Cigarette Smoking In Pss: Association With Earlier Onset, Male Sex And Serum Baff Increase In The Assess Cohort

Background Smoking is well known to contribute to the pathogenesis and severity of some systemic autoimmune rheumatic diseases. Objectives We therefore investigated the association between smoking and disease activity, dryness, autoantibody secretion, and markers of B-cell activation, in primary Sjogren’s syndrome, using the prospective ASSESS cohort. Methods Three hundred and ninety five patients with pSS according to American-European Consensus Criteria (AECG) were included from fifteen centers of Rheumatology and Internal Medicine in the “Assessment of Systemic Signs and Evolution of Sjogren’s Syndrome” (ASSESS) 5-year prospective cohort. At enrollment, disease activity was assessed using the EULAR Sjogren’s Syndrome Disease Activity Index (ESSDAI), and DNA, RNA and serum were collected. Patients were also asked about their current, former or absence of use of tobacco. Results 286 patients had never smoked (73.1%), 72 did previously (18.4%) and 33 (8.4%) were smoking at enrollment in the ASSESS cohort (4 missing data). 56.0% of men with pSS were ever smokers (current or past use of tobacco) compared to 24.0% of women (p=0.0007). Ever smokers were younger at diagnosis than never smokers (49 [41.3-56 years] vs 54 [44.9-61] years, P=0.006).No difference was observed regarding previous systemic involvement, including history of lymphoma, between ever and non smokers The ESSDAI score (2 [0-6.6] vs 2 [0-7], P=0.4) and proportion of patients with active systemic involvement at enrollment, (30.4% vs 31.0%), including lung involvement, were not significantly increased in current smokers. The ESSPRI score was not significantly different either. Unstimulated salivary flow was less frequently decreased in current smokers (28.0% vs 51.5%, P=0.04) but results of Schirmer’s test were similar. Positivity of anti-SSA/anti-SSB and RF was similar in ever than in non smokers. The proportion of focus score ≥1 was similar among ever and non smokers (92.3% vs 89.8%, P=0.3). Serum BAFF was significantly increased in active smokers (1091.8 [828.4-1422.7] vs 896.7 [705.1-1168.0], P=0.02). No increase in other markers of B-cell activation (beta2-microglobulin, IgG, IgA, and IgM, free light chains of immunoglobulins) was observed in current smokers. Conclusions Smoking is more frequent in male patients with pSS and is associated with an earlier disease onset and serum BAFF increase. These data are in accordance with a recent immunohistochemical study showing an increase of BAFF pulmonary expression in smokers, independently of autoimmunity. These results add to the rationale of discontinuing smoking in autoimmune diseases, including pSS. Disclosure of Interest None Declared