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P375. Primary response to infliximab therapy in IBD patients is reflected in the normalisation of the haemostatic profile

L. Bollen1, N. Vande Casteele1, M. Peeters1, P. Declerck1, M. Ferrante2, S. Vermeire2, A. Gils1, 1KU Leuven, Department of Pharmaceutical and Pharmacological Sciences, Therapeutic and Diagnostic Antibodies, Leuven, Belgium, 2KU Leuven, Department of Clinical and Experimental Medicine, Translational Research Center for GastroIntestinal Disorders (TARGID), Leuven, Belgium


Venous thromboembolic events (VTE) are an important extra-intestinal complication of patients with inflammatory bowel disease (IBD). Up to now, it is not known which factor is responsible for this increased risk of VTE. IBD patients in active state are much more prone to develop VTE compared to IBD patients in remission suggesting that the excessive inflammatory reaction is a potential trigger for VTE. Conflicting data about the influence of infliximab (IFX) therapy on VTE have been reported. Increased levels of Thrombin Activatable Fibrinolysis Inhibitor (TAFI) and/or Plasminogen Activator Inhibitor-1 (PAI-1), both antifibrinolytic proteins, are correlated with a higher risk of VTE.

We investigated the effect of IFX induction therapy on haemostatic parameters in IBD patients, taking into account the clinical response to treatment [i.e. primary responders vs. non-responders (PNR)].


In a prospective study, 103 IBD patients starting IFX therapy and 113 healthy controls (HC) were included. Plasma was collected before the first IFX infusion (week 0, w0) and after induction therapy (w14). Total PAI-1, active PAI-1, intact TAFI and activation peptide of TAFI (AP, marker for the extent of TAFI activation) were measured by ELISA. Area under the curve (AUC; global marker for coagulation/fibrinolysis), 50% clot lysis time (CLT; marker for fibrinolytic capacity) and amplitude (indicator for clot formation) were determined using a clot lysis assay.


Prior to IFX treatment, IBD patients had a significant increase in PAI-1, AUC and amplitude compared to HC (p < 0.05) whereas TAFI levels and 50% CLT did not differ between both groups. Upon induction therapy (w14 vs. w0), responders showed a significant decrease in AUC and amplitude (p < 0.05), which normalised to values observed in HC (Figure 1). In contrast, upon induction PNR did not show a significant decrease of AUC and amplitude. Three out of 103 IBD patients developed a VTE, all with an additional risk factor such as surgery, protein S deficiency and corticosteroid therapy.

Figure 1. Area under the curve (A) and amplitude (B). Healthy controls (grey), responders w0 (black), responders w14 (white). Bars reflect median + interquartile range (IQR). *P < 0.05 (unpaired data with Mann–Whitney test and paired data with Wilcoxon signed ranked test).


Compared to HC, IBD patients selected for treatment with IFX have increased PAI-1, AUC and amplitude levels. Following IFX induction therapy, responders had a normalisation of the AUC and amplitude. These data indicate that the response to IFX induction is reflected in the normalisation of the haemostatic profile of the IBD patient.