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Sleep quality in patients with alopecia areata: questionnaire‐based study

rapid progression and was given four monthly courses of 500 mg methylprednisolone pulse therapy administered intravenously. No clinical improvement was observed during the first two months of treatment, and persistent hair loss led to complete balding of the scalp (Fig. 1b). In month 3 after the start of steroid pulse therapy, regrowth of thin and depigmented hair was noted (Fig. 1c). Hair continued to grow without pigmentary recovery. Currently, at four years since the regrowth of hair was first noted, the patient’s hair is fully regrown and remains depigmented (Fig. 1d). The hair follicle melanocyte has been proposed as a target of autoimmunity in the pathogenesis of alopecia areata, and this hypothesis has been supported by a common clinical observation of the sparing of pre-existing non-pigmented hair follicles in the process of alopecia areata. It is also not uncommon to see white regrown hair focally in the initial recovery stage of alopecia areata. This phenomenon may be explained by the delayed recovery of the disrupted melanocytes in the hair follicles; the hair generally resumes its pigmented appearance shortly afterwards, usually within one anagen phase. Longterm persistent or permanent depigmentation of the hair shaft following recovery from alopecia areata has rarely been reported. Focal non-pigmented hair sustained for seven years was observed in a 17-year-old girl with a solitary patch of alopecia areata. Diffuse regrowth of nonpigmented hair sustained for six months was reported in a 62-year-old woman with diffuse alopecia areata. Our current patient’s presentation is unique in that it demonstrates long-lasting and near-complete hair depigmentation, which suggests that the autoimmune process of alopecia areata caused severe damage to the hair follicle melanocytes, possibly damaging the melanocyte stem cells that reside in the bulge area of hair follicles.