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Patients with axial spondyloarthritis who smoke and have elevated C-reactive protein levels respond less well to anti–tumor necrosis factor treatment than do nonsmokers, Swiss researchers reported.
The influence of smoking on treatment response is well known in rheumatoid arthritis, but the impact of tobacco use on patients with axial spondyloarthritis is only beginning to emerge.
In this study of 698 patients with confirmed axial spondyloarthritis who were taking a first anti–tumor necrosis factor (TNF) agent, the effect of smoking on treatment response was measured at 1 year using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and the Ankylosing Spondylitis Disease Activity Score (ASDAS) after adjustment for potential confounders, such as sex, amount of exercise, age, and disease duration (Ann. Rheum. Dis. 2015 Feb. 9 [doi:10.1136/annrheumdis-2013-205133]).
Dr. Adrian Ciurea of the University Hospital Zurich and associates found that patients with elevated C-reactive protein (CRP) levels who smoked achieved significantly smaller reductions in BASDAI and ASDAS scores after initiation of TNF inhibitors, compared with nonsmokers (0.75 BASDAI and 0.69 ASDAS units less, P = .005 and P = .001, respectively).
The odds of reaching a 50% improvement in BASDAI score or meeting ASAS criteria for 40% improvement after 1 year was significantly lower in current smokers than in nonsmokers (odds ratio, 0.54; P = .03; and OR, 0.43; P = .004, respectively).
Past smoking had no significant effect on response to treatment, the researchers said.
The underlying mechanisms on the influence of smoking are unclear, but could be related to an interference with the pharmacokinetics of anti-TNFs or smoking may increase pain levels or starve tissues of oxygen, the researchers suggested.
“Whether quitting smoking might ameliorate the course of disease during treatment with TNFi remains to be confirmed in prospective studies,” they concluded.
Patients in the study were part of the Swiss Clinical Quality Management Cohort during 2005-2014. Almost two-thirds (62%) were smokers; 38% were nonsmokers.
Dr. Ciurea and two coauthors have received consulting and/or speaking fees from a variety of companies marketing biologic drugs for rheumatic diseases. The study was funded by grants from the Foundation for Arthritis Research and the Swiss Spondylitis Foundation.
Patients with axial spondyloarthritis who smoke and have elevated C-reactive protein levels respond less well to anti–tumor necrosis factor treatment than do nonsmokers, Swiss researchers reported.
The influence of smoking on treatment response is well known in rheumatoid arthritis, but the impact of tobacco use on patients with axial spondyloarthritis is only beginning to emerge.
In this study of 698 patients with confirmed axial spondyloarthritis who were taking a first anti–tumor necrosis factor (TNF) agent, the effect of smoking on treatment response was measured at 1 year using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and the Ankylosing Spondylitis Disease Activity Score (ASDAS) after adjustment for potential confounders, such as sex, amount of exercise, age, and disease duration (Ann. Rheum. Dis. 2015 Feb. 9 [doi:10.1136/annrheumdis-2013-205133]).
Dr. Adrian Ciurea of the University Hospital Zurich and associates found that patients with elevated C-reactive protein (CRP) levels who smoked achieved significantly smaller reductions in BASDAI and ASDAS scores after initiation of TNF inhibitors, compared with nonsmokers (0.75 BASDAI and 0.69 ASDAS units less, P = .005 and P = .001, respectively).
The odds of reaching a 50% improvement in BASDAI score or meeting ASAS criteria for 40% improvement after 1 year was significantly lower in current smokers than in nonsmokers (odds ratio, 0.54; P = .03; and OR, 0.43; P = .004, respectively).
Past smoking had no significant effect on response to treatment, the researchers said.
The underlying mechanisms on the influence of smoking are unclear, but could be related to an interference with the pharmacokinetics of anti-TNFs or smoking may increase pain levels or starve tissues of oxygen, the researchers suggested.
“Whether quitting smoking might ameliorate the course of disease during treatment with TNFi remains to be confirmed in prospective studies,” they concluded.
Patients in the study were part of the Swiss Clinical Quality Management Cohort during 2005-2014. Almost two-thirds (62%) were smokers; 38% were nonsmokers.
Dr. Ciurea and two coauthors have received consulting and/or speaking fees from a variety of companies marketing biologic drugs for rheumatic diseases. The study was funded by grants from the Foundation for Arthritis Research and the Swiss Spondylitis Foundation.
Patients with axial spondyloarthritis who smoke and have elevated C-reactive protein levels respond less well to anti–tumor necrosis factor treatment than do nonsmokers, Swiss researchers reported.
The influence of smoking on treatment response is well known in rheumatoid arthritis, but the impact of tobacco use on patients with axial spondyloarthritis is only beginning to emerge.
In this study of 698 patients with confirmed axial spondyloarthritis who were taking a first anti–tumor necrosis factor (TNF) agent, the effect of smoking on treatment response was measured at 1 year using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and the Ankylosing Spondylitis Disease Activity Score (ASDAS) after adjustment for potential confounders, such as sex, amount of exercise, age, and disease duration (Ann. Rheum. Dis. 2015 Feb. 9 [doi:10.1136/annrheumdis-2013-205133]).
Dr. Adrian Ciurea of the University Hospital Zurich and associates found that patients with elevated C-reactive protein (CRP) levels who smoked achieved significantly smaller reductions in BASDAI and ASDAS scores after initiation of TNF inhibitors, compared with nonsmokers (0.75 BASDAI and 0.69 ASDAS units less, P = .005 and P = .001, respectively).
The odds of reaching a 50% improvement in BASDAI score or meeting ASAS criteria for 40% improvement after 1 year was significantly lower in current smokers than in nonsmokers (odds ratio, 0.54; P = .03; and OR, 0.43; P = .004, respectively).
Past smoking had no significant effect on response to treatment, the researchers said.
The underlying mechanisms on the influence of smoking are unclear, but could be related to an interference with the pharmacokinetics of anti-TNFs or smoking may increase pain levels or starve tissues of oxygen, the researchers suggested.
“Whether quitting smoking might ameliorate the course of disease during treatment with TNFi remains to be confirmed in prospective studies,” they concluded.
Patients in the study were part of the Swiss Clinical Quality Management Cohort during 2005-2014. Almost two-thirds (62%) were smokers; 38% were nonsmokers.
Dr. Ciurea and two coauthors have received consulting and/or speaking fees from a variety of companies marketing biologic drugs for rheumatic diseases. The study was funded by grants from the Foundation for Arthritis Research and the Swiss Spondylitis Foundation.
FROM ANNALS OF THE RHEUMATIC DISEASES
Key clinical point: Current smoking impairs treatment response to anti-TNFs in patients with axial spondyloarthritis who had elevated C-reactive protein levels.
Major finding: People with axial spondyloarthritis who smoked and had elevated C-reactive protein levels achieved significantly smaller reductions in BASDAI and ASDAS scores, compared with nonsmokers.
Source: A longitudinal study of 698 patients with axial spondyloarthritis who were taking a first anti-TNF agent and were part of the Swiss Clinical Quality Management Cohort between 2005 and 2014.
Disclosures: Dr. Ciurea and two coauthors have received consulting and/or speaking fees from a variety of companies marketing biologic drugs for rheumatic diseases. The study was funded by grants from the Foundation for Arthritis Research and the Swiss Spondylitis Foundation.
