Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
COVID-19, caused by SARS-CoV-2, can lead to severe inflammation and has been suggested to induce autoimmune phenomena. Multiple studies have reported autoantibodies in patients with COVID-19, particularly anti-cardiolipin, anti-β2-glycoprotein I and antinuclear antibodies.1 2 Anti-citrullinated protein antibodies (ACPA) and flaring of rheumatoid arthritis (RA) after SARS-Cov-2 infection have also been described.1 3 However, it is unclear how often ACPA occur after COVID-19 and whether they differ from ACPA normally found in patients with RA .
We have therefore performed a detailed investigation into ACPA positivity after COVID-19. To determine the seroprevalence of ACPA after COVID-19, ACPA was measured using routine tests or in-house ELISA in 61 patients visiting the post-COVID-19 outpatient clinic of the Leiden University Medical Center 5 weeks after hospitalisation. None of the patients tested positive for ACPA, except two patients previously diagnosed with ACPA-positive RA. Thus, we could not observe an increase in ACPA positivity after COVID-19.
Furthermore, we identified five patients across various Dutch rheumatology clinics presenting with polyarthritis compatible with RA after SARS-CoV-2 infection. To study the impact of COVID-19 on disease presentation, we closely examined their clinical phenotype and autoantibody characteristics (online supplemental table S1). All had suffered from moderate-to-severe COVID-19. On average, joint complaints started 6.6 weeks after infection, although two patients reported symptoms before infection. Four of five patients fulfilled …
Handling editor Josef S Smolen
Contributors VD, TH, RT and DvdW designed the study. FLK, AvdB, AV and AR collected the patient data and materials. VD and TK performed the experiments. VD, TK and DvdW analysed the data. VD drafted the manuscript. All authors revised the manuscript critically and gave approval of the version to be published.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
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.