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目的:研究被动吸烟对RA自身抗体的产生及疾病活动、远期预后的影响。方法:收集湖北民族大学附属民大医院住院部的RA患者233例，进行问卷调查，包括记录患者性别、年龄、病程、工作环境、居住环境、吸烟时间年限及既往吸烟时间年限、每天吸烟量、长期接触吸烟人数及共同生活及工作时间年限。并记录RA患者的关节肿胀数、关节压痛数、实验室指标（抗CCP抗体、RF、ESR、CRP）。计算疾病活动评分[DAS28、简化的疾病活动指数（SDAI）、临床疾病活动指数（CDAI）]和改良的van der Heijde-Sharp评分（Sharp）评分。研究采用单因素方差分析、非参数秩和检验，Spearman相关分析进行统计学分析。结果:初治RA患者中，被动吸烟者的抗CCP抗体、RF、CDAI明显高于不吸烟者（80±75，n t=1.965，n P=0.047；102±72，n t=3.025，n P=0.008；31±15，n t=2.129，n P=0.037），吸烟者的抗CCP抗体、RF、ESR、CRP、DAS28、SDAI、CDAI均明显高于不吸烟者[90±81，n t=2.223，n P=0.030；134±85，n t=3.885，n P=0.000；79±39，n t=2.215，n P=0.037；52.40（25.00，89.31），n P=0.010；6.6±1.3，n t=3.405，n P=0.003；104±73，n t=2.727，n P=0.004；33±14，n t=2.698，n P=0.011]。复治RA患者中，被动吸烟者的DAS28、CDAI评分高于不吸烟者（33±14，n t=3.025，n P=0.005；28±15，n t=2.729，n P=0.013），吸烟者的DAS28、SDAI、CDAI评分明显高于不吸烟者（6.3±1.7，n t=3.602，n P=0.000；92±70，n t=1.968，n P=0.045；33±17，n t=3.565，n P=0.001）。吸烟、被动吸烟、不吸烟患者之间Sharp评分差异无统计学意义，Sharp评分与病程呈正相关（n r=0.532，n P=0.000）。n 结论:暴露于被动吸烟同吸烟一样会影响抗体的产生和疾病活动，即使经过正规治疗后这种影响仍然存在。关节影像学毁损情况与病程密切相关。“,”Objective:To study the effect of passive smoking on rheumatoid arthritis autoantibody production and disease activity.Methods:A total of 233 inpatients with RA were collected and surveyed. The demographic information, smoking status, laboratory parameters [anti-cyclic citrulline peptide (CCP) antibody, rheumatoid factor (RF), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP)] were recorded, and disease activity score in 28 joints (DAS28), simplified disease activity index (SDAI), clinical diseaseactivity index (CDAI), Sharp scores were calculated. The analysis performed were one-way analysis of variance, non parametric rank sum test, and spearman correlation analysis.Results:Among the first diagnosed RA patients, the anti-CCP antibodies, RF, and CDAI of passive smokers were significantly higher than those of non-smokers (80±75n , t=1.965, n P=0.047; 102±72n , t=3.025, n P=0.008; 31±15n ,t=2.129, n P=0.037). The anti-CCP antibodies, RF, ESR, CRP, DAS28, SDAI, and CDAI of smokers were all significantly higher than non-smokers [90±81n , t=2.223, n P=0.030; 134±85n , t=3.885n , P=0.000; 79±39n , t=2.215n , P=0.037; 54.20 (25.00, 89.31)n , P=0.010; 6.6±1.3n , t=3.405, n P=0.003; 104±73n , t=2.727, n P=0.004; 33±14n , t=2.698, n P=0.011]. Among treated RA patients, the DAS28 and CDAI scores of passive smokers were higher than those of non-smokers (33±14n , t=3.025, n P=0.005; 28±15n , t=2.729, n P=0.013), and the DAS28, SDAI and CDAI scores of smokers were significantly higher than those of non-smokers (6.3±1.7n , t=3.602, n P=0.000; 92±70n , t=1.968, n P=0.045; 33±17n , t=3.565, n P=0.001). There was no difference in Sharp score between smokers, passive smokers and non-smokers. The Sharp score was positively correlated with the course of the disease (n r=0.532, n P=0.000).n Conclusion:Exposure to passive smoking, is just like smoking, can affect antibody production and disease activityeven after regular treatment. The joint damage shown on imagesis closely related to the course of the disease.