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- W2014371671 endingPage "101" @default.
- W2014371671 startingPage "91" @default.
- W2014371671 abstract "Epidermolysis bullosa acquisita (EBA) is a rare and acquired autoimmune subepidermal bullous disease of skin and mucosa. EBA includes various distinct clinical manifestations resembling genetic dystrophic epidermolysis bullosa (DEB), Bullous pemphigus, Brunsting-Perry pemphigoid, or cicatricial pemphigoid. These patients have autoantibodies against type VII collagen (C7), an integral component of anchoring fibrils (AFs), which are responsible for attaching the dermis to the epidermis. Destruction or perturbation of the normal functioning AFs clinically results in skin fragility, blisters, erosions, scars, milia, and nail loss, all features reminiscent of genetic dystrophic epidermolysis bullosa. These anti-C7 antibodies are pathogenic because when injected into a mouse, the mouse develops an EBA-like blistering disease. Currently, treatment is often unsatisfactory; however, some success has been achieved with colchicine, dapsone, photopheresis, plasmapheresis, infliximab, rituximab, and IVIG." @default.
- W2014371671 created "2016-06-24" @default.
- W2014371671 creator A5007855326 @default.
- W2014371671 creator A5027358797 @default.
- W2014371671 creator A5031646241 @default.
- W2014371671 creator A5073351087 @default.
- W2014371671 date "2011-09-28" @default.
- W2014371671 modified "2023-10-08" @default.
- W2014371671 title "Epidermolysis bullosa acquisita: Autoimmunity to anchoring fibril collagen" @default.
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