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Also, it has been recognized that early therapeutic intervention targeting remission improves clinical outcomes and reduces the accrual and progress of joint damage and disability.
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Currently, clinical remission or low disease activity are now realistic targets for the treatments, achieved by a large proportion of RA patients.
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However, the combined use of methotrexate, a standard synthetic disease-modifying anti-rheumatic drug (DMARD) and a biological DMARD targeting TNF, IL-6, and T cells has revolutionized treatment of RA. It is required to treat patients at a stage when the evolution of joint destruction can still be prevented. It is noteworthy that such a joint damage derived from synovial inflammation is apparent in the early stage of the disease. Auto-reactive T cells and inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin 6 (IL-6) play a pivotal role in the pathological processes of RA through the accumulation of inflammatory cells, the self-perpetuation of inflammation, and production of matrix metalloproteinase and induction and/or activation of osteoclasts, leading to destruction of cartilage and bone. It affects from 0.5% to 1.0% of adults with a 4-fold higher frequency in women than in men. Rheumatoid arthritis (RA) is a representative systemic autoimmune disease characterized with chronic and destructive inflammatory synovitis and multiple organ manifestations that causes severe disability and mortality. Contrarily, for established RA, fewer patients sustained remission after the discontinuation of biological DMARD and “deep remission” at the discontinuation was a key factor to keep the treatment holiday of biological DMARD. Recent reports indicate that more than half of early RA patients could discontinue TNF-targeted biological DMARD without clinical flare and functional impairment after obtaining clinical remission. On the other hand, discontinuation of a biological DMARD without disease flare is our next goal and desirable from the standpoint of risk reduction and cost effectiveness, especially for patients with clinical remission. Meanwhile, association of tofacitinib on carcinogenicity and malignancy is under debate and further investigation on post-marketing survey would be warranted. The efficacy was rapid and as strong as adalimumab, a TNF-inhibitor.
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Oral administration of tofacitinib targeting the Janus kinase (JAK) is significantly effective than placebo in active patients with methotrexatenaïve, inadequately responsive to methotrexate or tumor necrosis factor (TNF)-inhibitors. However, biological DMARD is limited to intravenous or subcutaneous uses and orally available small but strong molecules have been developed. Clinical remission is now realistic targets, achieved by a large proportion of RA patients, and rapid and appropriate induction of remission by intensive treatment with biological DMARD and methotrexate is prerequisite to halt joint damage and functional disabilities. However, the combined use of methotrexate, a synthetic disease-modifying antirheumatic drug (DMARD), and biologic DMARD has revolutionized treatment of RA. Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by inflammation and joint destruction that causes significant morbidity and mortality.