Abstract
Recently, several cases of bullous pemphigoid (BP) associated with the use of a dipeptidyl peptidase-4 (DPP-4) inhibitor, a type of antihyperglycemic drug, have been reported (DPP4i-BP).1,2 Béné reported a strong association between DPP-4 inhibitor use and the risk of BP.3 The juxtamembranous extracellular non-collagenous 16a (NC16a) domain of type XVII collagen (COL17, also termed BP180) is a major target epitope of autoantibodies in BP.4 A recent study found that BP cases whose autoantibodies bound to BP180 at regions other than NC16a exhibited a non-inflammatory phenotype with fewer erythemas. Intriguingly, half of these cases had taken DPP-4 inhibitors at the time of development of BP.5 In this study, we explored whether DPP4i-BP exhibited any unique clinical and serological features as suggested by the previous study.
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