Background: Few data are available concerning the efficiency of pulse corticosteroids in alopecia areata (AA). Objective: Our purpose was to assess the long-term outcomes of patients treated with methylprednisolone bolus. Methods: This study included 60 patients treated between 1995 and 2000. The short-term outcomes were analyzed in 2000. The long-term assessment of 30 patients was performed in 2010 by phone questionnaire. Results: Significant hair regrowth was observed in 10/30 patients at 6 months after the bolus treatment. Half of the plurifocalis AA patients were responders at 6 months, but less than one quarter of alopecia totalis (AT) and alopecia universalis (AU) patients responded. Long-term outcomes were assessed after a mean duration of 12.3 years; 8/10 initial responders had mild or no disease, and 14/20 initial nonresponders had severe AA. Conclusions: This study confirmed the low efficiency, both short- and long-term, of this treatment for AT and AU.

To report three cases of bullous pemphigoid in patients treated with vildagliptin. Case 1: An 86-year-old woman presented with bullous pemphigoid after 1 month of treatment with vildagliptin and metformin. After introduction of clobetasol, the symptoms resolved although vildagliptin was continued. However, the skin lesions reappeared 3 months later. Sustained remission was achieved only after definitive withdrawal of vildagliptin. Case 2: A 79-year-old man presented with bullous pemphigoid after 37-month treatment with gliclazide, vildagliptin and metformin. The disease at first responded to clobetasol but 3 months later the lesions reappeared. They finally regressed when the gliptin was discontinued. Case 3: A 77-year-old woman, treated with gliclazide and vildagliptin for 26 months, presented with bullous pemphigoid, which responded well to discontinuation of the gliptin and topical clobetasol. Gliptins are new molecules for treatment of type 2 diabetes mellitus, which have been suspected of implication in bullous pemphigoid. Such cases have been described in the literature (seven with vildagliptin and three with sitagliptin). In nine of these cases, the gliptin was associated with metformin, but the latter had never been considered responsible. The mechanism implicated in the development of bullous pemphigoid has not yet been clearly identified, but may involve a modified immune response or alteration of the antigenic properties of the epidermal basement membrane. These reports support the risk of bullous pemphigoid in patients exposed to gliptins.

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