Schiffenbauer A, et al. - Herein the authors assessed the contribution of smoking in causing polymyositis (PM) and dermatomyositis (DM) phenotypes. They also evaluated if the smoking effects of cigarette varied by race and genotype. In Caucasians, tobacco smoking was associated with clinical and autoantibody phenotypes. Results demonstrated probable interactions between HLA-DRB1*03:01 and smoking on the risk of PM and interstitial lung disease (ILD), along with anti-synthetase, anti-Jo-1 and anti-p155/140 autoantibodies in Caucasians.

Methods

• Using multiple logistic regressions, relationships of tobacco smoking with disease features, autoantibodies, HLA types and race were assessed in 465 patients.

Results

• Experts noted that 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 as compared to never-smokers.
• In African-Americans this association was inverted, but none of the trends reached statistical significance.
• Significant positive associations were found between pack-years of cigarette smoking 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 related to anti-p155/140 autoantibodies (adjusted OR=0.93, 95%CI:0.87-0.99) in Caucasians.
• Findings suggested that Caucasians 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) compared to never-smokers.
• While comparing Caucasians with 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.
• Intermediate risks were noted for those with only one of these two factors.
• Results demonstrated an inverse pattern regarding anti-p155/140 autoantibodies.