Procoagulant imbalance aggravated with falling liver function reserve, but not associated with the presence of portal vein thrombosis in cirrhosis

Abstract

Hypercoagulability, hemodynamic changes, and endothelial injury are the three major contributors to the development of thrombosis. However, the role of hypercoagulability in portal vein thrombosis (PVT) in liver cirrhosis is still controversial. The aim of this study is to elucidate the relationship between procoagulant imbalance and PVT in patients with liver cirrhosis. This study included 151 patients with cirrhosis with (n=20) or without PVT (n=131). Levels of procoagulant factor (FVIII) and anticoagulants [protein C (PC), protein S (PS), and antithrombin (AT)] were measured. Procoagulant imbalance was also evaluated using a thrombin generation test with/without Protac and the results were expressed as Protac-induced coagulation inhibition percentage (PICI%). The lower the PICI% value, the greater the procoagulant imbalance. The levels of PC (P<0.001), PS (P<0.05), and AT (P<0.001) decreased progressively from Child-Pugh A to C in all patients, whereas the levels of FVIII did not alter with the severity of cirrhosis (P>0.05), which indicated the balance tilting toward procoagulation in liver cirrhosis. Similarly, the PICI% values decreased from Child-Pugh A to C (P<0.001). However, there were no differences in the levels of PC, PS, AT, FVIII or PICI% between patients with and without PVT (P>0.05), even after stratification by Child-Pugh classification (P>0.05). Procoagulant imbalance is not associated with the presence of PVT in patients with cirrhosis, although the imbalance worsens with the severity of cirrhosis.