期刊
ANNALS OF THE RHEUMATIC DISEASES
卷 72, 期 -, 页码 124-127出版社
BMJ PUBLISHING GROUP
DOI: 10.1136/annrheumdis-2012-202350
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资金
- Ministry of Health, Labor and Welfare of Japan
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- University of Occupational and Environmental Health, Japan
- Mitsubishi-Tanabe Pharma Corporation
- Abbott Japan
- Eisai
- Chugai Pharmaceutical
- Janssen Pharmaceutical
- Santen Pharmaceutical
- Pfizer Japan
- Astellas Pharma
- Daiichi-Sankyo
- GlaxoSmithKline
- Astra-Zeneca
- Otsuka Pharmaceutical
- Actelion Pharmaceuticals Japan
- Eli Lilly Japan
- Nippon Kayaku
- UCB Japan
- Quintiles Transnational Japan
- Ono Pharmaceutical
- Bristol-Myers Squibb
- MSD
Biological agents targeting tumour necrosis factor (TNF) have revolutionised the treatment of rheumatoid arthritis (RA) and clinical remission has become a realistic treatment goal. Discontinuing anti-TNF therapy after sustained remission has emerged as an important area of investigation in rheumatology from the risk-benefit point of view, including health economic considerations. However, there is little information as to whether 'biologic-free remission' is possible after sustained remission following intensive treatment with TNF inhibitors in RA. European studies such as BeSt and OPTIMA in patients with early RA and Japanese studies such as remission induction by remicade in patients with RA and HONOR in patients with long-standing RA encountered during routine clinical practice have shown that, after a reduction in disease activity to clinical remission or low disease activity by infliximab or adalimumab in combination with methotrexate, patients can successfully remain in clinical remission without TNF inhibitors with no radiological and functional damage progression of articular destruction. Experimental findings in TNF-deficient mouse models suggest that TNF inhibitors may change the disease process of RA and bring about the potential of immunological remission, raising the possibility of a 'treatment holiday' of TNF inhibitors after intensive treatment.
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