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No sign of elevated cardiovascular risk in patients with seropositive rheumatoid arthritis who remain on stable antirheumatic therapy: results from the nationwide Norwegian Cardio-Rheuma Register
  1. Eirik Ikdahl1,
  2. Anne Grete Semb1,
  3. Anne M Kerola2,3
  1. 1 REMEDY Center for treatment of Rheumatic and Musculoskeletal Diseases, Diakonhjemmet Hospital, Oslo, Norway
  2. 2 Department of Rheumatology, Päijät-Häme Central Hospital, Lahti, Finland
  3. 3 Faculty of Medicine, University of Helsinki, Helsinki, Finland
  1. Correspondence to Dr Eirik Ikdahl; eirik.ikdahl{at}gmail.com

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The risk of cardiovascular disease (CVD) in patients with rheumatoid arthritis (RA) is closely linked to increasing levels of systemic inflammation.1 However, little is known about the CVD risk in patients with RA who maintain stable disease-modifying antirheumatic drug (DMARD) therapy. We evaluated the CVD risk in seropositive patients with RA who retained their first DMARD with no corticosteroid use later than 6 months after diagnosis.

Data came from the Norwegian Cardio-Rheuma Register (NCRR), which has previously been described in detail.2 NCRR spans the entire adult Norwegian population from January 2008 to December 2017 and includes: International Classification of Diseases 10th Revision (ICD-10) codes, dispensed prescriptions (anatomical therapeutic classification codes) and cause of death, from mandatory Norwegian health registers.

An initial 2-year washout period was applied to exclude individuals with previous inflammatory joint disease (IJD: ICD-10 codes or drug reimbursements for M05–M14, M45 and M46) or DMARD prescriptions. Only patients with ≥2 seropositive RA diagnosis codes (M05) and ≥1 prescription for DMARDs were included. This approach has been shown to have a diagnostic accuracy of 93%.3 Seronegative patients were not included due to lower diagnostic accuracy.

Two groups were formed: The stable treatment group consisted of …

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors All authors contributed to the planning, conduct and reporting of the work described in the article. EI is responsible for the overall content.

  • Funding The study was supported by internal funds at the REMEDY Center for treatment of Rheumatic and Musculoskeletal Diseases, Diakonhjemmet Hospital, Oslo, Norway.

  • Competing interests EI has nothing to declare. AGS has received speaker fees from Merck/Schering-Plough, BMS, UCB, Pfizer/Wyeth, Novartis, Lilly and Women’s College Hospital, Toronto, Canada. AMK has received speaker fees from Abbvie, Sanofi, Boehringer-Ingelheim and support for attending meetings/travel from Abbvie.

  • Patient and public involvement Patients and/or the public were involved in the design, or conduct, or reporting, or dissemination plans of this research. Refer to the Methods section for further details.

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

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.