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目的探讨肿瘤坏死因子-α(TNF-α)基因-238位点基因单核苷酸多态性(SNP)与Infliximab(英夫利昔单抗)治疗类风湿性关节炎(RA)疗效的相关性。方法对102例中国RA患者使用Infliximab进行治疗,以28处关节疾病活动度评分(DAS28)、健康评估问卷(HAQ)评分及美国风湿病学会(ACR)与欧洲抗风湿病联盟(EULAR)共同制定的RA临床缓解新标准为工具,评估Infliximab对RA的疗效。采用TaqMan MGB探针法检测TNF-α基因-238位点的SNP。统计分析TNF-α基因-238位点的SNP与Infliximab治疗RA疗效的相关性。结果具有GG基因型的RA患者在治疗后DAS28评分和HAQ评分均显著降低(P<0.05),而具有AA基因型及AG基因型的RA患者在治疗后DAS28评分和HAQ评分均无显著变化(P>0.05)。具有GG基因型的RA患者在治疗后达到临床缓解新标准的比例为91.8%,显著高于非GG基因型的RA患者。除有2例RA患者因对Inflix-imab过敏而退出试验外,未见结核、肿瘤发生等严重不良反应。结论 TNF-α基因-238位点的SNP与Inflix-imab治疗RA疗效可能相关,具有GG基因型的RA患者对Infliximab的疗效反应较好,而具有AA基因型及AG基因型的RA患者疗效反应则相对较差。
Objective To investigate the association between the single nucleotide polymorphism (SNP) at the -238 locus of tumor necrosis factor-α (TNF-α) and infliximab (rheumatoid arthritis) in the treatment of rheumatoid arthritis . Methods A total of 102 RA patients in China were treated with Infliximab, and 28 joint disease activity score (DAS28), health assessment questionnaire (HAQ) score and American College of Rheumatology (ACR) and European Rheumatism Alliance (EULAR) Of the RA clinical remission of new standards as a tool to assess the efficacy of Infliximab on RA. The SNP of -238 site of TNF-α gene was detected by TaqMan MGB probe. Statistical analysis of TNF-α gene -238 SNP and Infliximab treatment of RA correlation. Results The RA patients with GG genotype had significantly lower DAS28 scores and HAQ scores after treatment (P <0.05), while RA patients with AA genotype and AG genotype had no significant changes in DAS28 score and HAQ score after treatment P> 0.05). RA patients with GG genotype achieved 91.8% of new clinical remission criteria after treatment, significantly higher than non-GG genotype RA patients. In addition to two patients with RA due to allergies to Inflix-imab exit the test, no tuberculosis, tumor and other serious adverse reactions. Conclusions The SNP at -238 locus of TNF-α gene may be related to the efficacy of Inflix-imab in the treatment of RA. The RA patients with GG genotype respond better to Infliximab, while the RA patients with AA genotype and AG genotype respond to the response It is relatively poor.