It is theorized that high levels of circulating antigens initiate the formation of antigen-antibody complexes. A type III hypersensitivity reaction ensues because these complexes are deposited in blood vessel walls. The complement cascade system is activated by these deposited complexes which results in the chemotaxis of neutrophils. Neutrophils release lysosomal enzymes, which damage vessels, leading to thrombosis, embolization, occlusion, necrosis, haemorrhage, and ischaemia. Endothelial cells may show swelling, fibrinoid change or necrosis.
Cutaneous vasculitis occurs in the following conditions.
Clinically, skin involvement is characteristic of HV and usually manifested by palpable purpura in the skin. Polyarteritis nodosa is a multisystem, necrotizing vasculitis of medium-sized muscular arteries characterized by its involvement of the renal and visceral arteries. Nodular vasculitis is a form of lobular panniculitis associated with subcutaneous blood vessel vasculitis with subsequent ischaemic changes that produce lipocyte injury, necrosis, inflammation, and granulation. Particularly, subcutaneous nodules are seen on the posterior aspects of both lower legs. Giant cell arteritis is a systemic granulomatous vasculitis of medium and large-sized arteries.