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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. 1Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
  2. 2Department of Public Health and Clinical Medicine, Rheumatology, Umeå University, Umeå, Sweden
  3. 3Unit 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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