The regrowing hairs are often white at first and get darker with time. Obviously, melanocytes are affected by the inflammation and need time to recover. This is in line with the observation that pigmented hairs are more susceptible targets than white hairs. The reported overnight greying of hair in adults is the result of acute diffuse AA, which affects only pigmented hair while the white hairs are spared. This clinical and histological finding supports the hypothesis of melanocyte- and anagen-associated autoantigens as key players in the pathogenesis of AA [23]. However, because non-pigmented hair loss in AA is also reported, pigmented hair seems to be more susceptible but not exclusively affected.

Nail involvement is another feature of AA. Typical signs for AA are small pits, leukonycia punctata and vertical or longitudinal ridging. In severe forms, all 20 nails can be dystrophic. Nail involvement can precede or follow AA and often occurs in more widespread and recurring forms of AA.

The course of AA is unpredictable. Acute hair loss is often followed by spontaneous hair regrowth. As soon as one patch is gone another can appear. The hair loss can persist for many years or life. Alopecia areata is not scarring, hair follicles are usually preserved and hair can regrow even after many years. The prognosis depends on several factors (Box 149.1). Unfavourable prognostic factors include the early onset of disease, positive family history, atopic dermatitis and extensive trachyonychia.

Histological Features.

The typical characteristics of early AA are an increased number of catagen and telogen hair follicles. Around the lower hair follicle (peribulbar) an inflammatory lymphocytic infiltrate can be seen, which appears like a ‘swarm of bees’. CD4⁺ T cells predominate in the infiltrate around the hair bulb, while CD8⁺ T cells reside within the hair follicles. The bulge region containing the hair follicle stem cells in the upper region of the hair follicle is spared. This is the reason why AA is not scarring and hair follicles can even after years potentially regrow.

The infiltrate is mostly seen in terminal hair follicles reaching deep into the subcutaneous tissue. Affected anagen hair follicles rapidly enter telogen phase, the reason for sudden hair shedding. Afterwards follicles re-enter the next hair cycle but the lymphocytic infiltrate, which is still present, interrupts the anagen phase. Especially in repeated episodes of AA, miniaturization of the hair follicle occurs [24]. In long-standing AA, the lymphocytic infiltrate can be variable and mostly miniaturized hair follicles are seen.

Differential Diagnosis.

In children, the most common differential diagnosis is tinea capitis, which often appears as isolated patchy hair loss of the scalp but here the skin typically shows scalding and signs of inflammation in contrast to AA. Also important to keep in mind is trichotillomania in children. Trichotillomania is the mechanical pulling of hair shafts, which can be a habituation or a sign of psyochosomatic disorder. In trichotillomania, very short regrowing hair within the lesion can often be observed yielding a pattern in which hairs of multiple different lengths are seen and unusual or bizarre patterns that do not correlate with underlying anatomical or mosaic configurations. Traction alopecia is another differential diagnosis. Some types of hair styling using much pressure can be the reason for permanent patchy hair loss.

Associations.

Alopecia areata is associated with autoimmune diseases such as Hashimoto’s thyroiditis, diabetes mellitus, rheumatoid arthritis, pernicious anaemia, lupus erythematosus, myasthenia gravis, lichen planus, coeliac disease and vitiligo. The prevalence of an autoimmune disease in patients with AA is 16%. Thyroid disease and vitiligo have the strongest relationship to AA. Atopic diseases such as asthma, atopic dermatitis and hay fever have been reported in 10–60% of patients [25,26]. A strong association with AA has also been observed in patients with Down syndrome (10%).

Treatment.

The treatment of AA is difficult and often frustrating – in small children even more than in adults. Immunosuppressive or immunomodulating agents have been used and are variably effective in the treatment of AA, but there are still no definitive options to cure the disease or prevent relapses. Because of the high rate of spontaneous remission (25%), it is quite difficult to attribute successful regrowth to a particular treatment. In addition, there is an urgent need for double-blind placebo-controlled studies enrolling patients with extensive AA, AAT and AAU.

In general, it is reasonable to choose the treatment depending on the extent and duration of alopecia and age of the child. While limited lesions of AA respond favourably to a variety of treatments, long-standing AAT and AAU as well as association with atopy, early onset and nail symptoms are less responsive and difficult to treat (Table 149.1). Corticosteroids exert a potent anti-inflammatory effect and several ways of administration have been used: intralesional, topical and systemic. Therapeutic agents that have shown to be ineffective in the treatment of AA are listed in Table 149.2.

Table 149.1 Treatment options for alopecia areata in children

*Only in rare cases with rapid recent onset of hair loss, only three courses.

Table 149.2 Treatments without efficacy

Topical Corticosteroids

Intralesional corticosteroids (e.g. triamcinolone acetonide) have been used for treatment of AA for the past five decades in adults and several studies have reported successful regrowth at the site of injection although placebo-controlled studies are lacking. In children, intralesional corticosteroid injection into the scalp has been described [22]. Eighty per cent of the children treated with intralesional corticosteroids in limited AA showed an improvement of >50%. However, skin atrophy is a possible side-effect, and intralesional injection is painful and therefore not generally suitable for children under the age of 12 years.

Topically applied corticosteroids are very popular in the treatment of limited AA but there exist only two placebo-controlled studies using 0.05% clobetasol ointment with or without occlusion in adults. In multifocal AA, 0.05% clobetasol foam was effective in 30%, while AAT and AAU did not respond. Using occlusion, 17% of patients with AAU and AAT responded to the treatment [27,28]. Considering the difficulty of treating AAU and AAT at all, this is a good result. Another study reported that betamethasone valerate foam was an effective and well-tolerated treatment of mild-to-moderate AA [29]. In children, the risk of skin atrophy is higher than in adults and continuous uninterrupted treatment with a class IV corticosteroid for 6 months cannot be recommended. Therefore, further placebo-controlled studies with corticosteroids class II and III are needed.

Systemic Corticosteroids

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