FRI0345 Association between cigarette smoking and systemic lupus erythematosus (SLE) – an updated meta-analysis of case-control and cohort studies
Authors: M.H.Y. Chua, I. A. T. Ng, A. Mak
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> While the association between cigarette smoking and the occurrence of SLE has been studied over the past two decades, conflicting results have rendered such association controversial. With the global increase in woman smokers and more prospective data addressing the risk of the development of SLE and cigarette smoking being available, it is timely to provide an update on the evidence of the relationship between cigarette smoking and the occurrence of SLE. <h3>Objectives</h3> To study the association between cigarette smoking and the odds, as well as the risk of SLE occurrence by meta-analyses of case-control and cohort studies. <h3>Methods</h3> We performed an extensive literature search using the relevant keywords including "systemic lupus erythematosus"; "lupus'; "smoking"; "cigarette smoking"; "environmental"; "autoimmune disease" and "connective tissue disease" in various combinations to identify case-control and cohort studies addressing the relationship between cigarette smoking and SLE published in English in computerised databases including PubMed (from 1966 to , Jan 2018 Embase (1980 to Jan 2018 and Cochrane Central Register of Control Trials (last quarter of 2017). Effect sizes were pooled as odds ratio (OR) and relative risk (RR) and the corresponding 95% CI for case-control and cohort studies, respectively. Heterogeneity was studied by I<sup>2</sup>. If the effect sizes were associated with low heterogeneity (I<sup>2</sup> &lt;40), the fixed effects model was used. Otherwise (I<sup>2</sup> ≥40), the random effects model was used, based on the model suggested by DerSimonian and Laird. <h3>Results</h3> Thirteen relevant studies (10 retrospective case-control and 3 cohort) were selected for these meta-analyses. Data were aggregated based on smoking statuses comprising current, past, ever and never smoking. Analyses of case-control studies revealed significant relationships between the occurrence of SLE and current smoking (OR 1.639 [1.171–2.295], p=0.004, I<sup>2</sup>=85.8), and ever smoking (OR 1.438 [1.037–1.995], p=0.029, I<sup>2</sup>=86.3). However, no significant relationship was found between the occurrence of SLE and past smoking (OR 1.208 [0.853–1.711], p=0.286 I<sup>2</sup>=74.7). While no relationship was found between the development of SLE and current smoking (RR 1.002 [0.680–1.475], p=0.994, I<sup>2</sup>=51.6), and ever smoking (RR 1.163 [0.944–1.433], p=0.157, I<sup>2</sup>=0) when the effect sizes of cohort studies were amalgamated, a significant risk in the development of SLE was found amongst ex-smokers compared with never smokers when the prospective data were combined (RR 1.351 [1.085–1.681], p=0.007, I<sup>2</sup>=28.0). <h3>Conclusions</h3> Smoking is associated with the occurrence of SLE based on the aggregation of effect sizes from case-control and cohort studies. The higher risk of development of SLE in ex-smokers but not among current and ever smokers compared to never smokers based on prospective data warrants further mechanistic studies to unravel the actual immunologic impact of cigarette smoke on SLE development in different subsets of SLE patients. <h3>Disclosure of Interest</h3> None declared