Environmental Autoimmunity Group, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD.
Environmental Autoimmunity Group, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD.
Semin Arthritis Rheum. 2018 Dec;48(3):504-512. doi: 10.1016/j.semarthrit.2018.02.003. Epub 2018 Feb 14.
Cigarette smoking is associated with immune-mediated disorders. We explored the contribution of smoking to polymyositis (PM) and dermatomyositis (DM) phenotypes and attempted to determine whether cigarette smoking effects differ by race and genotype.
Associations of tobacco smoking with disease features, autoantibodies, HLA types, and race were evaluated using multiple logistic regressions in 465 patients.
Caucasian ever-smokers (n = 140) were more likely to have PM (adjusted OR = 2.24, 95% CI: 1.41\x963.57), anti-synthetase (adjusted OR = 1.93, 95% CI: 1.12\x963.34) and anti-Jo-1 autoantibodies (adjusted OR = 1.94, 95% CI: 1.08\x963.46) and less likely to have anti-p155/140 autoantibodies (adjusted OR = 0.36, 95% CI: 0.14\x960.92). In Caucasians, ever-smokers had a greater interstitial lung disease (ILD) frequency than never-smokers, while in African-Americans this relationship was inverted, but neither trend reached statistical significance. Pack-years of cigarette smoking showed significant positive associations with PM (adjusted OR = 1.02, 95% CI: 1.002\x961.04) and ILD (adjusted OR = 1.02, 95% CI: 1.001\x961.03) and was inversely associated with anti-p155/140 autoantibodies (adjusted OR = 0.93, 95% CI: 0.87\x960.99) in Caucasians. Caucasian heavy smokers (=20 pack-years) were more likely to have PM (adjusted OR = 2.52, 95% CI: 1.25\x965.09), ILD (adjusted OR = 2.48, 95% CI: 1.23\x965.00) and anti-Jo-1 autoantibodies (adjusted OR = 2.65, 95% CI: 1.16\x966.08) than never-smokers. In Caucasians, compared to never-smokers without HLA-DRB103:01 allele, ever-smokers with HLA-DRB103:01 allele had the highest odds of PM, ILD, ASA, and anti-Jo-1 autoantibodies. Risks for those with only one of these two factors were intermediate. An inverse pattern was observed regarding anti-p155/140 autoantibodies.
Tobacco smoking was associated with clinical and autoantibody phenotypes in Caucasians. Our findings also suggest possible interactions among HLA-DRB1*03:01 and smoking on the risk of PM and ILD, as well as, anti-synthetase, anti-Jo-1, and anti-p155/140 autoantibodies in Caucasians.
吸烟与免疫介导的疾病有关。我们探讨了吸烟对多发性肌炎(PM)和皮肌炎(DM)表型的贡献,并试图确定吸烟的影响是否因种族和基因型而异。
采用多元逻辑回归分析了 465 例患者的烟草吸烟与疾病特征、自身抗体、HLA 类型和种族的关系。
白种人曾吸烟者(n = 140)更易患 PM(调整后的 OR = 2.24,95%CI:1.41-3.57)、抗合成酶(调整后的 OR = 1.93,95%CI:1.12-3.34)和抗 Jo-1 自身抗体(调整后的 OR = 1.94,95%CI:1.08-3.46),不太可能患有抗 p155/140 自身抗体(调整后的 OR = 0.36,95%CI:0.14-0.92)。在白种人中,曾吸烟者比从不吸烟者更易发生间质性肺病(ILD),而在非裔美国人中则相反,但这两种趋势均未达到统计学意义。吸烟的烟龄与 PM(调整后的 OR = 1.02,95%CI:1.002-1.04)和 ILD(调整后的 OR = 1.02,95%CI:1.001-1.03)呈显著正相关,与抗 p155/140 自身抗体呈负相关(调整后的 OR = 0.93,95%CI:0.87-0.99)在白种人中。白种人重度吸烟者(≥20 包年)更易患 PM(调整后的 OR = 2.52,95%CI:1.25-5.09)、ILD(调整后的 OR = 2.48,95%CI:1.23-5.00)和抗 Jo-1 自身抗体(调整后的 OR = 2.65,95%CI:1.16-6.08)比从不吸烟者。在白种人中,与没有 HLA-DRB103:01 等位基因的从不吸烟者相比,携带 HLA-DRB103:01 等位基因的曾吸烟者患 PM、ILD、ASA 和抗 Jo-1 自身抗体的可能性最高。仅具有这两个因素之一的人的风险处于中间水平。关于抗 p155/140 自身抗体,观察到一种相反的模式。
吸烟与白种人的临床和自身抗体表型有关。我们的研究结果还表明,HLA-DRB1*03:01 和吸烟之间可能存在相互作用,可能会增加白种人患 PM 和 ILD 的风险,以及抗合成酶、抗 Jo-1 和抗 p155/140 自身抗体的风险。