Hypersensitivity vasculitis: (also known as leukocyte fragmentation vasculitis, allergic vasculitis) is a vasculitic disease caused by a variety of factors, mainly involving small blood vessels of the skin (especially postcapillary veins), and characterized pathologically by neutrophil infiltration and their nuclear fragmentation. The common allergens are drugs or chemicals, and can also be caused by certain autoimmune diseases, lymphoproliferative diseases or tumors, systemic vasculitis, or some kind of infection, all of which cause the disease, not only the rash morphology and systemic symptoms are similar, their histopathological changes are also similar, and the pathogenesis is mainly related to type III allergic reactions. (I) Clinical manifestations The onset is often acute, with various lesions appearing rapidly after exposure to a causative factor, such as purpura, urticaria, maculopapular rash, nodules, petechiae, macules, necrotizing ulcers, etc.; they may be accompanied by systemic symptoms, such as fever, myalgia, and arthralgia. The clinical manifestations vary widely, with only a few rashes seen in mild cases and extensive systemic lesions such as proteinuria, hematuria, and even renal insufficiency, pneumonia, and peripheral neuritis in severe cases. (B) Diagnosis The disease has no specific clinical manifestations and laboratory tests, so the diagnosis is difficult. It can be diagnosed if a skin biopsy shows vasculitis and a triggering drug or chemical can be found, which disappears within days or weeks after removal from the trigger. The American College of Rheumatology (ACR) 1990 classification criteria for the diagnosis of hypersensitivity vasculitis are: ① age of onset >16 years; ② history of drug use prior to onset; ③ elevated purpura that does not fade when pressed; ④ maculopapular rash (one or more skin sites, varying in size, flattened, protruding from the skin surface); ⑤ skin biopsy showing neutrophil infiltration in the walls of microarterial or microvenous vessels or in the periphery of the vessels. The diagnosis of hypersensitivity vasculitis can be made by having three or more of the above five items. However, in some patients, no precipitating factors can be found, and the symptoms persist without decreasing and are chronic in nature, and often need to be differentiated from allergic purpura, cryoglobulinemia, microscopic polyangiitis, etc. (C) Treatment The disease can be self-limiting after the cause is removed, so an individualized treatment plan is needed. The first step is to stop exposure to suspected allergic drugs or chemicals, actively treat infection if it is present, and use glucocorticoids, prednisone 30-60 mg/d if there is visceral damage or heavy skin lesions. colchicine 0.5 mg 2-3 times/day can be used for lower limb skin vasculitis without skin ulcers. For skin necrosis or if glucocorticoids are not tolerated, cyclophosphamide or azathioprine may be used.