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  • Investigation of an interleukin-6 receptor gene polymorphism (rs2228145) as a predictor of cardiovascular mortality in inflammatory polyarthritis: results from the Norfolk Arthritis Register

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Investigation of an interleukin-6 receptor gene polymorphism (rs2228145) as a predictor of cardiovascular mortality in inflammatory polyarthritis: results from the Norfolk Arthritis Register
  1. Ibrahim Ibrahim1,
  2. Kate McAllister1,
  3. Darren Plant1,2,
  4. Deborah Symmons1,2,
  5. Tarnya Marshall3,
  6. Anne Barton1,2,
  7. Stephen Eyre1
  1. 1 Arthritis Research UK Epidemiology Unit, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK
  2. 2 NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK
  3. 3 Norfolk and Norwich University Hospitals NHS Foundation Trust, Norwich, UK
  1. Correspondence to Dr Stephen Eyre, Arthritis Research UK Epidemiology Unit, Stopford Building, Oxford Road, University of Manchester, Manchester M13 9PT, UK; steve.eyre{at}manchester.ac.uk

https://doi.org/10.1136/annrheumdis-2013-204330

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    In patients with rheumatoid arthritis (RA), chronic inflammation on a background of established cardiovascular disease (CVD) risk factors is thought to contribute to atherosclerosis, resulting in the observed increased mortality from CVD.1

    Recent studies suggest a role for interleukin-6 receptor (IL6R) in both CVD2 ,3 and RA.4 A functional, non-synonymous genetic variant found within the IL6R gene (rs2228145) conferring an amino acid change (Asp358Ala) influential in determining levels of soluble IL6R5 has been convincingly associated with both CVD occurrence2 ,3 and RA.4 This amino acid change within the IL6R gene has a similar effect to the RA therapy, tocilizumab, which targets the IL6R pathway, leading to an increase in IL6R and soluble IL6 levels, as well as a decrease in C-reactive protein (CRP) levels. Although unlikely to be causal in disease,6 CRP levels …

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    Footnotes

    • II and KM both contributed equally to this work.

    • Contributors SE conceived the study, designed the study, drafted and revised the manuscript. II and DP cleaned the data, performed statistical analysis, drafted and revised the manuscript. KM performed the genotyping, performed statistical analysis, drafted and revised the manuscript. DS and TM drafted and revised the manuscript. AB conceived the study, designed the study, designed the data collection tools, monitored data collection, drafted and revised the manuscript. She is guarantor. All authors have read and approved the final manuscript for publication.

    • Funding We thank Arthritis Research UK for their support (grant ref 20385). This work was also supported by the NIHR Manchester Musculoskeletal Biomedical Research Unit.

    • Competing interests None.

    • Ethics approval Local Hospital (Norfolk and Norwich) LREC 2003-075.

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