title: The place of immunotherapy in the management of HCV-induced vasculitis: an update.
abstract: Patients with chronic hepatitis C virus (HCV) can develop systemic cryoglobulinemic vasculitis. Combination of pegylated-interferon α and ribavirin is the first-line treatment of this condition. However, in case of severe or life-threatening manifestations, absence of a virological response, or autonomized vasculitis, immunotherapy (alone or in addition to the antiviral regimen) is necessary. Rituximab is to date the only biologic with a sufficient level of evidence to support its use in this indication. Several studies have demonstrated that rituximab is highly effective when cryoglobulinaemic vasculitis is refractory to antiviral regimen, that association of rituximab with antiviral regimen may induce a better and faster clinical remission, and, recently, that rituximab is more efficient than traditional immunosuppressive treatments. Some issues with regard to the optimal dose of rituximab or its use as maintenance treatment remain unsolved. Interestingly, in balance with this anti-inflammatory strategy, a recent pilot study reported the significant expansion of circulating regulatory T lymphocytes with concomitant clinical improvement in patients with refractory HCV-induced cryoglobulinaemic vasculitis using low dose of subcutaneous interleukin-2. This paper provides an updated overview on the place of immunotherapy, especially biologics, in the management of HCV-induced cryoglobulinaemic vasculitis.
authors.affiliation: Department of Internal Medicine, Centre de Compétence pour les Maladies Autoimmunes Systémiques PACA Ouest, Hôpital de la Conception, Marseille, France. laurent.chiche@ap-hm.fr
authors.forename: Laurent
authors.initials: L
authors.lastname: Chiche
authors.forename: Stanislas
authors.initials: S
authors.lastname: Bataille
authors.forename: Gilles
authors.initials: G
authors.lastname: Kaplanski
authors.forename: Noemie
authors.initials: N
authors.lastname: Jourde
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D058846:Antibodies, Monoclonal, Murine-Derived / Q000494:pharmacology / Q000627:therapeutic use*; D000998:Antiviral Agents / Q000627:therapeutic use; D016174:Hepacivirus / Q000276:immunology / Q000472:pathogenicity; D006526:Hepatitis C / Q000150:complications; D018937:Hepatitis C Antibodies / Q000627:therapeutic use*; D006801:Humans; D007167:Immunotherapy; D016898:Interferon-alpha / Q000627:therapeutic use; D007376:Interleukin-2 / Q000627:therapeutic use; D011092:Polyethylene Glycols / Q000627:therapeutic use; D011994:Recombinant Proteins / Q000627:therapeutic use; D012254:Ribavirin / Q000627:therapeutic use; D000069283:Rituximab; D014657:Vasculitis / Q000628:therapy* / Q000821:virology
chemical_list: D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D000998:Antiviral Agents; D018937:Hepatitis C Antibodies; D016898:Interferon-alpha; D007376:Interleukin-2; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; D000069283:Rituximab; C100416:peginterferon alfa-2a