Automatic differentiation of u- and n-serrated patterns in direct immunofluorescence images

Epidermolysis bullosa acquisita (EBA) is a subepidermal autoimmune blistering disease of the skin. Manual u- and n-serrated patterns analysis in direct immunofluorescence (DIF) images is used in medical practice to differentiate EBA from other forms of pemphigoid. The manual analysis of serration patterns in DIF images is very challenging, mainly due to noise and lack of training of the immunofluorescence (IF) microscopists. There are no automatic techniques to distinguish these two types of serration patterns. We propose an algorithm for the automatic recognition of such a disease. We first locate a region where u- and n-serrated patterns are typically found. Then, we apply a bank of B-COSFIRE filters to the identified region of interest in the DIF image in order to detect ridge contours. This is followed by the construction of a normalized histogram of orientations. Finally, we classify an image by using the nearest neighbors algorithm that compares its normalized histogram of orientations with all the images in the dataset. The best results that we achieve on the UMCG publicly available data set is 84.6% correct classification, which is comparable to the results of medical experts

Inflammatory epidermolysis bullosa acquisita with coexistent IgA antibodies to plectin

We present a case of inflammatory epidermolysis bullosa acquisita (EBA) with IgA antibodies to plectin. Analysis of lesional skin biopsies by electron microscopy revealed the split level to be in the sublamina densa zone, corresponding to the diagnosis of EBA. Direct immunofluorescence of perilesional skin demonstrated u-serrated depositions of IgG and IgA that under immunoelectron microcopy were shown to be located in the sublamina densa. In contrast, indirect immunofluorescence on salt-split skin revealed circulating IgA antibodies that stained the roof rather than the floor of the blister. Immunoblotting showed these serum antibodies to be directed to the cytoplasmic hemidesmosomal antigen plectin. The antiplectin specificity of these antibodies was confirmed by 'knockout' immunofluorescence analysis; the serum IgA did not bind to skin sections of a patient with plectin-deficient epidermolysis bullosa. To our knowledge, this case demonstrates for the first time the existence of IgA antibodies against plectin