Allergic vasculitis is a vasculitis that mainly involves the small blood vessels of the skin (especially the postcapillary veins) and is characterized by neutrophil oiling and nuclear fragmentation. The common allergens are drugs or chemicals, and the pathogenesis is mainly related to type III allergic reactions. The pathogenesis is mainly related to type III allergic reactions. The onset of the disease is often acute: after exposure to a causative agent, a variety of rashes appear rapidly, such as purpura, urticaria, maculopapular rash, nodules, petechiae, macules, necrotizing ulcers; there may be systemic symptoms, such as fever, weight loss, myalgia, arthralgia: in mild cases, only a few rashes are seen; in severe cases, there may be proteinuria, hematuria, and even renal insufficiency, which may also cause pneumonia, peripheral neuritis, and other extensive systemic lesions. There are no specific changes in laboratory examination, white blood cell count is generally normal, sometimes it can be increased; platelets can be reduced during the acute rash period, and the sedimentation is increased; serum complement is reduced, some patients can be measured cold globulin, anti-cardiolipin antibodies (IgA type is common), histopathological biopsy can be seen microvein, microartery, capillary wall neutrophil or lymphocyte infiltration, leukocyte nuclear fragmentation and vascular wall fibrin-like necrosis. The disease may resolve on its own after the cause is removed. First, exposure to suspected allergic drugs or chemicals should be discontinued, and if there is an infection, the infection should be treated actively. If there is visceral damage or heavy skin lesions, glucocorticoids may be used, and for those with skin necrosis or intolerant glucocorticoids, cyclophosphamide or azathioprine may be used.