Allergic vasculitis

Introduction to allergic vasculitis Hypersensitivity vasculitis (hypersensitivityvasculitis), is one of the most common vasculitis, has been used to name leukocyte vasculitis, necrotizing nodular dermatitis, hypersensitivity vasculitis, nodular dermal allergic rash, allergic Arteritis and allergic vasculitis, the incidence of this disease can be acute and slow, the common symptoms of the system include fever, fatigue, fatigue, etc., local symptoms are mainly skin symptoms, a few patients have skin involvement, such as Joints, kidneys, lungs, digestive system, etc. Histopathological examination revealed fibrinous necrosis of the vessel wall and extensive neutrophil infiltration around the vessel. basic knowledge The proportion of the disease: the incidence rate in the youth population is about 0.052% Susceptible people: no specific population Mode of infection: non-infectious Complications: gastrointestinal bleeding, purpura nephritis, allergic purpura, abdominal pain, blood in the stool, intussusception, hematuria, headache, coma, nephrotic syndrome

Cause of allergic vasculitis

Drug factors (30%):

Many people with allergic constitutions develop an allergic reaction when they are exposed to allergenic substances. The drugs that are susceptible to sensitization include penicillin and its derivatives, sulfonamides, and aspirin.

Chemical substances (25%):

Allergic patients develop an allergic reaction when exposed to chemicals. Chemicals that are susceptible to sensitization include insecticides, herbicides, and petroleum preparations.

Allogeneic protein (28%):

Allergic reactions can occur in the body after exposure or ingestion of allergens, such as exposure to snake venom and various desensitizing agents.

Pathogenesis

After the exogenous antigen enters the body, it stimulates the body to produce corresponding antibodies, and forms an immune complex in the vascular wall. It activates complement activation by activating the classical pathway or the alternative pathway of complement. Activated complement can directly damage vascular endothelial cells. In addition, it also exerts strong chemotactic effects on neutrophils and monocytes, causing them to accumulate in the deposition site of immune complexes, causing inflammatory damage. In addition, during the inflammatory reaction, neutrophils, Monocytes, platelets, and mast cells also help or strengthen inflammatory damage by releasing a variety of inflammatory mediators. Platelets, through the release of ADP and prostaglandins, cause platelet aggregation and thrombosis, and therefore microcirculatory hemorrhage and local fibrinolysis It can also be the background of the disease.

Allergic vasculitis prevention

Quickly identify sensitizing drugs or chemicals, and warn patients to stop and ensure that they will not be exposed to such substances in the future, which can effectively prevent the occurrence of this disease.

Allergic vasculitis complications Complications, digestive tract hemorrhagic nephritis, allergic purpura, abdominal pain, bloody intestines, hematuria, headache, coma, nephrotic syndrome

Common complications of this disease are:

1. Gastrointestinal bleeding: related to intestinal mucosal damage.

2. Purpuric nephritis: associated with renal capillary allergic inflammation.

3. Allergic purpura: mild joint swelling and pain, abdominal pain, severe cases may have blood in the stool, hematemesis, and even develop intussusception, intestinal perforation, if not treated in time, it will cause liver and kidney damage, hematuria, Proteinuria, some children may have headaches, convulsions, coma, and even lead to a variety of complications, such as cerebrovascular disease, gastrointestinal bleeding and nephrotic syndrome.

Allergic vasculitis symptoms Common symptoms Allergic angioedema Joint pain Pain vascular wall and surrounding ... hemoptysis plaque papules double vision abdominal pain nodules

The onset of the disease can be acute and slow, and the common symptoms of the whole body include fever, fatigue, fatigue, etc. The local manifestations are mainly skin symptoms, and a few patients have extracutaneous involvement, such as joints, kidneys, lungs, and digestive system.

1. Skin manifestations : The skin lesions are symmetrical, often distributed in the lower limbs and buttocks, and can also occur in the upper limbs and chest and back. The skin manifests in various changes, mainly purpura, urticaria, papules, ecchymoses, nodules and necrosis. Ulcers, chronic patients may have reticular bluish spots, rashes often start from miliary to mung bean big red maculopapular rash and purpura, and soon develop into a touchable purpura, slightly protruding leather surface, touchable by hand, finger pressure is not Fading, easy to distinguish from non-inflammatory purpura, rash can vary from needle tip to broad bean size, small rash usually has no symptoms, large rash or rash with mutual fusion will have pain, rash episode irregular, lasting 1 to 4 weeks subsided There may be residual pigment spots, about 30% of patients have severe skin lesions, epidermal necrosis, ulceration, and scarring after healing.

2. Extra-cutaneous manifestations : joint pain may occur when the joint is involved, but generally no redness and swelling, when the lungs are invaded, the patient has shortness of breath, hemoptysis, abdominal pain, nausea, upper gastrointestinal bleeding, suggesting digestive tract involvement, central nervous system lesions There are headaches, double vision, etc., heart involvement is rare, manifested as arrhythmia, severe heart failure, kidney damage, edema, hematuria and so on.

Several special types of the disease are common:

(1) Acute viral hepatitis prodromal serum type: 10% to 20% of the disease develops into acute hepatitis B (type B or non-type B), and patients have more HBsAg titer, mostly in hepatitis. A rash, urticaria, and polyarthritis occur during the incubation period, and are often overlooked when the disease is mild or transient.

(2) hypocomplementic vasculitis: more common in young women, recurrent urticaria with decreased serum complement, may have fever, arthritis, abdominal pain, kidney involvement, renal biopsy suggests mild to moderate membrane hyperplasia Glomerulonephritis with IgG and complement deposition in the glomerular basement membrane, skin biopsy often shows necrotizing vasculitis.

