34-50% of patients will recover within 1 year, although almost all will experience more than one episode of the disease, and 14-25% progress to total loss of scalp hair (alopecia totalis, AT) or loss of the entire scalp and body hair (alopecia universalis, AU), from which full recovery is unusual (< 10%).[1,2] One study from Japan reported that spontaneous remission within 1 year occurred in 80% of patients with a small number of circumscribed patches of hair loss.[3] The prognosis is less favourable when onset occurs during childhood[1,4,5,6] and in ophiasis[6] (alopecia areata of the scalp margin). The concurrence of atopic disease has been reported to be associated with a poor prognosis[3,6] but this has been disputed.[7]

About 20% of people with alopecia areata have a family history of the disease, indicating a genetic predisposition.[8] Associations have been reported with a variety of genes, including major histocompatibility complex, cytokine and immunoglobulin genes, suggesting that the genetic predisposition is multifactorial in nature. The hair follicle lesion is probably mediated by T lymphocytes.[9] The association between alopecia areata and other autoimmune diseases suggests that alopecia areata is itself an autoimmune disease, although this is unproven.

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