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Ann Rheum Dis doi:10.1136/annrheumdis-2013-205159
  • Clinical and epidemiological research
  • Extended report

Cigarette smoking, antiphospholipid antibodies and vascular events in Systemic Lupus Erythematosus

  1. Elisabet Svenungsson1
  1. 1Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Solna, Karolinska Institutet, Stockholm, Sweden
  2. 2Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
  3. 3Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Huddinge, Karolinska Institutet, Stockholm, Sweden
  4. 4Department of Immunology, Genetics and Pathology, Rudbeck Laboratory C5, Uppsala University, Uppsala, Sweden
  5. 5Unit of Clinical Immunology, Department of Clinical Immunology and Transfusion Medicine, Karolinska University Hospital, Solna, Karolinska Institutet, Stockholm, Sweden
  1. Correspondence to Dr Johanna Gustafsson, Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Stockholm 171 76, Sweden; johanna.gustafsson{at}karolinska.se
  • Received 27 December 2013
  • Revised 10 March 2014
  • Accepted 16 March 2014
  • Published Online First 1 April 2014

Abstract

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-β2 glycoprotein-1 (aβ2GP1) 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 aβ2GP1 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.