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Updated: Apr 23, 2026
Reduced Complications after Arterial Reconnection in a Rat Model of Orthotopic Liver Transplantation
Published on: November 7, 2020
Abnormal hemostatic function one year after orthotopic liver transplantation can be fully attributed to endothelial
Freeha Arshad1, Jelle Adelmeijer2, Hans Blokzijl3
1Surgical Research Laboratory, Department of Surgery, University of Groningen, University Medical Center Groningen, Groningen, 9700 RB, Netherlands ; Section of Hepatobiliary Surgery and Liver Transplantation, Department of Surgery, University of Groningen, University Medical Center Groningen, Groningen, 9700 RB, Netherlands.
Background:
The long-term risk of thrombotic and vascular complications is elevated in liver transplant recipients compared to the general population. Patients with cirrhosis are in a hypercoagulable status during and directly after orthotopic liver transplantation, but it is unclear whether this hypercoagulability persists over time.
Aim:
We aimed to investigate the hemostatic status of liver transplant recipients one year after transplantation.
Methods:
We prospectively collected blood samples of 15 patients with a functioning graft one year after orthotopic liver transplantation and compared the hemostatic status of these patients with that of 30 healthy individuals.
Results:
Patients one year after liver transplantation had significantly elevated plasma levels of von Willebrand factor (VWF). Thrombin generation, as assessed by the endogenous thrombin potential, was decreased in patients, which was associated with increased plasma levels of the natural anticoagulants antithrombin and tissue factor pathway inhibitor. Plasma fibrinolytic potential was significantly decreased in patients and correlated inversely with levels of plasminogen activator inhibitor-1.
Conclusion:
One year after liver transplantation, liver graft recipients have a dysregulated hemostatic system characterised by elevation of plasma levels of endothelial-derived proteins. Increased levels of von Willebrand factor and decreased fibrinolytic potential may (in part) be responsible for the increased risk for vascular disease seen in liver transplant recipients.
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