Background/Purpose: Cardiovascular (CV) morbidity, mortality and perpetuated synovial angiogenesis have been associated with rheumatoid arthritis (RA). In our study we evaluated angiogenic factors in relation to vascular inflammation and function and clinical markers in RA patients undergoing one-year tofacitinib therapy.

Methods: Thirty RA patients treated with either 5 mg or 10 mg bid tofacitinib were included in a 12-month follow-up study. Eventually 26 patients completed the study and included in data analysis. Levels of various angiogenic cytokines (TNF-α, IL-6), growth factors (VEGF, bFGF, EGF, PlGF), cathepsin K (CathK), CXCL8, galectin-3 (Gal-3) and NT-proBNP were determined at baseline, 6 and 12 months after initiating tofacitinib treatment. In order to assess flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT) and carotid-femoral pulse-wave velocity (cfPWV) ultrasonography was performed. Synovial and aortic inflammation was also assessed by ¹³F-FDG-PET-CT.

Results: One-year tofacitinib therapy significantly decreased IL-6, VEGF, bFGF, EGF, PlGF and CathK, while increased Gal-3 production (p < 0.05). Basic FGF, PlGF and NT-proBNP levels were higher, while PECAM-1 levels were lower in RF seropositive patients (p < 0.05). TNF-α, bFGF and PlGF correlated with post-treatment synovial inflammation, while aortic inflammation was rather dependent on IL-6 and PECAM-1 as determined by PET/CT (p < 0.05). In the correlation analyses, NT-proBNP, CXCL8 and Cath variable correlated with ccIMT (p < 0.05).

Conclusion: Decreasing production of bFGF, PlGF or IL-6 by one-year tofacitinib therapy potentially inhibits synovial and aortic inflammation, respectively. Although NT-proBNP, CXCL8 and CathK were associated with ccIMT, their role in RA-associated atherosclerosis needs to be further evaluated.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/effects-of-one-year-tofacitinib-therapy-on-angiogenic-biomarkers-in-rheumatoid-arthritis/