Tobacco smoking was associated with clinical and autoantibody phenotypes in Caucasians. - GreenMedInfo Summary
The effect of cigarette smoking on the clinical and serological phenotypes of polymyositis and dermatomyositis.
Semin Arthritis Rheum. 2018 Feb 14. Epub 2018 Feb 14. PMID: 29703532
Adam Schiffenbauer
OBJECTIVE: 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.
METHODS: Associations of tobacco smoking with disease features, autoantibodies, HLA types, and race were evaluated using multiple logistic regressions in 465 patients.
RESULTS: Caucasian ever-smokers (n = 140) were more likely to have PM (adjusted OR = 2.24, 95% CI: 1.41-3.57), anti-synthetase (adjusted OR = 1.93, 95% CI: 1.12-3.34) and anti-Jo-1 autoantibodies (adjusted OR = 1.94, 95% CI: 1.08-3.46) and less likely to have anti-p155/140 autoantibodies (adjusted OR = 0.36, 95% CI: 0.14-0.92). 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: 1.002-1.04) and ILD (adjusted OR = 1.02, 95% CI: 1.001-1.03) and was inversely associated with anti-p155/140 autoantibodies (adjusted OR = 0.93, 95% CI: 0.87-0.99) in Caucasians. Caucasian heavy smokers (≥20 pack-years) were more likely to have PM (adjusted OR = 2.52, 95% CI: 1.25-5.09), ILD (adjusted OR = 2.48, 95% CI: 1.23-5.00) and anti-Jo-1 autoantibodies (adjusted OR = 2.65, 95% CI: 1.16-6.08) than never-smokers. In Caucasians, compared to never-smokers without HLA-DRB1*03:01 allele, ever-smokers with HLA-DRB1*03:01 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.
CONCLUSION: 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.
