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Systemic Vasculitis in Patients with Hepatitis C PATRICE CACOUB, THIERRY MAISONOBE, VINCENT THIBAULT, ANNE GATEL, JÉRÔME SERVAN, LUCILE MUSSET, and JEAN-CHARLES PIETTE
ABSTRACT.
Methods. We retrospectively compared 2 groups of patients with HCV presenting with systemic vasculitis: 10 with biopsy proven polyarteritis nodosa-type systemic vasculitis (PAN, Group 1) and 7 with mixed cryoglobulinemia syndrome (MC, Group 2). Results. Patients of Group 1 presented with different features than Group 2: life threatening systemic vasculitis (10 vs 0; p < 0.01), severe multifocal sensorimotor mononeuropathies versus distal moderate sensory polyneuropathies, malignant hypertension (5 vs 0; p = 0.04), cerebral angiitis (2 vs 0), ischemic abdominal pain (2 vs 0), kidney and liver microaneurisms (2 vs 0), increased erythrocyte sedimentation rate and C-reactive protein (7 vs 0; p < 0.01), renal insufficiency (5 vs 0; p = 0.04), HCV genotype 1b (3 vs 6; p = 0.06), and lower activity of chronic hepatitis (p = 0.02). Neuromuscular biopsies showed lesions of vasculitis in all patients, but the type of vasculitis was different in Group 1 compared to Group 2: medium size artery involvement (7 vs 0; p < 0.01), necrotizing vasculitis (10 vs 0; p < 0.01), and mononuclear cell infiltrate in perivascular areas (0 vs 7; p < 0.01). Using prednisone, plasma exchanges, and interferon-a, complete recovery was obtained in all PAN-type patients except one. In Group 2 patients, interferon-a did not have any effect on the peripheral neuropathy. Conclusion. HCV infection may be associated with different types of systemic vasculitis, i.e., polyarteritis nodosa or mixed cryoglobulinemia. Because of differences in clinical and pathological features and therapeutic strategy, PAN-type vasculitis should be distinguished from MC-type vasculitis in HCV patients. (J Rheumatol 2001;28:109-18) Key Indexing Terms:
HEPATITIS C VIRUS
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