Article Text
Abstract
Background Cigarette smoking is a well-established risk factor for several autoimmune diseases, but its role in primary Sjögren’s syndrome (pSS) remains unclear. Here, we investigated the association between cigarette smoking and subsequent development of pSS.
Methods Information on smoking habits was collected from lifestyle habit questionnaires of patients with pSS (n=815) and a matched control group (n=4425) for a case–control study. Differences in smoking exposure were analysed by conditional logistic regression. Potential interactions between smoking and risk-associated human leucocyte antigens (HLA) were assessed by multivariate regression.
Results The fraction of patients with pSS having ever smoked prior to diagnosis was lower than in controls (OR 0.67, 95% CI 0.55 to 0.81). Current smoking at diagnosis was also less prevalent in cases (OR 0.37, 95% CI 0.26 to 0.53). However, period prevalence of smoking during early adulthood was not statistically different from controls (OR 0.89, 95% CI 0.66 to 1.22) but markedly decreased over time. This was partly due to patients being more prone to stop smoking, starting already 30 years prior to diagnosis (OR 2.01, 95% CI 1.22 to 3.30). Smoking patterns were also stratified by autoantibody status, yielding similar estimates. No interaction effects between HLA-DRB1 haplotypes and smoking were observed.
Conclusion The observed smoking patterns indicate that individuals who develop pSS smoke equally much as the general population during early life but are then more prone to stop. The data can be interpreted as smoking conferring protective effects, or reflecting early symptoms of pSS that affect smoking habits, emphasising the slow, progressive development of the disease.
- Sjogren’s Syndrome
- Smoking
- Autoantibodies
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Footnotes
JM and AB contributed equally to this work.
Contributors AB, JM, LA and MW-H conceived the study. AB, ERA and MW-H coordinated data collection from patient questionnaires. MK, HFdE, SM-B, PE, TM, GN and AB recruited and characterised the patients. LP, IK and JH contributed with genotype and questionnaire data from controls. JM analysed the data with input from LA, MW-H and AB. AB and JM drafted the first manuscript with input from MW-H and LA. All authors participated in the editing of the manuscript until its final version.
Funding The study was supported by grants from the Swedish Research Council, the Swedish Rheumatism Association, the King Gustaf the V:th 80-year foundation, the Heart-Lung Foundation, the Freemason’s in Stockholm Foundation for Children’s Welfare, the Stockholm County Council, the Karolinska Institute, and the Torsten and Ragnar Söderberg Foundation. The SNP&SEQ Technology Platform in Uppsala is supported by Science for Life Laboratory, the Swedish Research Council (VR-RFI), Uppsala University, and the Knut and Alice Wallenberg Foundation.
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval The study was approved by the Regional Ethics Committee in Stockholm and all participants gave informed consent to participate.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement All data relevant to the study are included in the article or uploaded as supplemental information.
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