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