Association of the multi-biomarker disease activity score with arterial 18-fluorodeoxyglucose uptake in rheumatoid arthritis

Jon T Giles; Daniel H Solomon; Katherine P Liao; Pamela M Rist; Zahi A Fayad; Ahmed Tawakol; Joan M Bathon

doi:10.1093/rheumatology/keae242

Association of the multi-biomarker disease activity score with arterial 18-fluorodeoxyglucose uptake in rheumatoid arthritis

Rheumatology (Oxford). 2024 Apr 23:keae242. doi: 10.1093/rheumatology/keae242. Online ahead of print.

Authors

Jon T Giles¹, Daniel H Solomon², Katherine P Liao², Pamela M Rist³, Zahi A Fayad⁴, Ahmed Tawakol⁵, Joan M Bathon¹

Affiliations

¹ Division of Rheumatology, Columbia University, Vagelos College of Physicians & Surgeons, NY, USA, New York.
² Division of Rheumatology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
³ Division of Preventive Medicine, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA.
⁴ BioMedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
⁵ Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

PMID: 38652572
DOI: 10.1093/rheumatology/keae242

Abstract

Objectives: Rheumatoid arthritis (RA) and atherosclerosis share many common inflammatory pathways. We studied whether a multi-biomarker panel for RA disease activity (MBDA) would associate with changes in arterial inflammation in an interventional trial.

Methods: In the TARGET Trial, RA patients with active disease despite methotrexate were randomly assigned to the addition of either a TNF inhibitor or sulfasalazine+hydroxychloroquine (triple therapy). Baseline and 24-week follow-up 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography scans were assessed for change in arterial inflammation measured as the maximal arterial target-to-blood background ratio of FDG uptake in the most diseased segment of the carotid arteries or aorta (MDS-TBRmax). The MBDA test, measured at baseline and weeks 6, 18, and 24, was assessed for its association with the change in MDS-TBRmax.

Results: Interpretable scans were available at baseline and week 24 for n = 112 patients. The MBDA score at week 24 was significantly correlated with the change in MDR-TBRmax (Spearman's rho = 0.239; p= 0.011) and remained significantly associated after adjustment for relevant confounders. Those with low MBDA at week 24 had a statistically significant adjusted reduction in arterial inflammation of 0.35 units vs no significant reduction in those who did not achieve low MBDA. Neither DAS28-CRP nor CRP predicted change in arterial inflammation. The MBDA component with the strongest association with change in arterial inflammation was serum amyloid A (SAA).

Conclusions: Among treated RA patients, achieved MBDA predicts of changes in arterial inflammation. Achieving low MBDA at 24 weeks was associated with clinically meaningful reductions in arterial inflammation, regardless of treatment.

Keywords: Atherosclerosis; Biomarkers; Cardiovascular disease; Disease modifying antirheumatic drugs; Inflammation; Positron emission tomography; Prediction; Rheumatoid arthritis; Serum amyloid A; Tumor necrosis factor inhibitors.