Rheumatoid arthritis

Tofacitinib attenuates IL-6-mediated endothelial tissue factor induction in vitro without affecting platelet aggregation in vivo: mechanistic insights into cardiovascular risk in rheumatoid arthritis

Clin Exp RheumatolPublished Mechanistic study

Authors' conclusion

Despite clinical concerns raised by ORAL Surveillance, our findings indicate no direct enhancement of platelet reactivity by TOFA. Instead, TOFA attenuated IL-6-driven TF expression in endothelial cells, pointing to a possible protective effect on vascular thrombogenic pathways.

Study context

Population
Healthy volunteers, rheumatoid arthritis (RA) patients on tofacitinib (TOFA) and human umbilical vein endothelial cells (HUVECs)
Comparison
TOFA vs no TOFA on platelet aggregation and IL-6-induced endothelial tissue factor (TF)
  • Healthy volunteersn = 12
  • RAn = 14
Outcome
Effects of TOFA on platelet aggregation and TF-mediated coagulation pathways
Methodological detailsin vitro, ex vivo
  • In vitro
  • Ex vivo

Main finding

As reported in the abstract

  • TOFA did not alter ADP-induced platelet aggregation ex vivo in either healthy volunteers or RA patients
  • TOFA significantly reduced IL-6-induced TF mRNA expression and activity in HUVECs

Original publication

Tofacitinib attenuates IL-6-mediated endothelial tissue factor induction in vitro without affecting platelet aggregation in vivo: mechanistic insights into cardiovascular risk in rheumatoid arthritis. Clin Exp Rheumatol. Published 4 March 2025. doi:10.55563/clinexprheumatol/k0fdes

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