RESUMO
Current evidence strongly supports the theory that the lesions of pemphigus are due to binding of pemphigus antibody to an antigen in or near the epidermal cell membrane, which causes a release of at least one enzyme which results in dissolution of the intercellular attachments and acantholysis. Similarly, strong evidence supports the hypothesis that pemphigoid blisters are due to binding of antibody at the basement membrane, followed by activation of complement and release of anaphylatoxins which activate tissue mast cells to release eosinophil chemotactic factor. These eosinophils then release tissue-destructive enzymes and reactive oxygen intermediates directly onto the basement membrane zone, with loss of dermoepidermal adherence and formation of blisters.
Assuntos
Humanos , Anticorpos , Antígenos , Ativação Enzimática , Dermatopatias Vesiculobolhosas , Leucócitos , Mastócitos , Membrana Basal , Pele , Penfigoide Bolhoso , Proteínas do Sistema Complemento , PênfigoRESUMO
Necrotizing vasculitis is a term used to describe vessel wall necrosis due to neutrophil infiltration. Current evidence strongly suggests that these cells are responding to elaboration of chemotactic factors of the complement cascade released at the site of deposition of immune complexes in the vessel wall. The antibody is usually IgG or IgM (and rarely IgA), but the only antigens identified with even a minimum certainty are the streptococcal M protein, the hepatitis B surface antigen, and Mycobacterium tuberculosis. Vessels may be involved, leading to specific signs or symptoms, in a wide range of organs, but with those of the skin, kidney, joints, and gastrointestinal tract leading the list. Why vessels of different sizes or location become involved in individual patients is unknown. Therapy with nontoxic drugs, such as antihistamines or salicylates, is indicated when the disease is mild, but vital organ involvement may necessitate therapy with systemic corticosteroids and/or cyclophosphamide.