作者: William J. Sandborn , Stephen B. Hanauer
DOI: 10.1097/00054725-199905000-00008
关键词:
摘要: Tumor necrosis factor-alpha (TNFalpha), a proinflammatory cytokine, plays an important role in the pathogenesis of inflammatory bowel disease (IBD). Biotechnology agents including chimeric monoclonal anti-TNF antibody (infliximab), humanized (CDP571), and recombinant TNF receptor fusion protein (etanercept) have been used to inhibit TNFalpha activity. Controlled trials demonstrated efficacy for infliximab moderately severely active Crohn's (CD) fistulizing CD sufficient justify recent U.S. Food Drug Administration (FDA) approval. Additional completed rheumatoid arthritis (RA). Similarly, preliminary controlled suggested CDP571 RA. Larger etanercept RA patients who failed modifying antirheumatic drug (DMARD) therapy leading FDA approval Toxicities observed with therapies included formation human antichimeric antibodies (HACA) associated acute delayed hypersensitivity infusion reactions, antihuman (HAHAs), autoantibodies rare instances drug-induced lupus. Several cases non-Hodgkin's lymphoma also has described. Future studies should evaluate optimal timing duration therapy, utility adjuvant medical treatments during long-term safety various agents.