Platelets Activation and Liver TransplantationMasanobu Usui1, Hideo Wada2*, Shugo Mizuno1 and Shuji Isaji1
- *Corresponding Author:
- Hideo Wada
Department of Molecular and Laboratory Medicine
Mie University, Graduate School of Medicine, 2-174 Edobashi
Tsu, Mie 514-8507, Japan
E-mail: [email protected]
Received date: October 5, 2015; Accepted date: April 20, 2017; Published date: April 22, 2017
Citation: Usui M, Wada H, Mizuno S, Isaji S (2017) Platelets Activation and Liver Transplantation. J Liver 6:210. doi: 10.4172/2167-0889.1000210
Copyright: © 2017 Usui M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.