The effect of cigarette smoking on the clinical and serological phenotypes of polymyositis and dermatomyositis

Adam Schiffenbauer, Sara Faghihi-Kashani, Terrence P. O'Hanlon, Willy A. Flegel, Sharon D. Adams, Ira N. Targoff, Chester V. Oddis, Steven R. Ytterberg, Rohit Aggarwal, Lisa Christopher-Stine, Ejaz A. Shamim, Paul F. Dellaripa, Sonye K. Danoff, Andrew L. Mammen, Frederick W. Miller

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


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\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-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.

Original languageEnglish (US)
Pages (from-to)504-512
Number of pages9
JournalSeminars in Arthritis and Rheumatism
Issue number3
StatePublished - Dec 2018


  • Autoantibody
  • Autoimmunity
  • Cigarette smoking
  • Dermatomyositis
  • Polymyositis
  • Smoking

ASJC Scopus subject areas

  • Rheumatology
  • Anesthesiology and Pain Medicine


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