Master IgA Vasculitis (Formerly Henoch-Schonlein Purpura) with Picmonic for Medicine

IgA vasculitis most commonly affects children and is the most common vasculitis seen in the pediatric population.

IgA vasculitis often follows an upper respiratory or pharyngeal infection, as immune complex formation is typically triggered by a preceding infection, most commonly streptococcal.

The accumulation of circulating immunoglobulin A (IgA) immune complexes within small vessel walls, particularly in the skin, kidneys, and gastrointestinal tract. These complexes trigger complement activation and neutrophil recruitment, leading to inflammation, vessel damage, and tissue injury characteristic of IgA vasculitis

IgA vasculitis (Henoch-Schönlein Purpura) is a Type III hypersensitivity reaction in which galactose-deficient IgA1 forms circulating immune complexes that deposit in small vessel walls of the skin, kidneys, and gastrointestinal tract. This deposition activates complement and recruits neutrophils, producing leukocytoclastic vasculitis and tissue injury. The resulting immune complex–mediated inflammation causes the characteristic palpable purpura, arthralgia, abdominal pain, and renal involvement. Experimental models reproduce the disease using Type III hypersensitivity mechanisms, confirming that IgA1 immune complex deposition and subsequent inflammatory cascades are the central drivers of IgA vasculitis.

Arthralgia refers to joint pain caused by a non-inflammatory condition. Arthralgia is seen in IgA vasculitis due to joint involvement.

Colicky abdominal pain caused by IgA-mediated small vessel vasculitis of the gastrointestinal tract, leading to bowel wall edema, possible bleeding, and risk of intussusception

Gastrointestinal bleeding results from IgA-mediated small vessel vasculitis, causing mucosal hemorrhage, while bowel wall edema can act as a lead point for intussusception, presenting with severe abdominal pain and possible “currant jelly” stools.

IgA immune complex deposition in the mesangium leads to glomerulonephritis, resulting in hematuria, often with RBC casts, and mild to moderate proteinuria due to glomerular inflammation; this represents the most important complication and main determinant of long-term prognosis, typically occurring days to weeks after the rash, with pathology similar to IgA nephropathy, possible progression to nephritic syndrome, and usually normal complement levels, requiring close follow-up with serial urinalysis and renal function monitoring.

Black, tarry stool is a sign of intestinal hemorrhage, usually in the upper part of the gastrointestinal tract.

Lesions appear as red or purple discolorations on the skin that do not blanch with pressure. Palpable purpura results from the recruitment and activation of neutrophils within the small vessels of the skin, leading to vessel inflammation and leakage of blood into surrounding tissues. It is a hallmark of small-vessel vasculitis, most notably IgA vasculitis. The rash typically involves the buttocks and lower extremities, but may also appear on the face, arms, or trunk.

IgA vasculitis is usually a self-limited small vessel vasculitis in which symptoms such as palpable purpura, abdominal pain, and arthralgia resolve spontaneously within a few weeks, especially in children, although recurrence can occur, and renal involvement requires ongoing monitoring.

Management is primarily supportive, including hydration, pain control, and rest, as the disease is typically self-limited; NSAIDs may be used for arthralgia, while more severe symptoms such as significant abdominal or renal involvement may require corticosteroids.