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article · Annals of the Rheumatic Diseases

OP0069 GLP1 agonists mitigate the risk of cardiovascular events in Rheumatoid Arthritis patients treated with JAK inhibitors

20251 citationOpen accessAlexandria University

Abstract

<h2>Abstract</h2><h3>Background:</h3> Patients with rheumatoid arthritis (RA) face an increased risk of cardiovascular (CV) complications. Janus kinase (JAK) inhibitors, commonly used in the treatment of RA, have been associated with an increased risk of adverse CV events. Conversely, glucagon-like peptide-1 (GLP-1) receptor agonists have demonstrated possible cardioprotective effects in other patient populations. <h3>Objectives:</h3> This study investigates the role of GLP-1 receptor agonists as a protective measure against CV adverse effects in RA patients treated with JAK inhibitors. <h3>Methods:</h3> A retrospective cohort analysis was conducted using the TriNetX platform. Two cohorts of RA patients above 40 were identified: Group 1 consisted of RA patients on JAK inhibitors who subsequently initiated GLP-1 receptor agonists. Group 2 consisted of RA patients on JAK inhibitors without GLP-1 receptor agonist use. The index event for Group 1 was the initiation of GLP-1 receptor agonists while on JAK inhibitors, while the index event for Group 2 was the initiation of JAK inhibitors. Propensity score matching was performed to balance baseline characteristics, including age, sex, diabetes mellitus, hypertension, obesity, hyperlipidemia, primary thrombophilia, smoking, glucocorticoid use, and anticoagulant/ antiplatelet use. Patients with outcomes before the index event were excluded from the analysis.The primary outcomes occurring within 5 years after the index event were assessed, including the incidence of acute coronary syndromes, cerebral infarction, acute peripheral arterial thrombosis, deep venous thrombosis, and overall arterial CV events. <h3>Results:</h3> The analysis compares CV outcomes in RA patients on JAK inhibitors with and without GLP-1 receptor agonists. After Propensity score matching each cohort included 2,449 patients. Patients in the GLP-1 receptor agonist group had a significantly lower risk of acute coronary syndromes (Risk Ratio=0.645, p=0.0009). The GLP-1 receptor agonist-treated group exhibited a significantly reduced risk of deep venous thrombosis (Risk Ratio=0.69, p=0.007). Although the GLP-1 receptor agonist group showed a trend toward lower risk of acute cerebral infarction and peripheral arterial disease events, the difference was not statistically significant. The overall incidence of cardiovascular events was significantly lower in the group that received GLP-1 receptor agonists (Risk Ratio=0.673, p=0.0007). Kaplan-Meier survival analysis showed comparable survival probabilities between the two groups for all studied outcomes, with no significant difference in median survival. Figure 1overall arterial cardiovascular events in RA patients treated with JAK inhibitors with and without GLP1 agonists. <h3>Conclusion:</h3> The findings underscore the potential of GLP-1 receptor agonists to reduce CV risks in RA patients being treated with JAK inhibitors. However, the protective effects regarding other outcomes, like cerebral infarction and peripheral arterial thrombotic events, were less definitive. These findings emphasize the need for further research to validate the study results. <h3>REFERENCES:</h3> <b>NIL</b>. <h3>Acknowledgements:</h3> <b>NIL</b>. <h3>Disclosure of Interest:</h3> <b>None declared</b>. © The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.

Research topics

  • Systemic Lupus Erythematosus Research
  • Cytokine Signaling Pathways and Interactions
  • Hepatitis C virus research

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DOI: 10.1016/j.ard.2025.05.092

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