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Impaired response to treatment with tumour necrosis factor α inhibitors in smokers with axial spondyloarthritis

Impaired response to treatment with tumour necrosis factor α inhibitors in smokers with axial spondyloarthritis Impaired response to treatment with tumour necrosis factor α inhibitors in smokers with axial spondyloarthritis
Impaired response to treatment with tumour necrosis factor α inhibitors in smokers with axial spondyloarthritis Impaired response to treatment with tumour necrosis factor α inhibitors in smokers with axial spondyloarthritis

To investigate the impact of smoking on the response to treatment with a first tumour necrosis factor inhibitor (TNFi) in patients with axial spondyloarthritis (axSpA) in a real-life cohort.

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Key take away

The smokers suffering from Axial spondylitis (axSpA) might be deprived of the advantages of tumor necrosis alpha (TNF-α) blocking drugs. This can be seen especially if they have elevated levels of C-reactive protein.

Background

To investigate the impact of smoking on the response to treatment with a first tumour necrosis factor inhibitor (TNFi) in patients with axial spondyloarthritis (axSpA) in a real-life cohort.

Method

Patients fulfilling the Assessment of SpondyloArthritis international Society (ASAS) classification criteria for axSpA in the Swiss Clinical Quality Management Cohort were included in this study. The potential association between smoking status and differential response to TNFi in terms of Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Ankylosing Spondylitis Disease Activity Score (ASDAS) was analysed using multiple adjusted longitudinal mixed effect models. Binary response rates at 1 year were assessed with multiple adjusted logistic analyses.

Result

A first TNFi was initiated in 698 patients with axSpA with available smoking status and a baseline or follow-up BASDAI assessment, of which 490 (70%) had complete co-variate data. In comparison to non-smokers, current smokers demonstrated significantly smaller reductions in BASDAI and ASDAS scores upon treatment with TNFi (0.75 BASDAI units and 0.69 ASDAS units less, p=0.005 and 0.001, respectively) for patients with elevated baseline C-reactive protein (CRP) level. This effect was numerically smaller in patients with normal CRP. The odds for reaching a 50% improvement in BASDAI response or the ASAS criteria for 40% improvement after 1 year were significantly lower in current smokers than in non-smokers (0.54, 95% CI 0.31 to 0.95, p=0.03 and 0.43, 95% CI 0.24 to 0.76, p=0.004, respectively).

Conclusion

Current smoking is associated with an impaired response to TNFi in axSpA.

Source:

Ann Rheum Dis 2016;75:532-539

Article:

Impaired response to treatment with tumour necrosis factor α inhibitors in smokers with axial spondyloarthritis

Authors:

Adrian Ciurea et al.

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