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Understanding IgA Vasculitis – Causes, Symptoms, and Overview

Immunoglobulin A (IgA) vasculitis, previously called Henoch-Schönlein purpura, is a systemic small-vessel vasculitis caused by immune complex deposition in the blood vessels. It primarily affects children but can occur in adults, often presenting with a combination of skin, joint, gastrointestinal, and kidney symptoms. Although the exact cause is not fully understood, IgA vasculitis is generally triggered by immune system dysregulation, often following infections, medications, or vaccinations.


The hallmark symptom of IgA vasculitis is a purplish rash called palpable purpura, commonly appearing on the lower legs, buttocks, and sometimes arms. Unlike simple bruising, this rash is raised, firm, and may be accompanied by mild itching or tenderness. In some cases, the rash is the first sign noticed by caregivers or patients themselves.


Joint involvement is another common feature. Patients frequently experience swelling, stiffness, and pain, particularly in the knees and ankles. Although joint symptoms are typically transient, they can be uncomfortable and impact mobility, especially in children who are active.


Gastrointestinal symptoms often include abdominal pain, nausea, vomiting, and, occasionally, blood in stool. These symptoms arise from inflammation of the small blood vessels in the intestines. While mild abdominal discomfort is common, severe involvement may lead to complications such as intussusception, gastrointestinal bleeding, or perforation, which require urgent medical attention.


Kidney involvement, referred to as IgA nephropathy, can occur in both children and adults. It may manifest as hematuria (blood in urine) or proteinuria (protein in urine) and, if persistent, can progress to chronic kidney disease. Monitoring kidney function through urinalysis and periodic lab tests is a critical part of long-term management.


The immune system’s role in IgA vasculitis involves the deposition of IgA-containing immune complexes in the vessel walls, triggering inflammation. Upper respiratory infections are often implicated as a precipitating factor, leading to increased IgA production. Genetic and environmental factors may also influence susceptibility, although no single cause has been identified.



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