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.

Heparin-induced thrombocytopenia occurring early after living donor liver transplantation: a case report

“…[2,12,13] The spleen traps the platelets, and this is thought to cause thrombocytopenia after LT. Preoperative thrombocytopenia due to cirrhosis is a risk factor for persistent thrombocytopenia after LT, and residual hypersplenism is thought to be the main cause [14] ; however, several recent reports indicate that the spleen is not strongly involved in thrombocytopenia in the early phase of the postoperative period. [15][16][17] Graft liver dysfunction, medication, and infection also cause thrombocytopenia after LT. Graft liver dysfunction reduces the production of a disintegrin-like and metalloproteinase with thrombospondin type-1 motifs member 13 and thrombopoietin, leading to prolonged thrombocytopenia after LT. [18,19] Immunosuppressive medications, such as antithymocyte globulin, antiviral drugs, and trimethoprim-sulfamethoxazole, can cause thrombocytopenia after LT. [1] We used tacrolimus, a calcineurin inhibitor, and an antiviral drug. Thrombotic microangiopathy (TMA) after LDLT is well known as a rare but fatal complication, and drugs, including cal-cineurin inhibitors, are considered to be risk factors.…”

“…[2,12,13] The spleen traps the platelets, and this is thought to cause thrombocytopenia after LT. Preoperative thrombocytopenia due to cirrhosis is a risk factor for persistent thrombocytopenia after LT, and residual hypersplenism is thought to be the main cause [14] ; however, several recent reports indicate that the spleen is not strongly involved in thrombocytopenia in the early phase of the postoperative period. [15–17]…”

Thrombocytopenia after liver transplantation: Should we care?

“…Peck-Radosavljevic et al[ 75 ] observed that serum thrombopoietin levels increased significantly on the first day after LT, which preceded the increase in reticulated platelets by 3 d and in peripheral platelets by 5 d. This delayed rise in platelet count was compatible with the time lag between the appearance of reticulated platelets and peripheral platelets after in vivo administration of a recombinant human thrombopoietin analogue, and rules out the impaired production of TPO as a possible cause of post-transplant thrombocytopenia. Usui et al[ 76 ] reported the TPO levels in the prolonged thrombocytopenic group were significantly decreased. They considered that prolonged post-transplant thrombocytopenia was secondary to a decrease in TPO production suggesting graft dysfunction.…”