A 48-year-old woman with chronic hepatitis C infection develops episodic palpable purpura over the lower limbs, arthralgia, and weakness. Complement studies show C4 markedly reduced with normal C3. Rheumatoid factor is strongly positive. Skin biopsy shows leukocytoclastic vasculitis. What is the underlying mechanism?
- A Deposition of IgA immune complexes in dermal vessels
- B Granulomatous inflammation of medium-sized vessels driven by hepatitis B antigen
- C Direct endothelial injury by ANCA-activated neutrophils
- D Deposition of mixed IgG-IgM cryoglobulin immune complexes with complement activation ✓
Explanation
Type II mixed cryoglobulinemia, most often secondary to hepatitis C, consists of monoclonal IgM with rheumatoid factor activity binding polyclonal IgG; these complexes deposit in small vessels, fix complement (classically a disproportionately low C4), and produce palpable purpura, arthralgia, weakness, neuropathy, and membranoproliferative glomerulonephritis. Option A describes IgA vasculitis, which raises serum IgA and does not consume C4. Option C describes ANCA-associated vasculitides, which are pauci-immune, and option B describes polyarteritis nodosa, a hepatitis D linked medium-vessel disease.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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