Platelets Activation and Liver Transplantation

Abstract

Transient thrombocytopenia is a common phenomenon after living donor liver transplantation (LDLT), and severe thrombocytopenia after LDLT is associated with graft loss and poor patient outcomes. The various causes of thrombocytopenia include bone marrow hematopoiesis failure due to decreased thrombopoietin (TPO) production in the injured liver, platelet destruction associated with splenomegaly, and the activation and consumption of platelets due to various forms of thrombosis, including disseminated intravascular coagulation (DIC), thrombotic microangiopathy (TMA), and venous thromboembolism (VTE). The observation of biomarkers such as soluble platelet glycoprotein VI (sGPVI), TPO, von Willebrand factor (VWF), VWF propeptide (VWFpp), and disintegrin-like and metalloproteinase with thrombospondin type-1 motifs member 13 (ADAMTS13) is useful in the evaluation of the mechanisms of thrombocytopenia in patients who undergo LDLT. The presence of these biomarkers, including sGPVI, ADAMTS13, VWF and VWFpp, suggests that platelet activation occurs in the early phase of LDLT and that vascular endothelial cell injury occurs on postoperative days 7-14.