The effect of cigarette smoking on the clinical and serological phenotypes of polymyositis and dermatomyositis.
Słowa kluczowe
Abstrakcyjny
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.
CONCLUSIONS
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.
