Funding sources This work was supported by a grant of the National Center of Science, Poland (no. N N402 661940) and a grant of the Medical University of Warsaw, Poland (no. 1WY/NK1W/2009).
Fluorescence overlay antigen mapping using laser scanning confocal microscopy differentiates linear IgA bullous dermatosis from epidermolysis bullosa acquisita mediated by IgA
Article first published online: 28 FEB 2013
© 2012 The Authors. BJD © 2012 British Association of Dermatologists
British Journal of Dermatology
Volume 168, Issue 3, pages 634–638, March 2013
How to Cite
Wozniak, K., Hashimoto, T., Ishii, N., Koga, H., Huczek, M. and Kowalewski, C. (2013), Fluorescence overlay antigen mapping using laser scanning confocal microscopy differentiates linear IgA bullous dermatosis from epidermolysis bullosa acquisita mediated by IgA. British Journal of Dermatology, 168: 634–638. doi: 10.1111/bjd.12017
Conflicts of interest None declared.
- Issue published online: 28 FEB 2013
- Article first published online: 28 FEB 2013
- Accepted manuscript online: 27 AUG 2012 10:20AM EST
- Accepted for publication 17 August 2012
Background Linear IgA bullous dermatosis (LABD) and epidermolysis bullosa acquisita (EBA) mediated by IgA antibodies belong to the group of autoimmune subepidermal bullous diseases mediated by IgA autoantibodies. Early and correct diagnosis is crucial because the management and prognosis of the diseases are different.
Objectives To determine whether fluorescence overlay antigen mapping using laser scanning confocal microscopy (FOAM-LSCM) is helpful in the differentiation between these diseases.
Methods FOAM-LSCM and immunoblot studies were performed in 19 patients with disseminated tense blisters who presented with in vivo bound and circulating IgA antibasement membrane zone (BMZ) antibodies on immunofluorescence.
Results Using FOAM-LSCM, in vivo bound IgA above type IV collagen, which is characteristic for LABD, was seen in 14 of the 19 cases, whereas five of the 19 cases had IgA deposits below type IV collagen, typical for EBA. Immunoblot studies showed that IgA antibodies in 11 of the 14 patients with deposits above type IV collagen reacted with different epitopes on BP180, mainly with LAD-1, which is a target antigen in LABD. Among the five patients with deposits below type IV collagen, one showed IgA antibodies to the 200-kDa laminin γ-1 and one had antibodies to the 290-kDa type VII collagen, EBA antigen. Additionally, enzyme-linked immunosorbent assay with recombinant type VII collagen was positive in three of the five cases who presented with IgA deposits below type IV collagen on FOAM-LSCM.
Conclusions The results using FOAM-LSCM were consistent with those obtained on immunoblotting. FOAM-LSCM is useful in routine diagnostics in cases with undetectable circulating anti-BMZ antibodies, and can differentiate LABD from IgA-EBA, the former with in vivo bound IgA above type IV collagen and the latter with IgA deposits below type IV collagen.