Urticarial vasculitis is an immune complex disease with complex mechanisms and causes. Common causes include allergic reactions caused by some drugs and autoantibody problems. This disease often occurs in middle-aged women. 1. Causes This disease is an immune complex disease with complex etiology and pathogenesis. 1. The factors that induce urticarial vasculitis are unknown. There are reports that it may be a hypersensitivity vasculitis caused by chemicals, drugs (such as iodine), and pathogen antigens. 2. In low-complement urticarial vasculitis, autoantibodies (low molecular weight serum complement C1q precipitants) directly target the collagenous region of C1q, leading to a decrease in serum C1q, which then activates the complement pathway and produces anaphylatoxins and neutrophil chemotactic factors. These inflammatory mediators can damage vascular endothelial cells and lead to the occurrence of vasculitis. Some scholars pointed out that the relationship between this disease and connective tissue diseases should be taken seriously. 2. Clinical manifestations 1. This disease is more common in middle-aged women, with the age of onset mostly between 30 and 40 years old. The onset is often accompanied by irregular fever, sometimes reaching 38 to 39°C. 2. The main skin feature is wheal-like lesions, which are similar to urticaria, but the wheal lesions last for a long time, often 24 to 72 hours, or even several days. The skin lesions are infiltrated when touched, and purpura may sometimes be seen at the lesions. A few cases have blisters but no necrosis. After the lesions subside, pigmentation or desquamation remains. You may feel itching or burning. 3. This disease is often accompanied by joint pain and arthritis, mainly in the joints of the limbs, sometimes with joint swelling, abdominal discomfort, swollen lymph nodes, etc. In the late stage, kidney damage may occur, and in a few cases, epilepsy, meningitis, and unilateral optic neuritis may occur. 4. Urticarial vasculitis is often an early symptom of diseases such as dermatomyositis and systemic lupus erythematosus, so the course of the disease should be closely observed. 3. Inspection Laboratory examinations showed increased erythrocyte sedimentation rate, decreased serum complement levels, positive autoantibody titers (ANA, dsDNA antibodies, anti-SSA/SSB antibodies), positive rheumatoid factor, and increased levels of circulating immune complexes. There are two commonly used auxiliary inspection methods: 1. Routine blood examination may reveal normal or increased peripheral white blood cell count, increased neutrophil proportion, and rapid erythrocyte sedimentation rate. The most common is severe and persistent hypocomplementemia, especially a more obvious decrease in C4. 2. Direct fluorescence examination shows granular deposits of immunoglobulins and complement in and around the blood vessel walls. |
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