Alopecia and hair disorders in children — structured clinical encounter

Station 1 — recognition and confirmation

Asked for my first impression, I would recognise this as alopecia areata. The completely smooth, non-scaly bald patch with exclamation-mark hairs at the edge is the signature of an autoimmune attack on the anagen hair bulb. I would confirm the pattern with dermoscopy, expecting yellow dots, black dots and short regrowing vellus hairs, and the absence of scale, broken stubs and lymphadenopathy would distinguish it from tinea capitis at the bedside. [1]

Station 2 — the autoimmune association and screening

Asked about associations and screening, I would state that the key association is with other autoimmune disease, most importantly autoimmune thyroid disease, and that I would screen thyroid function, with thyroid antibodies where clinically indicated. I would ask about vitiligo and type 1 diabetes, take a family history of autoimmune disease, and note the increased prevalence in Down syndrome. These associations are why thyroid screening is built into the work-up even when the child is clinically well. [4]

Station 3 — the stepwise management

Asked how I would manage limited patchy disease, I would start a potent or ultrapotent topical corticosteroid, with or without topical minoxidil five per cent. For a few discrete patches I would use intralesional triamcinolone acetonide at around five to ten milligrams per millilitre in small volumes per site, repeated every four to six weeks. I would escalate to topical immunotherapy with diphenylcyclopropenone or squaric acid dibutylester for extensive or active disease, add a short oral corticosteroid course to halt rapid shedding, and reserve systemic therapy, oral minoxidil and JAK inhibitors for refractory disease under dermatology guidance. [1] [2]

Station 4 — setting prognostic expectations

Asked which features predict a worse outcome, I would name the ophiasis pattern, the totalis and universalis patterns, and the features of atopy, early childhood onset, nail involvement, long duration before treatment, extensive involvement and a family history. I would set honest expectations with the family, explaining that limited patchy disease has a good prognosis with a high rate of regrowth but that relapse is common enough to warrant clear follow-up planning. [4]

Station 5 — the pivot to trichotillomania and the tinea trap

Finally I describe how I would handle a twelve-year-old with an irregular patch over the crown, hairs broken to wildly varying lengths and a completely normal scalp, who denies pulling. I would recognise this as trichotillomania, a body-focused repetitive behaviour, distinguished from alopecia areata by the varying hair lengths on a normal scalp and the absence of exclamation-mark hairs. First-line management is habit-reversal and cognitive behavioural therapy, with pharmacotherapy only as an adjunct given the modest evidence in the Cochrane review. I would ask about hair eating because of the trichobezoar risk. And asked about a scaly bald patch with broken stubs, black dots and lymphadenopathy, I would diagnose tinea capitis, confirm it with potassium hydroxide microscopy, and warn against the trap of treating it as alopecia areata with a topical steroid, which causes tinea incognito, because tinea capitis always needs an oral antifungal. [8] [9] [12]