医学
巴斯代人
强直性脊柱炎
内科学
轴性脊柱炎
队列
戒烟
HLA-B27
混淆
人口
物理疗法
队列研究
疾病
银屑病性关节炎
骶髂关节炎
免疫学
人类白细胞抗原
病理
环境卫生
抗原
作者
Adrian Ciurea,Almut Scherer,Ulrich Weber,Michael J. Nissen,Pascale Exer,Jürg Bernhard,Giorgio Tamborrini,Ruediger B. Müeller,Bettina Weiss,R Kissling,BA Michel,Axel Finckh
标识
DOI:10.1136/annrheumdis-2012-eular.1779
摘要
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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