Interferon-alpha and ribavirin treatment in patients with hepatitis C virus-related systemic vasculitis

Hepatitis C virus (HCV)-related vasculitis may involve multiple organs, including the skin, kidneys, and nervous system, and may be life-threatening. Although HCV is increasingly recognized as a cause of systemic vasculitis, limited data are available regarding the optimal treatment of this potentially serious condition. Therefore, we retrospectively analyzed the response to treatment in patients with chronic hepatitis C complicated by systemic vasculitis who had received antiviral therapy with interferon-alpha (IFNalpha) and ribavirin.

This retrospective study included 27 patients with systemic vasculitis and chronic HCV infection. Each patient had received treatment with IFNalpha and ribavirin for at least 6 months. The response to antiviral treatment was analyzed by comparing clinical, immunologic, and virologic data at the time of entry and during followup. Clinical response was defined according to the evolution of weight, arthralgia, nervous system, renal system, and cutaneous involvement. The virologic and immunologic responses were defined by the absence of HCV RNA and the absence of cryoglobulinemia, respectively, both 6 months after stopping antiviral therapy and at the end of followup.

Patients received IFNalpha for a mean +/- SD of 20 +/- 14 months and ribavirin (at a mean +/- SD dosage of 895 +/- 250 mg/day) for 14 +/- 12 months. Other treatments included low-dose corticosteroids and plasma exchange. After a mean +/- SD followup of 57 +/- 29 months, 25 of 27 patients are alive and are being followed up as outpatients. Because of the heterogeneity of anti-HCV treatments received, the main results were stratified according to patients with 6 months of followup after stopping antiviral treatment (group 1, n = 14) and those who were still undergoing antiviral therapy at the time of analysis (group 2, n = 13). Nine patients in group 1 had a sustained virologic response and were clinical and immunologic complete responders. Four patients in group 1 were virologic nonresponders, and 3 of these patients had partial clinical and immunologic responses. Overall, 10 patients in group 1 had a complete clinical and immunologic response of their vasculitis (all 9 of the sustained virologic responders and 1 of the 5 patients who remained viremic). At the end of followup, 7 patients in group 2 were negative for HCV RNA; 6 were complete clinical responders. Among the other 6 patients in group 2, who had persistent viremia, 4 had a partial clinical response. Among the patients in group 1, HCV RNA was more often undetectable and genotype 1 was less frequent in complete clinical responders compared with partial/nonresponders. Age, sex, clinical vasculitic involvement, mean duration or total cumulative dose of IFNalpha or ribavirin, and use of steroids or plasmapheresis did not differ significantly according to clinical response.

Treatment with IFNalpha and ribavirin can achieve a complete clinical response in most patients with HCV-related systemic vasculitis. Complete clinical response correlates with the eradication of HCV.