AB0740 Smoking Impact in the Effectiveness of Anti-Tumour Necrosis Factor-Alpha Therapy in Portuguese Spondyloarthritis Patients
Authors: F. Aguiar, D. Rosa-Gonçalves, R. Fonseca, R. Vieira, P. Madureira, A. Bernardo, M. Bernardes, I. Brito, L. Costa
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Background</h3> Tumour necrosis factor alpha (TNF-α) plays an important role in the pathogenesis of spondyloarthritis (SpA) and the advent of anti-TNF-α therapy represented a major therapeutic advancement in its treatment. There is evidence that cigarette smoking increases the production of TNF-α and reduces the effectiveness of anti-TNF drugs in patients with rheumatoid arthritis. In early axial SpA it was demonstrated that smoking was independently associated with higher disease activity, increased structural axial damage, poorer functional status and poorer quality of life. However, there are few studies investigating the effect of smoking in SpA patients using anti-TNF-α drugs. <h3>Objectives</h3> To investigate whether smoking influences the effectiveness of anti-TNF-α therapy in SpA patients. <h3>Methods</h3> This is a retrospective study, including all SpA patients that started anti-TNFα treatment in the last decade at a Rheumatology Department of a Portuguese University Hospital. All the information, including demographic and clinical features, measures of disease activity, functional impairment and metrology at baseline, as well as outcome measures at 6 and 12 months after starting an anti-TNF-α agent were obtained from our national database for rheumatic patients. Sixteen out of a total of 128 patients were excluded from the study due to incomplete data. The statistical analysis was performed using SPSS 21.0 software, and p&lt;0.05 was taken to indicate statistical significance. To compare the differences in the groups of ever-smokers and never smokers at baseline, 6 and 12 months Mann-Whitney U, χ<sup>2</sup> and Fisher tests were used. <h3>Results</h3> A total of 112 patients were included, with 59.8% males, median age of 45 (range 26-73), 52.3% never-smokers, 18.3% ex-smokers and 29.2% current smokers. Patients were stratified into 2 groups: ever-smokers (52.3%) (current smokers and ex-smokers) and non-smokers (47.7%). At baseline, there were significant differences between ever-smokers and non-smokers for gender (p=0.002), BASDAI (p=0.02) and BASMI (p=0.014): ever-smokers were more likely to be male; BASDAI was lower in ever-smokers (median 5.8) than in non-smokers (median 6.7) and BASMI was lower in non-smokers (median 4.6) than in ever-smokers (median 6.4). There were no statistic significant differences in age, disease duration, baseline BASFI or ASDAS. In the evaluation of the response to anti-TNF-α therapy there was no difference between the two groups in the proportion of patients meeting ASAS 40 at 6 (p=0.678) and 12 months (p=0.4) or at ASDAS response at 12 months (p=0.692). However we found difference in the ASDAS response at 6 months (p=0.042), which was more favorable in ever-smokers. <h3>Conclusions</h3> In this study it was not possible to demonstrate that smoking had an effect on the response to anti-TNF-α therapy, even though there was a more favorable ASDAS response at 6 months in ever-smokers. However, this was a heterogeneous group of patients, with some different baseline characteristics, and possibly other variables not included in the analysis could have confounded the results. More studies, with larger sample sizes and longer follow-up time, should be undertaken to assess this subject. <h3>Disclosure of Interest</h3> None declared