Recipient levels and function of von Willebrand factor prior to liver transplantation and its consumption in the course of grafting correlate with hepatocellular damage and outcome*

Abstract

Summary Von Willebrand factor (vWF) is a major platelet adhesion molecule at sites of vascular injury, such as observed in ischemia/reperfusion injury following orthotopic liver transplantation (OLT). Thirty‐three OLT patients were divided into groups with elevated or low markers of hepatocellular damage (high and low‐HD). Whole‐blood aggregometry was performed to evaluate platelet function. Multimeric analysis was utilized to evaluate functional vWF levels in the course of OLT. Donor and recipient demographics were comparable among groups. Low‐HD patients demonstrated better preserved coagulation parameters on POD 1–6 if contrasted to high‐HD patients. One year graft survival for the high‐HD group was lower than low‐HD patients (P = 0.037). Preoperative vWF‐dependent platelet aggregation and functional vWF plasma levels correlated directly with alanine transaminase levels early after OLT as did the decrease of functional vWF to reperfusion. In summary, these data suggest that vWF may serve as a significant mediator of platelet recruitment and hepatocellular injury in the graft following reperfusion.

Mesenchymal stromal cells in renal ischemia/reperfusion injury

“…In fact, platelets have been suggested to be involved in the inflammatory response of I/R injury in various organs. They are able to roll and adhere to post-reperfusion endothelium in a P-selectin-dependent mechanism (Massberg et al, 1998; Sindram et al, 2000; Khandoga et al, 2002; am Esch et al, 2005). In mouse myocardial tissue, the first activated platelets are present within minutes after reperfusion (Xu et al, 2006), and then accumulate in the infarcted myocardium (Liu et al, 2011).…”

Platelets Boost Recruitment of CD133+ Bone Marrow Stem Cells to Endothelium and the Rodent Liver—The Role of P-Selectin/PSGL-1 Interactions

“…Interestingly, we recently demonstrated CD133 + BMSC when co-incubated with platelets to control their thrombogenic responses in a CD39-dependent manner [ 8 ]. Furthermore, a major role for platelets was described in the mediation of hepatic injury [ 9 , 10 , 11 ]. There is increasing evidence that points to a crucial complex orchestrated role for platelets in various preclinical and clinical scenarios of hepatic regeneration following injury and resection, respectively [ 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 ].…”