Hypersensitivity vasculitis, which is usually represented histopathologically as leukocytoclastic vasculitis (LCV), is a term commonly used to denote a small-vessel vasculitis. There are many potential causes of hypersensitivity vasculitis; however, up to 50% of cases are idiopathic. Hypersensitivity vasculitis may present clinically as cutaneous disease only or it may be a cutaneous manifestation of systemic disease. The internal organs most commonly affected in hypersensitivity vasculitis are the joints, gastrointestinal tract, and kidneys. Hypersensitivity vasculitis may be acute and self-limited, recurrent, or chronic. Overall, hypersensitivity vasculitis has a orable prognosis, paicularly when no internal involvement is present . Hypersensitivity vasculitis tends to affect the skin and occasionally the kidney. The loss of integrity of the capillaries and post capillary venules results in extravasation of red blood cells, usually causing purpura and a burning or minimally pruritic sensation. Hypersensitivity vasculitis is thought to be mediated by immune complex deposition.In this form of vasculitis, circulating antigens in the body (produced by factors such as medications, infections, and neoplasms) induce antibody formation. These antibodies bind to the circulating antigen and create immune complexes, which then deposit within vessels, activating complement and inducing inflammatory mediators. Inflammatory mediators, adhesion molecules, and local factors may affect the endothelial cells and play a role in the manifestations of this disease. Additionally, autoantibodies, such as antineutrophil cytoplasmic antibody (ANCA), may be associated with disease manifestations. In ANCA-mediated vasculitis, intracellular proteins from neutrophils become expressed on the cell surface, leading to formation of antibodies (ANCA). These autoantibodies then bind neutrophils, subsequently leading to neutrophil adhesion to vessel walls and cellular activation. Ref - medscape.com