British Association of Dermatologists' Guidelines for the Management of Alopecia Areata 2012

A.G. Messenger; J. McKillop; P. Farrant; A.J. McDonagh; M. Sladden


The British Journal of Dermatology. 2012;166(5):916-926. 

In This Article

6.0 Background

Alopecia areata is a chronic inflammatory disease that affects the hair follicle and sometimes the nail. 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.

6.1 Prognosis

Hair follicles are preserved in alopecia areata and the potential for recovery of hair growth is maintained, even in longstanding disease. 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] Data from secondary and tertiary referral centres are less favourable indicating that 34–50% of patients will recover within 1 year. 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%).[4,5] Disease severity at presentation is the strongest predictor of long-term outcome. In an Italian study, 191 patients with alopecia areata who presented to a university dermatology clinic between 1983 and 1990 were contacted by telephone in 2005 to give self-reports of their clinical status.[6] Patients with less severe disease at presentation were more likely to report being free of disease at follow-up (68% with less than 25% hair loss initially; 32% with 25–50% hair loss initially; 8% with more than 50% hair loss initially). Patients with more severe disease initially were also more likely to report worsening patterns of alopecia such as AT and AU.

The prognosis is also less favourable when onset occurs during childhood[4,7–9] and in ophiasis.[9] The concurrence of atopic disease has been reported to be associated with a poor prognosis[3,9] but this has been disputed.[10]

6.2 Aetiology

About 20% of people with alopecia areata have a family history of the disease indicating a genetic predisposition.[11] Associations have been reported with a variety of genes, including major histocompatibility complex (MHC) and cytokine genes, suggesting that the genetic predisposition is multifactorial in nature. A genome-wide association study confirmed the link with the MHC genes and also identified associations with other genes involved in regulating immune and inflammatory responses, and with some genes expressed in the hair follicle.[12] The hair follicle lesion is probably mediated by T lymphocytes.[13] The association between alopecia areata and other autoimmune diseases suggests that alopecia areata is itself an autoimmune disease although this is unproven. It has been proposed that the hair follicle is an immunologically 'privileged tissue' which is sheltered from immune surveillance by autoreactive T cells, and that failure of such immune privilege plays a key role in the pathogenesis of alopecia areata.[14,15]


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as: