Session Information
Date: Monday, November 9, 2015
Session Title: Epidemiology and Public Health II: RA and Lifestyle Factors
Session Type: ACR Concurrent Abstract Session
Session Time: 2:30PM-4:00PM
Background/Purpose:
Increased salt concentration enhances the production of TH17 cells, which are highly proinflammatory and are pivotal in rheumatoid arthritis (RA) pathogenesis.1, 2 A population-based study has identified an increased RA risk among smokers who also consume a high amount of sodium, as well as a significant additive interaction between smoking and high sodium intake for the development of ACPA-positive RA.3 Based on these results, we aimed at investigating the role of salt consumption, together with smoking, with regard to the development of ACPA-positivity.
Methods:
The analysis involved 1294 newly diagnosed cases recruited from the EIRA project during 2009-2011. Smoking status (categorized as never/ever smoking), smoking intensity (cut-off at 20 pack-years) and other lifestyle related factors were reported through self-administrated questionnaires at baseline. Sodium consumption was calculated using an algorithm based on data from food questionnaire and was categorized as low, median and high intake. We calculated the odds ratio (OR) and 95% confidence intervals (95%CI) associated with combinations of smoking and salt regarding the development of ACPA positivity in a case-only analysis.
Results:
We identified an increased risk of belonging to the ACPA-positive RA subset among ever smokers (OR=1.4, 95%CI: 0.9-2.1) and heavy smokers (OR=2.6, 95%CI: 1.6-4.1) who had a medium to high sodium intake compared with never smokers with low intake. We further observed a dose response effect between pack-years of smoking and sodium intake with regard to ACPA-positivity (light or never smokers/median sodium intake: 1.0 (0.7-1.4); light or never smokers/high sodium intake: 0.9 (0.6-1.3); heavy smokers/low sodium intake: 1.4 (0.8-2.4); heavy smokers/median sodium intake: 2.1 (1.2-3.7); heavy smokers/high sodium intake: 3.2 (1.7-6.0); p-trend <0.0001).
Conclusion: We observed an increased risk of ACPA-positivity among high sodium intake (heavy) smokers, compared with never smokers with low sodium intake, as well as a dose response effect of sodium intake among heavy smokers.
References:
1. Kleinewietfeld M, Manzel A, Titze J, et al. Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature 2013;496:518-522.
2. Wu C, Yosef N, Thalhamer T, et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature 2013;496:513-517.
3. Sundstrom B, Johansson I, Rantapaa-Dahlqvist S. Interaction between dietary sodium and smoking increases the risk for rheumatoid arthritis: results from a nested case-control study. Rheumatology (Oxford) 2015;54:487-493.
To cite this abstract in AMA style:
Jiang X, Sundström B, Alfredsson L, Klareskog L, Rantapaa-Dahlqvist S, Bengtsson C. Sodium Chloride Consumption, Together with Smoking, Is Associated with ACPA Positivity [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/sodium-chloride-consumption-together-with-smoking-is-associated-with-acpa-positivity/. Accessed February 21, 2020.« Back to 2015 ACR/ARHP Annual Meeting
ACR Meeting Abstracts - https://acrabstracts.org/abstract/sodium-chloride-consumption-together-with-smoking-is-associated-with-acpa-positivity/