Biological therapies: new treatment options for ANCA-associated vasculitis?

Expert Opin Biol Ther. 2007 Apr;7(4):521-33. doi: 10.1517/14712598.7.4.521.

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.

Publication types

  • Review

MeSH terms

  • Antibodies, Antineutrophil Cytoplasmic* / adverse effects
  • Antibodies, Antineutrophil Cytoplasmic* / immunology
  • Antibodies, Antineutrophil Cytoplasmic* / physiology
  • Antibodies, Monoclonal / adverse effects
  • Antibodies, Monoclonal / blood
  • Antibodies, Monoclonal / therapeutic use
  • Antibodies, Monoclonal, Murine-Derived
  • Antirheumatic Agents / adverse effects
  • Antirheumatic Agents / therapeutic use*
  • Biological Therapy / methods*
  • Churg-Strauss Syndrome / drug therapy*
  • Etanercept
  • Granulomatosis with Polyangiitis / drug therapy*
  • Granulomatosis with Polyangiitis / etiology
  • Granulomatosis with Polyangiitis / physiopathology
  • Humans
  • Immunoglobulin G / adverse effects
  • Immunoglobulin G / blood
  • Immunoglobulin G / therapeutic use
  • Immunologic Factors / therapeutic use*
  • Infliximab
  • Interferon-alpha / therapeutic use*
  • Randomized Controlled Trials as Topic
  • Receptors, Tumor Necrosis Factor / blood
  • Receptors, Tumor Necrosis Factor / therapeutic use
  • Rituximab
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / immunology
  • Vasculitis / drug therapy*
  • Vasculitis / etiology
  • Vasculitis / immunology

Substances

  • Antibodies, Antineutrophil Cytoplasmic
  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Murine-Derived
  • Antirheumatic Agents
  • Immunoglobulin G
  • Immunologic Factors
  • Interferon-alpha
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Rituximab
  • Infliximab
  • Etanercept