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OP0096 Tobacco smoking is associated with increased disease activity in HLA-B27 positive axial spondyloarthritis patients, but does not alter the course of disease activity
  1. A. Ciurea1,
  2. A. Scherer2,
  3. U. Weber3,
  4. M. Nissen4,
  5. P. Exer5,
  6. J. Bernhard6,
  7. G. Tamborrini7,
  8. R. Mueller8,
  9. B. Weiss3,
  10. R. Kissling3,
  11. B.A. Michel1,
  12. A. Finckh4
  13. on behalf of the Rheumatologists of SCQM
  1. 1University Hospital Zurich
  2. 2SCQM
  3. 3Balgrist University Hospital, Zurich
  4. 4University Hospital, Geneva
  5. 5Rheumatology Private practice, Basel
  6. 6Cantonal Hospital, Solothurn
  7. 7University Hospital, Zurich
  8. 8Cantonal Hospital, St.Gallen, Switzerland

Abstract

Background Smoking is associated with increased disease activity in patients with ankylosing spondylitis (AS) and early axial spondyloarthritis (SpA) in cross-sectional studies, however causation has not been established.

Objectives To investigate the impact of smoking on disease activity in patients with axial SpA.

Methods We included all patients from a Swiss population-based axial SpA cohort (SCQM) with available smoking and HLA-B27 status fulfilling the ASAS 2009 criteria for axial SpA. The primary and secondary outcomes for this analysis were the BASDAI and the AS disease activity score (ASDAS-CRP) respectively. The primary exposure of interest was smoking (ever/never) and a secondary analysis examined smoking as current/past/never. We compared clinical and demographic characteristics between smokers and non-smokers cross-sectionally. The course of BASDAI and ASDAS were analysed using random slope multivariate longitudinal regression models, adjusted for the following potential confounders: baseline levels of BASDAI or ASDAS, anti-TNF treatment, age at first symptoms, disease duration, gender, HLA-B27, BMI and education.

Results Of the 1129 patients who fulfilled our inclusion criteria, 60% fulfilled the modified New York criteria, 62% were smokers (37% current smokers, 25% past smokers), 84% were HLA-B27 positive, 66% were male, mean age was 39.7 years and mean symptom duration at baseline was 13,5 years. As shown in previous reports, smoking was associated with a higher level of baseline disease activity. Mean BASDAI levels were +0.7 (95% CI: +0.4;+1.0) higher in smokers, with no difference between former and current smokers (wilcoxon test p=0.6). The association of smoking and BASDAI levels varied with regards to HLA-B27 status in the adjusted model (effect modification by HLA-B27, p=0.004). The adjusted mean BASDAI levels were 0.8 (95% CI: +0.3;+1.4) higher in HLA-B27 smokers compared to non-smokers, while no significant differences were observed in HLA-B27 negative smokers (-0.35 [95% CI: -0.9;+0.2]). The adjusted longitudinal evolution of BASDAI was similar between smokers and non-smokers (p=0.7). Similar results were found using ASDAS as the outcome.

Conclusions In this large observational cohort of axial SpA, the cross-sectional associations between smoking and BASDAI or ASDAS levels depended on the HLA-B27 status; only HLA-B27 positive patients demonstrated increased disease activity with smoking. However, smoking did not alter the long-term evolution of BASDAI and ASDAS in axial SpA, challenging the notion of a causal effect of this environmental factor on disease activity.

Disclosure of Interest None Declared

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