Abstract
An assessment of hemostasis was carried out in patients with compensated and decompensated liver cirrhosis.
Materials and methods. A total of 320 patients with liver cirrhosis. 254 patients were assigned to the decompensated cirrhosis group. 66 patients were assigned to the compensated group. Evaluation of the procoagulant pathway included determination of platelet count, prothrombin index, activated partial thromboplastin time, fibrinogen levels, and coagulation factor FVIII activity. Assessment of the anticoagulant pathway included determination of Protein C activity. The ratio of factor F VIII activity to protein C activity (FVIII/PC ratio) was calculated. Markers of thrombosis were evaluated based on fibrinogen "B" and D-dimer levels.
Results. In patients with compensated disease, reduction in the levels of standard procoagulant parameters was observed in 37.9% of those examined. Concurrently, factor F VIII activity was at the upper limit of normal in 65.2% of patients, while in 36.4% of cases, it exceeded the reference range. Plasma activity of the Protein C was within the lower limit of normal in 72.7% of subjects and below the reference range in 27.3%. The FVIII/PC ratio slightly exceeded normal values in 82.4% of patients, ranging from 1.1 to 1.3, indicating relative imbalance favoring hypercoagulability.
Among decompensated patients, 60-70% exhibited reduction in standard procoagulant parameters of the hemostasis system upon admission. Conversely, Factor FVIII activity levels were above the reference range in nearly all patients. Protein C activity was below the normal limit in over 60% of patients presenting with either hemorrhage or ascites. The FVIII/PC ratio exceeded normal values by 3- to 4-fold in 100 % of patients with bleeding and 40-60 % of those with ascites, indicating a marked baseline imbalance favoring a hypercoagulability.
The observed reduction in platelet counts, prothrombin index, and fibrinogen levels, alongside prolonged aPTT during hemorrhage in decompensated patients, can be interpreted as a manifestation of disseminated intravascular coagulation syndrome. Upon admission, D-dimer levels in 75.0%-97.0 % of patients—presenting with both hemorrhage and ascites—exceeded reference values by more than five-fold. Among deceased patients, D-dimer concentrations remained persistently elevated in 100.0 % of cases.
Conclusions. Hemostatic status in compensated liver cirrhosis is characterized by relative imbalance between hepatocyte-derived pro- and anticoagulants and the endothelial-derived extrahepatic clotting factor FVIII, favoring a hypercoagulability.
Hemostatic status in hospitalized patients with decompensated liver cirrhosis is characterized by reduction in both hepatocyte-derived pro- and anticoagulants, signaling hepatic functional decompensation. Conversely, the activity levels of the extrahepatic coagulation factor F VIII were elevated above the reference range in nearly all patients, indicating underlying endothelial dysfunction. The FVIII/PC ratio in the majority of patients was 3- to 4-fold higher than the reference range, indicating underlying baseline thrombophilia.
The presence of hypocoagulation is attributed to the development of disseminated intravascular coagulation syndrome of varying severity. This is laboratory-confirmed by thrombocytopenia, decreased prothrombin index, reduced fibrinogen levels, prolonged aPTT, and the presence of fibrin degradation products, including fibrinogen B and D-dimer.