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 journalArticle

5 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
JournalSeminars in Arthritis and Rheumatism
DOIs
StateAccepted/In press - Jan 1 2018

Fingerprint

Dermatomyositis
Autoantibodies
Smoking
Polymyositis
Phenotype
Interstitial Lung Diseases
Ligases
Alleles
Immune System Diseases
African Americans
Logistic Models
Genotype

Keywords

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

ASJC Scopus subject areas

  • Rheumatology
  • Anesthesiology and Pain Medicine

Cite this

Schiffenbauer, A., Faghihi-Kashani, S., O'Hanlon, T. P., Flegel, W. A., Adams, S. D., Targoff, I. N., ... Miller, F. W. (Accepted/In press). The effect of cigarette smoking on the clinical and serological phenotypes of polymyositis and dermatomyositis. Seminars in Arthritis and Rheumatism. https://doi.org/10.1016/j.semarthrit.2018.02.003

The effect of cigarette smoking on the clinical and serological phenotypes of polymyositis and dermatomyositis. / Schiffenbauer, Adam; Faghihi-Kashani, Sara; O'Hanlon, Terrence P.; Flegel, Willy A.; Adams, Sharon D.; Targoff, Ira N.; Oddis, Chester V.; Ytterberg, Steven R; Aggarwal, Rohit; Christopher-Stine, Lisa; Shamim, Ejaz A.; Dellaripa, Paul F.; Danoff, Sonye K.; Mammen, Andrew L.; Miller, Frederick W.

In: Seminars in Arthritis and Rheumatism, 01.01.2018.

Research output: Contribution to journalArticle

Schiffenbauer, A, Faghihi-Kashani, S, O'Hanlon, TP, Flegel, WA, Adams, SD, Targoff, IN, Oddis, CV, Ytterberg, SR, Aggarwal, R, Christopher-Stine, L, Shamim, EA, Dellaripa, PF, Danoff, SK, Mammen, AL & Miller, FW 2018, 'The effect of cigarette smoking on the clinical and serological phenotypes of polymyositis and dermatomyositis', Seminars in Arthritis and Rheumatism. https://doi.org/10.1016/j.semarthrit.2018.02.003
Schiffenbauer, Adam ; Faghihi-Kashani, Sara ; O'Hanlon, Terrence P. ; Flegel, Willy A. ; Adams, Sharon D. ; Targoff, Ira N. ; Oddis, Chester V. ; Ytterberg, Steven R ; Aggarwal, Rohit ; Christopher-Stine, Lisa ; Shamim, Ejaz A. ; Dellaripa, Paul F. ; Danoff, Sonye K. ; Mammen, Andrew L. ; Miller, Frederick W. / The effect of cigarette smoking on the clinical and serological phenotypes of polymyositis and dermatomyositis. In: Seminars in Arthritis and Rheumatism. 2018.
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title = "The effect of cigarette smoking on the clinical and serological phenotypes of polymyositis and dermatomyositis",
abstract = "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.",
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author = "Adam Schiffenbauer and Sara Faghihi-Kashani and O'Hanlon, {Terrence P.} and Flegel, {Willy A.} and Adams, {Sharon D.} and Targoff, {Ira N.} and Oddis, {Chester V.} and Ytterberg, {Steven R} and Rohit Aggarwal and Lisa Christopher-Stine and Shamim, {Ejaz A.} and Dellaripa, {Paul F.} and Danoff, {Sonye K.} and Mammen, {Andrew L.} and Miller, {Frederick W.}",
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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.

PY - 2018/1/1

Y1 - 2018/1/1

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: 1.41–3.57), 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.

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: 1.41–3.57), 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.

KW - Autoantibody

KW - Autoimmunity

KW - Cigarette smoking

KW - Dermatomyositis

KW - Polymyositis

KW - Smoking

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