Hyperfibrinolysis underlies abnormal hemostasis in patients with advanced liver cirrhosis

Abstract

Background Hemostasis is a dynamic process resulting from the balance between procoagulant and anticoagulant factors. The liver plays a key role in blood coagulation, being the site of synthesis of almost all coagulation factors and inhibitors. In addition to synthesis, the hepatic reticuloendothelial system is also involved in the clearance of activated coagulation factors as well as enzyme-inhibitor complexes. Plasma levels of fragment D-dimer represent an accurate marker of fibrinolytic activity. Thus, coagulation abnormality is a predictable feature of acute and chronic liver diseases. Aim The aim of the study was to evaluate fibrinolytic activity in patients with various degrees of liver parenchymal damage and its relation to the synthetic function of hepatic coagulation. Patients and methods We studied 40 patients with liver cirrhosis, who were classified into two groups according to Child-Pugh classification: group I, comprising patients with Child class A or B (n = 17), and group II, comprising patients with Child class C (n = 23). In addition, there was a control group (group III) (n = 15). Results Platelet count was significantly low in group II compared with groups I and III (P = 0.001); platelet distribution width was significantly high in group II compared with groups I and III (P = 0.009). There was nonsignificant difference between the studied groups as regards the mean platelet volume (P = 0.4). Fibrinogen and factor VII were significantly decreased in group II when compared with group I and group III (P = 0.01 and 0.001, respectively). D-dimer was significantly increased in group II when compared with group I and group III (P = 0.04). In group II (Child class C) there was significant positive correlation between fibrinogen level, prothrombin concentration, and factor VII (r = 0.53 and 0.58; P = 0.009 and 0.004, respectively) and significant negative correlation between fibrinogen level, activated partial thromboplastin time, and D-dimer concentration (r = −0.50 and −0.39; P = 0.01 and 0.05, respectively). There was significant negative correlation between D-dimer concentration and prothrombin concentration (r = −0.59; P = 0.003). Conclusion Patients with liver cirrhosis suffer from complex coagulation changes. There is a state of hyperfibrinolysis in decompensated cirrhosis. Abnormal fibrinolytic activity is a major hemostatic defect in patients with liver parenchymal damage.