Lupus & antiphospholipid syndrome
Janus kinase inhibitors enhance prostanoid biosynthesis in human whole blood in vitro: implications for cardiovascular side effects and prevention strategies
Authors' conclusion
The enhanced biosynthesis of TXA2 in platelets, with a minor contribution from leukocytes, may contribute to the increased cardiovascular risk associated with JAKis.
Study context
- Population
- Whole blood (WB) from healthy subjects, patients with systemic lupus erythematosus (SLE), and treatment-naïve patients with axial spondyloarthritis (axSpA)
- Comparison
- Janus kinase inhibitors (JAKis) effect on TXB2 biosynthesis in whole blood
- Baricitinibn = 10
- Upadacitinibn = 7
- Filgotinibn = 7
- Outcome
- TXB2 production in clotting WB and in 24-hour LPS-stimulated WB
Methodological detailsin vitro, human whole blood
- In vitro
- Human whole blood
Main finding
As reported in the abstract
TXB2 production
- Tofacitinib (1 μM), lipopolysaccharide (LPS)-stimulated WB, HSs (n = 17): increase in TXB2
- 42% ± 33%
- Tofacitinib (1 μM), LPS-stimulated WB, SLE (n = 12): increase in TXB2
- 57% ± 39%
- Tofacitinib (1 μM), LPS-stimulated WB, axSpA (n = 15): increase in TXB2
- 31% ± 23%
- Baricitinib (1 μM), HSs (n = 10): increase in TXB2
- 30% ± 22%
- Upadacitinib, trend towards increased TXB2 (n = 7)
- 46% ± 40%
- Filgotinib, no increase in TXB2 (n = 7)
- 21% ± 19%
Original publication
Janus kinase inhibitors enhance prostanoid biosynthesis in human whole blood in vitro: implications for cardiovascular side effects and prevention strategies. Ann Rheum Dis. Published 5 May 2025. doi:10.
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