https://orcid.org/0000-0001-6356-7192
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Y. Mai, W. Nishie, K. Izumi, N. Yoshimoto, Y. Morita, M. Watanabe, E. Toyonaga, H. Ujiie, H. Iwata, Y. Fujita, T. Nomura, K.C. Sato‐Matsumura, S. Shimizu, H. Shimizu, Detection of anti‐BP180 NC16A autoantibodies after the onset of dipeptidyl peptidase‐IV inhibitor‐associated bullous pemphigoid: a report of three patients, British Journal of Dermatology, Volume 179, Issue 3, 1 September 2018, Pages 790–791, https://doi.org/10.1111/bjd.16656
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Funding sources: no external funding.
Conflicts of interest: none declared.
Dear Editor, Bullous pemphigoid (BP) is a common autoimmune blistering disorder in which autoantibodies (autoAbs) target two hemidesmosomal components (BP180/collagen XVII and BP230) in basal keratinocytes,1 and 80–90% of patients with BP have autoAbs targeting the juxtamembranous extracellular NC16A domain of BP180 (anti‐BP180 NC16A autoAbs).1 Recently, increasing numbers of patients with BP associated with the administration of dipeptidyl peptidase‐IV inhibitors (DPP4i) for the treatment of type 2 diabetes have been reported,2,3,4 although the association remains controversial.5 Our recent reports suggested that DPP4i‐associated BP (DPP4i‐BP) tends to show a ‘noninflammatory’ phenotype characterized by no or mild erythema, and these patients with DPP4i‐BP have autoAbs that preferentially target the mid‐portion of the extracellular domain of BP180 but not the NC16A domain.6,7 However, Fania et al.4 reported five cases of DPP4i‐BP that shared overlapping features of classical BP, including the presence of anti‐BP180 NC16A autoAbs and the inflammatory phenotype. It is uncertain whether anti‐BP180 NC16A autoAbs may develop during the course of DPP4i‐BP in those patients in whom anti‐BP180 NC16A autoAbs were initially undetectable. In this report, we present three patients with DPP4i‐BP in whom anti‐BP180 NC16A autoAbs were initially undetectable but became positive during the course of BP.
