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Maintenance of remission once achieved is becoming a critical goal for patients with rheumatoid arthritis (RA) as outcomes improve and advances in therapies continue.1 2 Identification of biomarkers to facilitate tailoring of treatment is often linked to modest response criteria, but less frequently to the more stringent target of sustained remission. We have previously implicated monocytes as potential predictor of response to anti-tumour necrosis factor (TNF) through modulation of regulatory T cells, which may promote maintenance of remission through re-establishment of immune tolerance.3 Circulating monocyte numbers are increased in RA but fall in patients who respond to TNF blockade.4 Whether changes in monocyte numbers can also predict loss of remission, once achieved, to anti-TNF therapy is unknown. We therefore addressed whether the change in monocyte counts in the first year from initiation of anti-TNF therapy (baseline) would predict loss of remission (LOR) in patients who achieved sustained remission.
We extracted data (June 2020) from two independent cohorts of adult biologic-naïve patients with RA who attained sustained remission while treated with anti-TNF between January 2008 and December 2019 (online supplemental table 1). In this retrospective study, Disease Activity Score-28 (DAS28) with erythrocyte sedimentation rate ≤2.6 on at least two occasions (3–6 months apart) after initiation of anti-TNF therapy was used as the definition of remission, as this index was routinely calculated at the treating hospitals. A more stringent definition of remission based on the Clinical Disease Activity Index (CDAI ≤2.8) …
Handling editor Josef S Smolen
Twitter @RajAmarr, @MikeEhrenstein
Contributors MRAS, S-AY and MRE were involved in the design of the study and data interpretation, and wrote the manuscript. RA and MDM collected the data. MRAS analysed the data. All authors reviewed and approved the manuscript’s content before submission.
Funding MRAS is funded by vs Arthritis. S-AY is funded by the Royal College of Physicians, Rosetrees Trust, NIHR University College London Hospitals (UCLH) Biomedical Research Centre, UCLH Charities and Versus Arthritis. MRE is supported (in part) by the UCLH Biomedical Research Centre.
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.