Tofacitinib does not affect platelet function or coagulation in patients with ulcerative colitis

Tofacitinib is a Janus kinase inhibitor used to treat inflammatory diseases, including rheumatoid arthritis and ulcerative colitis (UC). Previous studies have reported an increased risk of thromboembolic events in patients with rheumatoid arthritis treated with tofacitinib. Therefore, evaluating whether these effects are also present in other inflammatory diseases such as UC is important.

In this exploratory study, we evaluated the impact of tofacitinib on platelet function and coagulation profiles in patients with active UC receiving tofacitinib (n=10), compared with patients treated with anti-TNF agents (n=10) and healthy controls (HC; n=10). Patients were assessed at baseline and after 14 weeks of treatment. Platelet aggregation was assessed by lumiaggregometry, while platelet activation was evaluated by flow cytometry through PAC-1 binding and surface expression of CD62P and CD63. Coagulation was assessed by rotational thromboelastometry (ROTEM^®) using extrinsic (EXTEM) and intrinsic (INTEM) pathway activation assays. Longitudinal analyses evaluated the effects of time, treatment, and their interaction.

Tofacitinib did not significantly affect platelet aggregation or the expression of platelet activation markers compared with either anti-TNF-treated patients or HC. Regarding thrombus dynamics, a significant difference was observed only in the INTEM assay when comparing the tofacitinib and anti-TNF groups, showing longer clot formation times in tofacitinib-treated patients; however, neither group differed from HC.

In this study, tofacitinib treatment was not associated with increased platelet aggregation, platelet activation, or enhanced coagulation in patients with UC.