(3) mixed cryoglobulinemia: more common in middle-aged women, clinical manifestations of cutaneous vasculitis, Raynaud's phenomenon, recurrent purpura, joint muscle pain, renal failure, hepatosplenomegaly, lymphadenopathy and Anemia, renal pathology can show proliferative glomerulonephritis or diffuse proliferative glomerulonephritis, immune complexes and complement deposition in the vascular wall and glomerular basement membrane.

3. Henouh-Schonlein purpura: This disease is more common in children, the vast majority have typical triads (purpura, joint pain and abdominal pain), more than half have hematuria, proteinuria, nephrotic syndrome, and even kidney Functional failure, renal pathology suggests focal segmental sclerosing glomerulonephritis or diffuse mesangial proliferative glomerulonephritis, a few severe cases of crescentic nephritis, immunofluorescence showing IgA, complement glomerular mesangial area Deposition, with pathological changes similar to primary IgA nephropathy.

Whether the treatment of the disease is effective, it is very important to identify and remove the cause, especially the discontinuation of suspected antigenic sensitizers has a key role in determining the prognosis. Other treatment principles are basically similar to nodular polyarteritis.

Examination of allergic vasculitis

Laboratory inspection

1. Blood test: blood eosinophils often increase, white blood cells can increase, erythrocyte sedimentation rate increases, high hyperglobulinemia and ADP and prostaglandin increase, generally no anemia, normal platelet count, out, normal clotting time There is cryoglobulinemia of IgG-IgM. Laboratory tests show hypergamma and hypo-complementemia, and RF and HBsAg may be positive.

2. Urine examination: There may be protein, red blood cells, white blood cells and casts. In severe cases, there may be proteinuria in the range of nephrotic syndrome. When renal function is reduced, there may be an increase in urea nitrogen and creatinine.

3. Dung routine examination: some patients can see parasite eggs and red blood cells, occult blood test can be positive.

4. Bone marrow: normal bone marrow, eosinophils can be high.

5. Capillary fragility test is positive.

Auxiliary inspection

1. Histopathological examination: pathological examination showed diffuse small perivascular inflammation, neutrophils gathered around the blood vessels, and immunofluorescence showed that IgA and C3 were deposited in the vascular wall of the dermis.

(1) Skin changes: The main pathological feature of this disease is acute fibrinoid necrosis, which begins in the endothelium or subendothelial matrix and then spreads throughout the vessel wall, with significant polymorphic cellular responses and eosinophil infiltration, vascular disease. The lesions progress in the same period, unlike the nodular polyarteritis.

Examination of visible skin tissue dermal papillary to reticular layer with arteritis, phlebitis and capillary vasculitis, vasodilation, endothelial cell edema, exudation, luminal stenosis, thrombosis, fibrinoid degeneration or necrosis of the vessel wall In the early stage of the disease, neutrophils are infiltrated around the blood vessels, and leukocyte disruption and nuclear dust and red blood cell extravasation are observed. In the late stage of the disease, mononuclear cell infiltration is the main cause.

(2) Kidney changes: In addition to the skin, the kidney is the most susceptible part of the disease. The size of the kidney is normal or enlarged by the naked eye. There are bleeding spots on the surface. Small interlobular arteries, small arteries, veins and Capillary cells have cellulose-like necrosis, with glomerular lesions most prominent, occasional granulomatous lesions around the ball, capillary cell proliferation, and visible segmental or epithelial-like crescent and diffuse necrotic glomerulus Nephritis, the kidney has many pathological types, including no or less immune complex crescentic nephritis, renal interstitial round cell infiltration and hemorrhage, partial tubule atrophy, immunofluorescence showing mesothelial area and capillary wall with a little IgG, IgM and complement deposition or no immunoglobulin components, but in the renal capsule, glomerular necrosis area has more fibrinogen precipitation, no obvious characteristic changes in electron microscopy, and no more electronic compact.

The characteristic lesion of kidney involvement in this disease is necrotizing glomerulitis or focal necrotic glomerulitis, and diffuse necrotic glomerulonephritis can be seen in the worsened cases.

2. X-ray examination: When the lung is involved, the chest radiograph may show focal or diffuse pulmonary infiltration, or small nodular, occasional pleural effusion.

Diagnosis and diagnosis of allergic vasculitis

Diagnostic criteria

According to the characteristics of the disease, the diagnosis of typical allergic vasculitis is not difficult. In 1990, the American College of Rheumatology (ARA) developed a diagnostic standard for this disease.

1. Age of onset > 16 years old.

2. Have a history of taking drugs before the illness.

3. Tactile purpura.

4. A maculopapular rash, that is, one or more skins have flattened skins of different sizes, higher than the skin rash.

5. Vein venules or arterial sections show neutrophil infiltration in or outside the blood vessels.

Those with 3 or more of the above 5 items can be diagnosed as allergic vasculitis with a sensitivity of 71% and a specificity of 93%.

Differential diagnosis

Typical allergic vasculitis is mainly identified by the following diseases:

1. Allergic purpura: occurs in children and young people, skin, joints, gastrointestinal tract and kidneys are often invaded at the same time, the shape of lesions is relatively simple, characterized by palpable wheal purpura and ecchymoses Protein and red blood cells may appear in the urine, and there may be gastrointestinal bleeding.

2. Pap necrotizing tuberculosis rash: mostly occurs in young people, the lesion is symmetrically distributed on the extremities of the extremities, near the joints and buttocks, with dark red parenchyma or central necrotic nodules, no purpura, tuberculosis history or tuberculosis, tissue Pathological examination has a change in tuberculosis.

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