title: Biological therapies: new treatment options for ANCA-associated vasculitis?
abstract: Biological therapies enable us to apply highly selective targeting components to modulate the immune response. Until now, a few controlled studies investigated the efficacy of TNF-alpha blocking agents in systemic vasculitis have been carried out, but, in general, they were falling short of expectations. However, there is conducive evidence that TNF-alpha blockers are advantageous in antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis, at least in selected disease stages. Likewise, although the efficacy of the monoclonal CD20 antibody rituximab in ANCA-associated vasculitis is obvious, the effect on predominantly granulomatous disease activity in Wegener's granulomatosis is less clear. In addition, interferon-alpha is used for induction treatment particularly in Churg-Strauss syndrome. Even though the effectiveness and safety of short-term administration was confirmed by case series, severe side effects after long-term treatment relativized the initial results. This review presents the recent data on the use of biologicals in vasculitis and appraises the knowledge in the clinical context.
authors: University Hospital Schleswig-Holstein, Campus Luebeck, Department of Rheumatology and Rheumaklinik Bad Bramstedt, Ratzeburger Allee 160, 23538 Lübeck, Germany. Rheumatologie@hamburg.de
authors: Peer M
authors: PM
authors: Aries
authors: Peter
authors: P
authors: Lamprecht
authors: Wolfgang L
authors: WL
authors: Gross
mesh_terms: D019268:Antibodies, Antineutrophil Cytoplasmic / Q000009:adverse effects / Q000276:immunology / Q000502:physiology; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000097:blood / Q000627:therapeutic use; D058846:Antibodies, Monoclonal, Murine-Derived; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001691:Biological Therapy / Q000379:methods*; D015267:Churg-Strauss Syndrome / Q000188:drug therapy*; D000068800:Etanercept; D014890:Granulomatosis with Polyangiitis / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects / Q000097:blood / Q000627:therapeutic use; D007155:Immunologic Factors / Q000627:therapeutic use*; D000069285:Infliximab; D016898:Interferon-alpha / Q000627:therapeutic use*; D016032:Randomized Controlled Trials as Topic; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood / Q000627:therapeutic use; D000069283:Rituximab; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000097:blood / Q000276:immunology; D014657:Vasculitis / Q000188:drug therapy* / Q000209:etiology / Q000276:immunology
chemical_list: D019268:Antibodies, Antineutrophil Cytoplasmic; D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D007155:Immunologic Factors; D016898:Interferon-alpha; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069283:Rituximab; D000069285:Infliximab; D000068800:Etanercept