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High sodium chloride consumption enhances the effects of smoking but does not interact with SGK1 polymorphisms in the development of ACPA-positive status in patients with RA
  1. Xia Jiang1,
  2. Björn Sundström2,
  3. Lars Alfredsson1,
  4. Lars Klareskog3,
  5. Solbritt Rantapää-Dahlqvist2,
  6. Camilla Bengtsson1
  1. 1 Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
  2. 2 Department of Public Health and Clinical Medicine, Rheumatology, Umeå University, Umeå, Sweden
  3. 3 Unit of Rheumatology, Department of Molecular medicine, Karolinska Institutet Hospital, Stockholm, Sweden
  1. Correspondence to Xia Jiang, Institute of Environmental Medicine, Karolinska Institutet Solna, Box 210, Nobels väg 13, Stockholm 17172, Sweden; xia.jiang{at}

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Two recent studies using both animal models and human cells reported that increased salt concentration induces serum glucocorticoid kinase 1 (SGK1) expression, which enhances production of interleukin-17-producing CD4+ helper T cells (TH17). These T cells are highly proinflammatory1 ,2 and may contribute to the pathogenesis of rheumatoid arthritis (RA).3 A population-based nested case–control study identified an increased RA risk among smokers with high sodium intake and also a significant additive interaction between smoking and high sodium intake of developing anticitrullinated protein/peptide antibodies (ACPA)-positive RA.4 Based on these results, we used data from the large EIRA study5 on genetic and environmental risk for RA to investigate the impact of sodium consumption on the development of ACPA-positivity among smokers as well as the effect of smoking on ACPA-positivity according to different levels of sodium intake. Furthermore, we studied whether medium/high sodium consumption might influence SGK1 polymorphisms regarding the risk of ACPA-positivity.

A case–case design contrasting ACPA-positive versus ACPA-negative RA cases was used in all analyses. In total, 1285 …

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  • XJ and BS contributed equally.

  • Contributors XJ and BS designed the study, conducted the statistical analysis and wrote the manuscript; LA, LK, SR-D and CB contributed to the interpretation of the findings and the modification of manuscript. All authors participated and approved the submission of the final version of the manuscript.

  • Funding This project was funded by grants from the Swedish Medical Research Council; from the Swedish Research Council for Health, Working Life and Welfare, the AFA foundation, Vinnova, King Gustaf V's 80-year foundation, the Swedish Rheumatic Foundation and Swedish Foundation for Strategic Research.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Ethics approval Institutional Review Board at the Karolinska Institutet.

  • Provenance and peer review Not commissioned; externally peer reviewed.