[Studies on the mechanism of hyperfibrinolysis in liver cirrhosis--changes of plasma t-PA, PAI-1 and active PAI-1 levels in liver cirrhosis].

Liver cirrhosis is known to have abnormal fibrinolysis. In order to investigate the changes of fibrinolytic system in liver cirrhosis, plasma levels of various fibrinolytic molecular markers were measured in patients with different stages of liver cirrhosis, 20 compensated liver cirrhosis (c-LC) and 14 decompensated liver cirrhosis (d-LC) and were compared with those in normal subjects. Both the plasma levels of plasmin alpha 2-plasmin inhibitor complex (PIC) and the plasma levels of total fibrin/fibrinogen degradation products (T-FDP) were significantly elevated in patients with both c-LC and d-LC as compared with normal controls. Moreover, both factors in d-LC were significantly higher than those in c-LC. These findings indicate that patients with liver cirrhosis have hyperfibrinolysis. Then, in order to investigate the mechanisms of hyperfibrinolysis in liver cirrhosis, plasma levels of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) were determined in these patients. The plasma levels of t-PA significantly increased in both c-LC and d-LC as compared with normal controls. Its levels were higher in patients with LC at their decompensated stage than at their compensated stage. In patients with LC, plasma PAI-1 levels showed significantly higher values than those in normal controls. However, the plasma levels of active PAI-1 in patients with LC were similar to those in normal controls. These results suggest that hyperfibrinolysis in patients with LC is mainly due to increased concentrations of t-PA, without increased active PAI-1 levels.