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The following is a summary of “Impact of RA treatment strategies on lipids and vascular inflammation in rheumatoid arthritis: a secondary analysis of the TARGET randomized active comparator trial,” published in the June 2024 issue of Rheumatology by Liao et al.

Rheumatoid arthritis (RA) treatments are known to induce complex alterations in lipid profiles and lipoproteins, potentially affecting cardiovascular (CV) risk. This study aimed to investigate the changes in lipids and lipoproteins associated with two prevalent RA treatment strategies—triple therapy and tumor necrosis factor inhibitor (TNFi) therapy—and their association with CV risk.

In this secondary analysis of the TARGET trial, patients with RA who were inadequate responders to methotrexate (MTX) were randomized to receive either triple therapy (adding sulfasalazine and hydroxychloroquine) or TNFi for 24 weeks. The primary outcome was the change in arterial inflammation, measured by FDG-PET/CT in the carotid arteries or aorta, quantified as the target-to-background ratio (TBR) in the most diseased segment (MDS) at baseline and 24 weeks. Routine lipid profiles and advanced lipoproteins were assessed at both time points, with patients on statin therapy at baseline being excluded from the analysis. Lipid changes were compared within and between treatment arms, and associations between lipid changes and MDS-TBR changes were evaluated.

A total of 122 participants, evenly divided between the two treatment arms (61 each), were included in the study, with a median age of 57 years, 76% female, and a median RA disease duration of 1.5 years. In comparing the treatment strategies, triple therapy showed a significantly larger reduction in triglycerides (15.9 mg/dL, p = 0.01), total cholesterol to HDL-C ratio (0.29, p = 0.01), and LDL particle number (111.2, p = 0.02) relative to TNFi therapy. Conversely, TNFi therapy led to a greater increase in HDL particle number (1.6 umol/L, p = 0.006). No significant correlations were found between lipid measurement changes and MDS-TBR changes within or across treatment arms.

Both RA treatment strategies improved lipid profiles, albeit through different lipid and lipoprotein modifications. However, these changes did not correlate with alterations in CV risk, as assessed by vascular inflammation using FDG-PET/CT. This suggests that while both treatments positively impact lipid profiles, they do not directly translate to changes in CV risk markers, highlighting the need for further research to understand the clinical implications of these findings in managing RA-associated CV risk.

Source: arthritis-research.biomedcentral.com/articles/10.1186/s13075-024-03352-3