The role of biologics in treatment of ANCA-associated vasculitis.
The vast majority of patients with anti-neutrophil cytoplasmic autoantibody-associated vasculitis (AAV) who receive conventional treatment with glucocorticoids and cyclophosphamide experience frequent relapses and treatment-related side-effects. Increasing knowledge of the pathogenesis of AAV has permitted the development of targeted therapies against tumour necrosis factor (TNF)-α and T and B lymphocytes. Therapy with TNF-α blocking drugs has so far proved disappointing, and this approach is not recommended. B cell depletion using rituximab is effective for remission induction, especially in refractory patients. The long-term side-effects and the best method of using rituximab to maintain remission are still to be determined.
Department of Rheumatology, Ipswich Hospital NHS Trust, Heath Road, Ipswich, IP4 5PD, UK.
Chethana
C
Dharmapalaiah
Richard A
RA
Watts
D056648:Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis / Q000188:drug therapy*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D058846:Antibodies, Monoclonal, Murine-Derived / Q000627:therapeutic use*; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D000069285:Infliximab; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D000069283:Rituximab; D016896:Treatment Outcome
D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D007074:Immunoglobulin G; D007166:Immunosuppressive Agents; D018124:Receptors, Tumor Necrosis Factor; D000069283:Rituximab; D000069285:Infliximab; D000068800:Etanercept