Premium
A case of vancomycin‐associated linear I g A bullous dermatosis and I g A antibodies to the α3 subunit of laminin‐332
Author(s) -
Zenke Y.,
Nakano T.,
Eto H.,
Koga H.,
Hashimoto T.
Publication year - 2014
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/bjd.12720
Subject(s) - laminin , antibody , protein subunit , vancomycin , medicine , immunoglobulin a , immunology , secretory iga , microbiology and biotechnology , immunoglobulin g , biology , bacteria , staphylococcus aureus , biochemistry , gene , genetics , cell
Summary Linear I g A bullous dermatosis ( LABD ) is a rare autoimmune bullous disease, which is defined by the histopathological finding of subepidermal vesicles with neutrophilic infiltration and linear I g A deposits in the basement membrane zone, revealed by immunofluorescence study. We present a case of LABD in which vancomycin ( VCM ) administration triggered LABD , and immunoblot analysis showed I g A antibodies reactive to the 145‐ and 165‐kDa α3 subunits of laminin‐332. This is the first report of VCM ‐associated LABD in which the target antigen was laminin‐332. In the present case, we were compelled to continue administration of VCM along with systemic steroids, which eventually led to the attenuation of the symptoms, normalization of the serum I g A level, and negative results on both indirect immunofluorescence of 1 mol L −1 N a C l‐split skin and immunoblot analysis.