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Bullous pemphigoid induced by dipeptidyl peptidase‐4 inhibitors. Eight cases with clinical and immunological characterization
Author(s) -
GarcíaDíez Irene,
IvarsLleó Marta,
LópezAventín Daniel,
Ishii Norito,
Hashimoto Takashi,
Iranzo Pilar,
Pujol Ramon M.,
España Agustín,
HerreroGonzalez Josep E.
Publication year - 2018
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1111/ijd.14005
Subject(s) - bullous pemphigoid , medicine , pemphigoid , vildagliptin , linagliptin , immunology , antibody , endocrinology , diabetes mellitus , type 2 diabetes mellitus , metformin , insulin
Abstract Background Dipeptidyl peptidase‐4 (DPP‐4) inhibitors have increasingly been identified as causative agents of bullous pemphigoid. The clinical and immunological characteristics of this pemphigoid variant are still unclear. The objective of our study was to analyze the clinical and immunological features of patients with pemphigoid induced by DPP‐4 inhibitors. Methods All patients diagnosed with DPP‐4 inhibitor‐associated bullous pemphigoid at dermatology departments in three Spanish centers during the period 2013 to 2015 were included. ELISA assays for the NC16A domain of BP180 and BP230 were performed. Immunoblot studies using epidermal/dermal extracts and the C‐terminal, NC16A and LAD‐1 regions of BP180 were also carried out. Results A total of eight patients were identified (5 treated with vildagliptin, 2 with linagliptin, and one with sitagliptin). Of these, four presented the classical inflammatory phenotype of bullous pemphigoid and four a noninflammatory phenotype. The ELISA for BP180 (NC16A domain) was positive in six patients at diagnosis. Most patients reacted to more than one BP180 antigenic site (LAD‐1 and/or C‐terminal domain) on the immunoblot. Two patients showed no reaction against the NC16A domain of BP180 on either the ELISA or immunoblot but recognized either LAD‐1 or both LAD‐1 and the C‐terminal domain. Only one of the NC16A‐negative patients had a noninflammatory subtype of bullous pemphigoid. Conclusions Patients with DPP‐4 inhibitor‐induced BP may present either an inflammatory or a noninflammatory phenotype of BP. IgG response against other BP180 regions different from the NC16A domain, such as LAD‐1 and the C‐terminal domain, could be pathogenically relevant to the onset of DPP‐4 inhibitor‐induced BP.