Jeremy Sokolove1,2, Catriona A Wagner3,2, Lauren J Lahey3,2, Harlan Sayles4,5, Michael J Duryee4,5, Andreas M Reimold6,7, Gail Kerr8,9,10, William H Robinson3,2, Grant W Cannon11,12, Geoffrey M Thiele4,5, Ted R Mikuls4,5. 1. VA Palo Alto Health Care System sokolove@stanford.edu. 2. Division of Immunology and Rheumatology, Stanford University School of Medicine, Palo Alto, CA. 3. VA Palo Alto Health Care System. 4. VA Nebraska Western-Iowa Health Care System. 5. Nebraska Arthritis Outcomes Research Center, University of Nebraska Medical Center, Omaha, NE. 6. Dallas VA Medical Center. 7. Division of Rheumatic Diseases, University of Texas Southwestern University Medical Center, Dallas, TX. 8. DC VA Medical Center. 9. Division of Rheumatology, Georgetown University. 10. Division of Rheumatology, Howard University, Washington, DC. 11. George E. Wahlen VA Medical Center. 12. Division of Rheumatology, University of Utah Health Care, Salt Lake City, UT, USA.
Abstract
OBJECTIVES: Cigarette smoking is a major risk factor for RA and has been associated with increased disease severity and lower rates of disease remission. We hypothesized that inflammation and disease activity would be associated with smoking status and this would be related to levels of ACPA. METHODS: RA patients from the Veterans Affairs RA registry were studied (n = 1466): 76.9% anti-CCP2 positive, 89% male, median age 63 years (interquartile range 57-72), median disease duration 8.45 years (interquartile range 2.8-18). Baseline serum samples were evaluated for levels of anti-CCP2, RF, 19 distinct ACPAs and 17 cytokines. Smoking status at baseline was recorded as current, former or never. The association of smoking status with cytokines, autoantibodies and disease activity (DAS28) was evaluated. RESULTS: Among anti-CCP-positive RA patients, RA-associated cytokines (false-discovery rates q < 0.1%) and DAS28 (P < 0.01) were higher in current smokers compared with former or never smokers. DAS28 and cytokine levels were similar between former and never smokers. In contrast, ACPA concentrations were higher among both current and former smokers compared with never smokers, and levels of ACPA were not associated with DAS28 or cytokine levels. CONCLUSION: Among anti-CCP2-positive RA patients, current smoking status is associated with elevations in pro-inflammatory cytokines and increased RA disease activity. Similar levels of inflammation and disease activity among former and never smokers suggests that the detrimental effects of smoking could be ameliorated through tobacco cessation. The effect of tobacco cessation on RA disease activity should be evaluated prospectively. Published by Oxford University Press on behalf of the British Society for Rheumatology 2016. This work is written by US Government employees and is in the public domain in the United States.
OBJECTIVES: Cigarette smoking is a major risk factor for RA and has been associated with increased disease severity and lower rates of disease remission. We hypothesized that inflammation and disease activity would be associated with smoking status and this would be related to levels of ACPA. METHODS:RApatients from the Veterans Affairs RA registry were studied (n = 1466): 76.9% anti-CCP2 positive, 89% male, median age 63 years (interquartile range 57-72), median disease duration 8.45 years (interquartile range 2.8-18). Baseline serum samples were evaluated for levels of anti-CCP2, RF, 19 distinct ACPAs and 17 cytokines. Smoking status at baseline was recorded as current, former or never. The association of smoking status with cytokines, autoantibodies and disease activity (DAS28) was evaluated. RESULTS: Among anti-CCP-positive RApatients, RA-associated cytokines (false-discovery rates q < 0.1%) and DAS28 (P < 0.01) were higher in current smokers compared with former or never smokers. DAS28 and cytokine levels were similar between former and never smokers. In contrast, ACPA concentrations were higher among both current and former smokers compared with never smokers, and levels of ACPA were not associated with DAS28 or cytokine levels. CONCLUSION: Among anti-CCP2-positive RApatients, current smoking status is associated with elevations in pro-inflammatory cytokines and increased RA disease activity. Similar levels of inflammation and disease activity among former and never smokers suggests that the detrimental effects of smoking could be ameliorated through tobacco cessation. The effect of tobacco cessation on RA disease activity should be evaluated prospectively. Published by Oxford University Press on behalf of the British Society for Rheumatology 2016. This work is written by US Government employees and is in the public domain in the United States.
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