Hypersensitivity vasculitis (HV) encompasses a heterogeneous group of vasculitides associated with hypersensitivity to antigens from infectious agents, drugs, or other exogenous or endogenous sources, characterized pathologically by involvement of postcapillary venules and inflammation and fibrinoid necrosis. Clinically, skin involvement is characteristic, manifested by "palpable purpura." Systemic vascular involvement occurs, chiefly in the kidney, muscles, joints, GI tract, and peripheral nerves. Schonlein-Henoch purpura is a type of HV associated with IgA.
The most frequently postulated mechanism for the production of necrotizing vasculitis is the deposition in tissues of circulating immune complexes. Initial alterations in venular permeability, which may facilitate the deposition of complexes at such sites, may be due to the release of vasoactive amines from platelets, basophils, and/or mast cells. Immune complexes may activate the complement system or may interact directly with Fc receptors on endothelial cell membranes. When the complement system is activated, the generation of anaphylatoxins C3a and C5a can degranulate mast cells. Also, C5a can attract neutrophils that could release lysosomal enzymes during phagocytosis of complexes and subsequently damage vascular tissue.
* A slightly elevated, purple-red rash over one or more areas of skin. The rash doesn't whiten when pressed.
* Flat and raised lesions of different sizes over one or more areas of skin
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