Journal
ANNALS OF THE RHEUMATIC DISEASES
Volume 74, Issue 8, Pages 1537-1543Publisher
BMJ PUBLISHING GROUP
DOI: 10.1136/annrheumdis-2013-205159
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Funding
- Swedish Heart-Lung Foundation
- Stockholm County Council
- Karolinska Institutet (ALF)
- The King Gustaf V 80th Birthday Fund
- The Swedish Rheumatism Association
- The Swedish research council
- The Ake Wiberg Foundation
- Alex and Eva Wallstroms Foundation
- Karolinska Institutet's Foundations
- The Foundation in memory of Clas Groschinsky
- Swedish Society of Medicine
- Strategic Research Program in Epidemiology at Karolinska Institutet, Sweden
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Objective Smoking can induce autoantibodies in persons who are genetically predisposed to rheumatoid arthritis. We investigated the association between smoking and antiphospholipid antibodies (aPL) in systemic lupus erythematosus (SLE), a question not previously addressed. Further, we explored the relationship between smoking, aPL and vascular events (arterial and venous, VE). Methods In this cross-sectional study, clinical evaluation and questionnaire data were collected from 367 prevalent SLE patients. At the same time, we measured aPL (anticardiolipin (aCL), anti-beta(2) glycoprotein-1 (a beta(2)GP1) antibodies IgG/IgM/IgA, and lupus anticoagulant (LA)), and a large set of other SLE-associated autoantibodies for comparison. Association analyses using logistic regression models with smoking, (ever, former and current with never as reference) and antibody status as outcome variable were performed. As a secondary outcome, we investigated the associations between aPL, smoking and VE. Results In multivariable-adjusted models ever, and in particular former, cigarette smoking was associated with the most pathogenic aPL; LA, aCL IgG and a beta(2)GP1 IgG. Other SLE-associated autoantibodies were not associated with smoking. The combination of smoking and aPL was strongly associated with VE. We noted a positive interaction between smoking-LA and smoking-'triple aPL' positivity for previous VE. Conclusions We investigated a large set of commonly occurring autoantibodies in SLE, but only aPL were positively associated with a history of smoking. This association was especially apparent in former smokers. Among ever regular smokers who were aPL positive, we observed a strikingly high frequency of former VE. The underlying mechanisms and temporality between smoking, aPL and VE need further investigations.
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