TY - JOUR
T1 - The effect of cigarette smoking on the clinical and serological phenotypes of polymyositis and dermatomyositis
AU - Schiffenbauer, Adam
AU - Faghihi-Kashani, Sara
AU - O'Hanlon, Terrence P.
AU - Flegel, Willy A.
AU - Adams, Sharon D.
AU - Targoff, Ira N.
AU - Oddis, Chester V.
AU - Ytterberg, Steven R.
AU - Aggarwal, Rohit
AU - Christopher-Stine, Lisa
AU - Shamim, Ejaz A.
AU - Dellaripa, Paul F.
AU - Danoff, Sonye K.
AU - Mammen, Andrew L.
AU - Miller, Frederick W.
N1 - Funding Information:
This research was supported in part by the Intramural Research Programs of the NIH, National Institute of Environmental Health Sciences, National Institute of Arthritis and Musculoskeletal and Skin Diseases, and NIH Clinical Center (Project ID Z99 CL999999)
Funding Information:
Ira Targoff reports grants and non-financial support from Oklahoma Medical Research Foundation during the conduct of the study. Rohit Aggarwal reports personal fees from BMS, personal fees from Novartis, personal fees from Octapharma, personal fees from Mallinckrodt, grants from BMS, grants from Mallinckrodt, grants from Pfizer and grants from Momenta outside the submitted work. Lisa Christopher-Stine reports personal fees from Novartis, personal fees from Option Care, personal fees from Idera, grants from CSL Behring, personal fees from Mallinckrodt, and other from Inova Diagnostics outside the submitted work. In addition, Lisa Christopher-Stine has a patent on Detection of HMGCoA reductase (HMGCR) Antibodies in Patient Sera with royalties paid outside the submitted work. Paul Dellaripa reports non-financial support from Boehringer Ingelheim, other from UpToDate and other from Genentech outside the submitted work. The other authors have nothing to disclose.
Publisher Copyright:
© 2018 Elsevier Inc.
PY - 2018/12
Y1 - 2018/12
N2 - 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.
AB - 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.
KW - Autoantibody
KW - Autoimmunity
KW - Cigarette smoking
KW - Dermatomyositis
KW - Polymyositis
KW - Smoking
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U2 - 10.1016/j.semarthrit.2018.02.003
DO - 10.1016/j.semarthrit.2018.02.003
M3 - Article
C2 - 29703532
AN - SCOPUS:85046152397
SN - 0049-0172
VL - 48
SP - 504
EP - 512
JO - Seminars in Arthritis and Rheumatism
JF - Seminars in Arthritis and Rheumatism
IS - 3
ER -