Abstract

Bullous pemphigoid (BP) is an uncommon chronic, autoimmune, and subepidermal disease (1). Tense blisters occur over normal or erythematous skin. (1) BP may be localized or generalized. It may involve both skin of extremities and trunk and mucosa. Pruritus may precede bullae formation by weeks or months. It can be associated with drugs, UV irradiation, and X-ray therapy (1). There is a number of reports on bullous pemphigoid (BP) induced by DPP-IV inhibitors (vildagliptin, sitagliptin) used for treatment of type 2 DM (2-6). Although skin lesions were not observed at an increased incidence in clinical trials, there have been post-marketing reports of bullous and exfoliative skin lesions. The enzyme dipeptidyl peptidase (DPP-IV) degrades glucagon like peptide 1 (GLP-1), which is a potent stimulator of insulin production and secretion (7). DPP-IV is expressed by diverse tissues including skin (7). In the skin, many cell types (including keratinocytes) express DPP-4, giving rise to cytokine production, tissue differentiation and collagen metabolism (7). Some factors Bullous pemphigoid (BP) is an uncommon chronic, autoimmune, and subepidermal disease. Tense blisters occur over normal or erythematous skin. It can be associated with drugs. There is a number of reports on bullous pemphigoid (BP) induced by DPP-IV inhibitors (vildagliptin, sitagliptin, saxagliptin). DPP-IV (CD26), present as a cell surface molecule on immune cells, also plays an important costimulatory role in immune activation. We present a case of BP induced by vildagliptin. A 59 yr old male patient who was diagnosed type 2 DM had initial haemoglobin A1c level of 12.90%. Initial therapy with premix biphasic aspart insulin bid was switched to metformin and vildagliptin 50/1000 mg combo pill bid after A1c level dropped to 5.7% at 9 months of insulin therapy, Five months after vildagliptin was started, tense vesicles 8-10 in number with an erythematous base developed over forearms and cruris. Histologic examination of the lesions confirmed bullous pemphigoid. Oral antidiabetics were discontinued. He was followed up with diet alone. The lesions regressed spontaneously after cessation of antidiabetics and clobetasol propionate cream bid treatment. A1c was 5.7% 5 months after discontinuation of vildagliptin and metformin. In the literature onset of BP lesions took 10 days to 2 years. Mostly the patients were on combo therapy with metformin. The lesions improved dramatically after cessation DPP-IV inhibitors avoiding necessity for systemic treatment for BP. Elder males predominate. This is the first case of BP induced by DPP-IV inhibitors Turkey.

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