Dr. Marcellin has received speaking fees (less than $10,000 each) from Roche, Schering-Plough, Gilead Sciences, Bristol-Myers Squibb, GlaxoSmithKline, and Indenix/Novartis, has served as an investigator and expert witness for Roche, Schering-Plough, Gilead Sciences, Bristol-Myers Squibb, GlaxoSmithKline, Vertex, Idenix/Novartis, Valeant Pharmaceuticals, Human Genome Sciences, Cytheris, InterMune, and Wyeth, and has served as an expert witness for Coley Pharma. Dr. Cacoub has received consulting fees, speaking fees, and/or honoraria (less than $10,000 each) from Servier, Schering-Plough, Sanofi, and Bristol-Myers Squibb.
Relapse of hepatitis C virus–associated mixed cryoglobulinemia vasculitis in patients with sustained viral response
Article first published online: 31 JAN 2008
Copyright © 2008 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 58, Issue 2, pages 604–611, February 2008
How to Cite
Landau, D.-A., Saadoun, D., Halfon, P., Martinot-Peignoux, M., Marcellin, P., Fois, E. and Cacoub, P. (2008), Relapse of hepatitis C virus–associated mixed cryoglobulinemia vasculitis in patients with sustained viral response. Arthritis & Rheumatism, 58: 604–611. doi: 10.1002/art.23305
- Issue published online: 31 JAN 2008
- Article first published online: 31 JAN 2008
- Manuscript Accepted: 5 OCT 2007
- Manuscript Received: 9 MAY 2007
To investigate the clinical characteristics, outcomes, and results of hepatitis C virus (HCV) RNA analyses in a group of patients with HCV-associated mixed cryoglobulinemia (MC) vasculitis who experienced a relapse of vasculitis despite achieving a sustained viral response to treatment with antiviral agents.
HCV RNA testing was performed by the transcription-mediated amplification (TMA) method in sera and cryoprecipitates (detection limit 2.5 IU/ml). HCV replication was assessed in peripheral blood mononuclear cells (PBMCs) by a modified real-time polymerase chain reaction assay (detection limit 15 IU/106 cells).
We identified 8 patients with relapse of HCV-MC vasculitis despite their having achieved a sustained viral response to treatment. Relapse appeared early after the end of treatment (mean ± SD 2.5 ± 3.5 months) and included mainly purpura (n = 7) and arthralgia (n = 5). Relapse was associated with an increase in serum cryoglobulin levels as compared with end-of-treatment levels (mean ± SD 0.3 ± 0.09 gm/liter and 0.08 ± 0.04 gm/liter, respectively; P < 0.01) and a decrease in C4 levels. In most patients, the relapse was brief, and the MC vasculitis manifestations subsided. A search for HCV RNA by TMA was negative in all patients tested (7 of 8 patients), both in sera and in cryoprecipitates. HCV replication was not found in PBMCs from any of the patients tested (6 of 8 patients). In 3 patients, the MC vasculitis symptoms persisted and were associated with elevated cryoglobulin levels. B cell lymphoma was diagnosed in 2 of these 3 patients.
Relapse of MC vasculitis does occur in a few patients with HCV infection, despite achieving a sustained viral response, and this relapse is not related to persistence of virus. Relapse is short-lived and may be induced by the withdrawal of interferon alfa therapy. However, in patients with persistent MC vasculitis symptoms, a different underlying condition should be considered, especially B cell lymphoma.