RT Journal Article SR Electronic T1 Systemic Vasculitis in Patients with Hepatitis C Virus Infection with and without Detectable Mixed Cryoglobulinemia JF The Journal of Rheumatology JO J Rheumatol FD The Journal of Rheumatology SP jrheum.100191 DO 10.3899/jrheum.100191 A1 Benjamin Terrier A1 Damien Sène A1 Agnès Dechartres A1 David Saadoun A1 Nicolas Ortonne A1 Philippe Rouvier A1 Lucile Musset A1 Matthieu Resche Rigon A1 Thierry Maisonobe A1 Patrice Cacoub YR 2010 UL http://www.jrheum.org/content/early/2010/10/13/jrheum.100191.abstract AB Objective To describe hepatitis C virus (HCV)-related systemic vasculitis in patients without detectable mixed cryoglobulinemia (MC) and to compare them to typical cases of HCV-MC vasculitis. Methods Twelve HCV RNA+ patients with histologically proven vasculitis in the absence of detectable MC (cases) were retrospectively compared with 48 HCV RNA+ patients with MC vasculitis (controls). Each case was matched with 4 controls for age and sex. Results The main epidemiological and virologic features were similar between cases and controls. No clinical difference was found, except for lower rates of arthralgias (33% vs 71%; p = 0.02) and purpura (50% vs 83%; p = 0.03) in cases. Cases showed higher mean serum C3 (1.17 ± 0.21 vs 0.93 ± 0.23 g/l; p = 0.01) and median C4 levels (0.25 vs 0.04 g/l; p < 0.001), lower median serum IgM levels (0.6 vs 1.9 g/l; p < 0.001), and lower rates of rheumatoid factor positivity (8% vs 82%; p < 0.001) than controls. The main histologic features were similar between cases and controls. Immunofluorescence analysis of skin biopsy from 1 case revealed perivascular deposits of C3 and IgA. After treatment, overall clinical response of vasculitis (75% vs 83%) and sustained virological response (40% vs 64%; p = 0.3) were similar between cases and controls, except for higher complete clinical response (42% vs 73%; p = 0.05) in controls. Conclusion HCV-related systemic vasculitis may occur in the absence of detectable MC. Our findings suggest that such vasculitis probably results from immune complex-mediated mechanisms, and that the therapeutic management of such vasculitis should be similar to that of HCV-MC vasculitis.