类风湿关节炎药物治疗进展（Advances in the treatment of rheumatoid arthritis）.docVIP

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类风湿关节炎药物治疗进展（Advances in the treatment of rheumatoid arthritis）.doc

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类风湿关节炎药物治疗进展（Advances in the treatment of rheumatoid arthritis）

类风湿关节炎药物治疗进展（Advances in the treatment of rheumatoid arthritis） Advances in the treatment of rheumatoid arthritis 2011-01-16 Ye Shuangsun Lingyun! The treatment for rheumatoid arthritis (RA) is divided into classic nonsteroidal anti-inflammatory drugs (NSAIDs) and antirheumatic drugs (DMARDs), or slow acting antirheumatic drugs (SAARDs), that are used as second-line drugs. Since bone erosion occurs in 90% of RA patients within 2 years of onset, strategies for early active use of DMARDs have been widely accepted [1]. However, due to the severe side effects and / or poor efficacy of the drugs, the average length of time for patients to use DMARDs is only 2~3 years, and only 20% of the total number of patients over 5 years. In recent years, with the in-depth study of the pathogenesis of RA, new immunosuppressive agents and modulators for blocking the target sites in the pathogenesis of RA have been published, and have achieved encouraging results. Several new drugs are introduced as follows. 1 cytokine antagonists (etanercept/remicade) The pathological characteristics of RA are: activated T cells, macrophages, plasma cells and other inflammatory cells infiltration of synovial membrane, and secrete a large number of cytokines, which mediated the formation of synovial immune inflammation. In the study of RA cytokines, tumor necrosis factor (TNF) has attracted much attention [2]. TNF alpha is now thought to initiate a cascade reaction of RA cytokines (cytokine, cascade). Animal experiments confirmed that transgenic mice overexpressing TNF gene may develop arthritis, and anti TNF alpha monoclonal antibody can inhibit the disease; in addition, anti TNF alpha monoclonal antibody has inhibitory effect on collagen induced arthritis. The anti rheumatism action mechanism of gold salt may also play a therapeutic effect through transcriptional repression of TNF alpha and other DMARDs such as methotrexate (MTX) and D- penicillamines also interfere with the role of TNF produced, sug