To study the effect of fexofenadine on extensive alopecia areata (AA), we evaluated retrospectively 121 patients with AA having alopecia in more than 50% of the scalp and followed them for at least 6 months. Patients were treated by immunotherapy using diphenylcyclopropenone or squaric acid dibutylester with or without oral fexofenadine. The regrowth score was estimated as decrease of Severity of Alopecia Tool (SALT) score. In AA with atopic background (atopic AA), the mean regrowth score of the fexofenadine group was 1.333 (n = 33) and that of the control 0.471 (n = 34). The fexofenadine group showed significantly better regrowth than control by Mann-Whitney's U-test (P = 0.00213). In non-atopic AA, the mean regrowth score of the fexofenadine group was 1.303 (n = 33) and that of the control 1.048 (n = 21). There was no significant difference by Mann-Whitney's U-test (P = 0.872). Together, fexofenadine is a helpful reagent in the treatment extensive atopic AA with contact immunotherapy.

Pigmentary complication by contact immunotherapy (CI) for alopecia areata (AA) has been reported but its pathophysiology remains unknown. To characterize pigmentary complication by CI and its pathophysiology, we examined the incidence of hyperpigmentation in 186 consecutive patients treated with CI using diphenylcyclopropenone. From clinical data of AA totalis (AAT) or universalis (AAU) patients (n = 78), we studied the correlations between this complication and age, sex, atopic background, duration and treatment responsiveness, duration of CI, final concentration of diphenylcyclopropenone and administration of anti-histamines by χ(2)-test or Mann-Whitney U-test. Additionally, the histopathology of pigmentation was studied. As a result, 11 (5.91%) of the 186 patients had hyperpigmentation in this series. All of them had AAT or AAU, suggesting that the pigmentation is apt to occur in severe AA. When the AAT or AAU patients with (n = 11) and without hyperpigmentation (n = 67) were compared, those with pigmentation showed poorer responsiveness to CI (P < 0.05) but no significant tendency for other factors. Histopathologically, skin specimens showed lichenoid or vacuolar interface dermatitis with necrotic keratinocytes and dermal melanophages, consistent with pigmented contact dermatitis (PCD). Together, pigmentary complication by CI corresponds to PCD from therapeutic sensitizer, representing clinical indicator of poor responsiveness.