Vasculitis is a group of diseases associated with necrosis and inflammation of blood vessels. Damage to the lumen causes insufficient blood supply to the corresponding organ or tissue. Clinical manifestations vary depending on the type, size and location of the involved vessels, the stage of inflammation and the characteristics of the lesions. Most of the etiologies are unknown, while a few are more clearly defined, such as serum sickness, pharmacological metabolic reactions and infections. Hepatitis B virus has been shown to be the cause of many types of vasculitis, and more recently cytomegalovirus, herpes simplex virus, and adult T-cell leukemia virus have been found to cause vasculitis. The pathogenesis of most vasculitides is related to the immune response. Immunocomplexes can be detected in the blood, suggesting that immune complexes are an important mechanism for causing vasculitis. Vasculitis can involve any blood vessel in the body and can be classified according to the type of infiltrating cells and pathological characteristics into: (1) leukocytoclastic vasculitis; (2) lymphocytic granulomatous vasculitis; (3) giant cell vasculitis; and (4) necrotizing vasculitis. These lesions constitute a narrowing of the lumen of the vessel or a neoplastic change in the wall, which results in insufficient blood supply to the local integrated tissues. Pathological changes are also characterized by the following: (1) the lesions are segmental or limited; (2) the lesions in different antibody stages and their severity are often inconsistent; (3) the lesions sometimes involve only a corner of the wall of the tube, so the pathological diagnosis can be difficult. Classification I Primary vasculitis (a) Involving large, medium, and small vessels Aortitis (Takayasu’s arteritis) Temporal arteritis (giant cell arteritis) Isolated central nervous system vasculitis (b) Involving medium and small vessels Nodular polyarteritis Allergic granulomatous vasculitis (Churg-Strauss syndrome) Wegener’s granulomatosis (c) Involving small blood vessels Microscopic vasculitis (Churg-Strauss syndrome) ) Involving small vessels Microscopic polyarteritis Anaphylactic purpura (HenochSchonlein purpura) Cutaneous leukocyte-crushing vasculitis (iv) Other Occlusive thrombotic vasculopathy (Buerger’s disease) Cogan’s syndrome Leukoarthritis (Behcet’s disease) Kawasaki’s disease II. Secondary vasculitides Infection-associated vasculitides Connective tissue disease-associated vasculitides Secondary to Mixed primary cryoglobulinemic vasculitis Malignancy-associated vasculitis Hypocomplementemia Urticarial vasculitis Vasculitis after organ-same transplantation Pseudo vasculitis syndromic gynecological signs (mucinous neoplasms, endocarditis, Sneddon’s syndrome) Classification of vasculitides according to their etiology is difficult because most etiologies are not known, and the same etiology can cause several different types of vasculitis. For example, hepatitis B virus infection can induce urticarial vasculitis, cryoglobulinemic vasculitis, and classic nodular polyarteritis. Classification in terms of the type, size, and distribution of the affected vessels and the histologic features of the grafts is also problematic because many vasculitides overlap; for example, vasculitides complicated by Wegener’s granulomatosis and rheumatoid aspects of arthritis can both present with acute necrotizing arteritis, granulocytic or lymphocytic small-vessel vasculitides, and granulomatous vasculitides. The clinical manifestations of vasculitis also have many overlaps, so called clinical sometimes roughly divided vasculitis into primary and secondary two categories. In short, there is no satisfactory solution so far, and the classification of vasculitis combining clinicopathology is generally used. Clinical manifestations: I. Clinical manifestations Vasculitis should be thought of when the following symptoms occur: (1) multi-system damage; (2) active glomerulonephritis; (3) ischemic or bruising signs and symptoms, especially in young people; (4) raised purpura and other nodular necrotic rashes; (5) multiple mononeuritis; (6) unexplained fever. Autoantibodies (i) Anti-neutrophil plasma antibody (ANCA) There are two patterns when examined by fluorescent immunoassay: ① Cytoplasmic (C-ANCA), with uniform coloration of granulocyte plasma, which is highly specific for Wegener’s granuloma. The majority of patients with active systemic Wegener’s granuloma are positive, and after remission, the potency usually decreases or becomes negative. The antigen recognized by C-ANCA is a serine protease with a molecular weight of 29 KD, which is located in the granules of neutrophils; ② Perinuclear (P-ANCA), in which the coloration is concentrated in the nuclear periphery of the nucleus of the lobular nucleus, except in the case of Wegener’s granuloma. Perinuclear (P-ANCA), the coloration is concentrated in the nucleus of the lobulated nucleus, which is seen in Wegener’s granuloma, but also in other vasculitides, such as microscopic polyarteritis, crescentic nephritis, and connective tissue disorders, such as lupus erythematosus, rheumatoid arthritis, and scleroderma, etc. The antigen recognized by P-ANCA is mainly myeloperoxidase (MPO), and it is likely to have a pathogenetic effect on vasculitides. It causes vascular inflammation by activating neutrophils, causing them to produce respiratoryburst and degranulation. (ii) Anti-Endothelial Cell Antibodies (AECA) are found in a variety of vasculitides and connective tissue diseases. They are specific antibodies directed against endothelial cell membrane antigens and generally do not bind complement or produce a cytotoxic response. AECA has been shown to play a pathologically damaging role only in Kawasaki’s disease. Examinations: Ultrasound, x-ray tomography, and magnetic resonance can detect lesions such as thickening of the vessel wall and narrowing of the lumen. Tissue biopsy is important for diagnosis. The positive detection rate of blind biopsy is very low. Samples should be taken from tissue with lesions. Tissue after treatment and in the chronic phase tends to lose characteristic changes. Therefore the amount of tissue taken should be adequate. Needle biopsies yield too little tissue to be adequate. Since vascular lesions are sometimes segmental, the blood vessels sent for examination should be of a certain length to increase the detection rate. Diagnosis and differential diagnosis: Vasculitis should generally be differentiated from the following categories of diseases, including other connective tissue diseases, infections, tumors, atherosclerosis, and thromboembolic diseases Treatment and prevention: 1. Remove the cause of the disease, e.g., avoiding or eliminating drug allergens, and treating the cause of the disease with antibody therapy, e.g., anti-infective. 2.Treat the underlying disease, such as connective through tissue disease, tumor. 3, for vasculitis confined to the skin commonly used antihistamines, such as chlorpheniramine 12mg / d, phenindamine 75mg / d, divided into 3 times, and non-steroidal anti-inflammatory drugs, such as grinning Pomaxin, 75 ~ 150mg / d, ibuprofen 1.2 ~ 2g / d, divided into 3 times. 4.Systemic vasculitis generally need to use adrenal glucocorticoids, such as necrotizing vasculitis usually should be added immunosuppressive agents, such as cyclophosphamide, according to the condition of the choice of oral administration or intravenous shock therapy. 5, can be added with antiplatelet aggregating agents, such as aspirin 3 ~ 10mg/kg-d, vasodilators, such as nifedipine 30mg/d, isosorbide nitrate 30mg/d, divided into 3 times. Heparin and bicoumarin anticoagulants should not be used in patients with necrotizing vasculitis to avoid serious bleeding. 6, other plasma replacement therapy can be used to treat cryoglobulinemic vasculitis. It is not effective in other types of vasculitis. High-dose static injection of gammaglobulin is an experimental therapy, which may aggravate the condition of lupus nephritis patients.