慢性関節リウマチ Rheumatoid arthritis.:Rheumatoid arthritis

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Rheumatoid arthritis is a chronic inflammatory disease of joints with the potential to cause substantial joint damage and disability. Proinflammatory cytokines(TNF<I>α</I>, IL-6, IL-1) have recently been shown to play important roles in the pathogenesis of rheumatoid arthritis. In addition, advances in the field of genetic engineering have made possible therapies using monoclonal antibody targeting specific inflammatory mediators. Infliximab is a chimeric anti-TNF<I>α</I> monoclonal antibody that is already available for rheumatoid arthritis patients in the United States and European countries following the results of multiple double-blinded placebo-controlled trials. Infliximab has been demonstrated to improve symptoms and signs of synovitis, and to prevent radiographic evidence of progeressive joint damage in a majority of patients with rheumatoid arthritis. However, increased susceptibility to infection is a potential concern with agents inhibiting TNF<I>α</I> as the cytokine plays a central role in host defense. In fact, several kinds of infection, including tuberculosis, have been reported as adverse events following anti-TNF<I>α</I> blockade therapy. Physicians are therefore recommended to screen patients for latent tuberculosis infection or disease before initiating such therapies. IL-6 is likely to be involved in the pathogenesis of rheumatoid arthritis in addition to TNF<I>α</I>. Clinical trials into IL-6 blockade therapy using complementarity determining regions (CDR)-grafted anti-human IL-6 receptor monoclonal antibody have therefore started. In the near future, these anti-cytokine therapies will become part of the standard armamentarium for the treatment of rheumatoid arthritis in Japan.

収録刊行物

  • Drug delivery system

    Drug delivery system 17(1), 50-57, 2002-01-10

    日本DDS学会

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各種コード

  • NII論文ID(NAID)
    10008132059
  • NII書誌ID(NCID)
    AN10084591
  • 本文言語コード
    JPN
  • 資料種別
    REV
  • ISSN
    09135006
  • データ提供元
    CJP書誌  CJP引用  J-STAGE 
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