Serum levels of anti-type VII collagen antibodies detected by enzyme-linked immunosorbent assay in patients with epidermolysis bullosa acquisita are correlated with the severity of skin lesions

Background  Epidermolysis bullosa acquisita (EBA) is a chronic autoimmune subepidermal bullous disease characterized by circulating autoantibodies against type VII collagen. Detecting these autoantibodies is crucial for the diagnosis of this disease, and is also useful for measuring disease activity...

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Veröffentlicht in:Journal of the European Academy of Dermatology and Venereology 2013-02, Vol.27 (2), p.e224-e230
Hauptverfasser: Kim, J.H., Kim, Y.H., Kim, S., Noh, E.B., Kim, S-E., Vorobyev, A., Schmidt, E., Zillikens, D., Kim, S-C.
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Sprache:eng
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Zusammenfassung:Background  Epidermolysis bullosa acquisita (EBA) is a chronic autoimmune subepidermal bullous disease characterized by circulating autoantibodies against type VII collagen. Detecting these autoantibodies is crucial for the diagnosis of this disease, and is also useful for measuring disease activity. Enzyme‐linked immunosorbent assay (ELISA), a quantitative method to measure anti‐type VII collagen antibody levels, is currently available to diagnose EBA. Objective  The aim of this study was to investigate the relationship of ELISA with overall clinical severity. Methods  Sera from patients with EBA (n = 30), bullous pemphigoid (n = 20), anti‐laminin γ1 pemphigoid (n = 9) and healthy donors (n = 24) were tested using ELISA, using the recombinant non‐collagenous 1 (NC1) and 2 (NC2) domains of type VII collagen. Relationships between clinical characteristics, indirect immunofluoroscence (IIF) titres and ELISA values were investigated. Results  The sensitivity and specificity of the EBA ELISA were 96.7% and 98.1%, respectively. There was no significant difference between ELISA results for classic and inflammatory types. The severity of skin involvement was positively correlated with both ELISA value (r = 0.87, P 
ISSN:0926-9959
1468-3083
DOI:10.1111/j.1468-3083.2012.04617.x