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This affects about 2% of the patients seen at our skin clinics.
An immunological basis is suspected because of an association with thyroid disease, vitiligo and atopy.
Histologically, T lymphocytes cluster like a swarm of bees around affected hair bulbs, having been attracted and made to divide by cytokines from the dermal papilla. Alopecia areata is probably inherited as a complex genetic trait, with an increased occurrence in the first-degree relatives of affected subjects and twin concordance. The existence of trigger factors, such as stress, fits with this idea.
A typical patch is uninflamed, with no scaling, but with easily seen empty hair follicles (Fig. 13.4). Pathog-nomonic ‘exclamation-mark’ hairs may be seen around the edge of enlarging areas. They are broken off about 4 mm from the scalp, and are narrowed and less pigmented proximally (Figs 13.5 and 13.6). Patches are most common in the scalp and beard but other areas, especially the eyelashes and eyebrows, can be affected too. An uncommon diffuse pattern is recognized, with exclamation-mark hairs scattered widely over a dif-fusely thinned scalp. Up to 50% of patients show fine pitting or wrinkling of the nails.
The outcome is unpredictable. In a first attack, regrowth is usual within a few months.
New hairs appear in the centre of patches as fine pale down, and gradually regain their normal thickness and colour, although the new hair may remain white in older pati-ents. Subsequent episodes tend to be more extensive and regrowth is slower. Hair loss in some areas may coexist with regrowth in others. A few patients lose all the hair from their heads (alopecia totalis) or from the whole skin surface (alopecia universalis).
Regrowth is tiresomely erratic but the following suggest a poor prognosis.
1 Onset before puberty.
2 Association with atopy or Down’s syndrome.
3 Unusually widespread alopecia.
of the scalp margin (ophiasiform type), especially at the nape of the neck.
Patches are not scaly, in contrast to ringworm, and are usually uninflamed, in contrast to lupus erythematosus and lichen planus. In the hair-pulling habit of children, and in traction alopecia, broken hairs may be seen but true exclamation-mark hairs are absent. Secondary syphilis can also cause a ‘moth-eaten’ patchy hair loss.
None are usually needed. Syphilis can be excluded with serological tests if necessary. Organ-specific auto-antibody screens provide interesting information but do not affect management.
A patient with a first or minor attack can be reassured about the prospects for regrowth. Tranquillizers may be helpful at the start. The use of systemic steroids should be avoided in most cases, but the intradermal injection of 0.2 mL of intralesional triamcinolone acetonide (10 mg /mL), raising a small bleb within an affected patch, leads to localized tufts of regrowth (Fig. 13.7) while not affecting the overall outcome. This may be useful to re-establish eyebrows or to stimulate hope. Spirit-based steroid lotions and mild irritants, such as 0.1–0.25% dithranol, are often used but with limited success.
Ultraviolet radiation or even psoralen with ultraviolet A (PUVA) therapy may help extens-ive cases, but hair fall often returns when treatment stops. Contact sensitizers (e.g. diphencyprone) seemed promising (Figs 13.8) but the long-term effect of per-sistent antigen stimulation is worrying; they are still being used only in a few centres under trial conditions. The efficacy of topical immunosuppressive agents (e.g. tacrolimus) has yet to be proved in a randomized clinical trial. Wigs are necessary for extensive cases.
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