Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of dyshydrosiform pemphigoid. Multiple small bullae were noticed in the bilateral hands and feet of an 85 year old Japanese male about 1 month before admission to hospital, and these lesions gradually worsened and expanded generally. Clinical appearance on the initial examination showed a collection of erosions, bullae, and pustules with haemorrhagic pompholyx. Serum anti-BP180 antibody index was more than 150. Histopathologic appearance of the bullous leision revealed a subepidermal bulla with an inflammatory infiltrate and fibrinous exudate, with aggregated eosinophils, neutrophils, and lymphocytes in the upper dermis. In direct immunofluorescence, the epidermal basement membrane was stained strongly for complement C3 and weakly for IgG. Based on these features, especially from the particular clinical aspects, we finally diagnosed one subtype of bullous pemphigoid, namely dyshidrosiform pemphigoid. Although he got better by orally taking steroids, the eruptions recurred just after tapering off. Thereafter, he died due to worsened general condition partly complicated by pancreatitis.
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PMID:[A case of dyshidrosiform pemphigoid]. 2170 23

The study of autoimmunity mediated by immunoglobulin E (IgE) autoantibodies, which may be termed autoallergy, is in its infancy. It is now recognized that systemic lupus erythematosus, bullous pemphigoid (BP), and chronic urticaria, both spontaneous and inducible, are most likely to be mediated, at least in part, by IgE autoantibodies. The situation in other conditions, such as autoimmune uveitis, rheumatoid arthritis, hyperthyroid Graves' disease, autoimmune pancreatitis, and even asthma, is far less clear but evidence for autoallergy is accumulating. To be certain of an autoallergic mechanism, it is necessary to identify both IgE autoantibodies and their targets as has been done with the transmembrane protein BP180 and the intracellular protein BP230 in BP and IL-24 in chronic spontaneous urticaria. Also, IgE-targeted therapies, such as anti-IgE, must have been shown to be of benefit to patients as has been done with both of these conditions. This comprehensive review of the literature on IgE-mediated autoallergy focuses on three related questions. What do we know about the prevalence of IgE autoantibodies and their targets in different diseases? What do we know about the relevance of IgE autoantibodies in different diseases? What do we know about the cellular and molecular effects of IgE autoantibodies? In addition to providing answers to these questions, based on a broad review of the literature, we outline the current gaps of knowledge in our understanding of IgE autoantibodies and describe approaches to address them.
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PMID:Immunoglobulin E-Mediated Autoimmunity. 2968 78