Assessment of hemostasis in patients with compensated and decompensated liver cirrhosis

Abstract

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 hospitalized between 2020 and 2025 were examined. 254 patients were assigned to the decompensated cirrhosis group: 164 presented with gastrointestinal bleeding, and 90 presented with ascites. 66 patients were assigned to the group with compensated passage of disease. At the time of examination, they presented with no specific complaints. 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 as a marker of hemostatic imbalance. Additionally, markers of thrombosis were evaluated based on fibrinogen "B" and D-dimer levels.
Results. In patients with compensated disease, a reduction in the levels of standard procoagulant parameters (prothrombin index, fibrinogen) was observed in 37.9% of those examined. Platelet counts were below 60?109/L in only 6,0 %. 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 a relative imbalance favoring a hypercoagulable state.
Among decompensated patients, 60-70% exhibited a reduction in standard procoagulant parameters of the hemostasis system (prothrombin index, fibrinogen) 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 hypercoagulable state.
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 of varying severity. 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 a relative imbalance between hepatocyte-derived pro- and anticoagulants and the endothelial-derived extrahepatic clotting factor FVIII, favoring a hypercoagulable state. The FVIII-to-Protein C activity ratio may serve as an objective marker for the presence or absence of thrombophilia this ratio was elevated in 82.4 % of the subjects examined.
Hemostatic status in hospitalized patients with decompensated liver cirrhosis is characterized by a 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 an underlying baseline thrombophilia.
The presence of a hypocoagulation state is attributed to the development of disseminated intravascular coagulation syndrome of varying severity. This is laboratory-confirmed by thrombocytopenia, a decreased prothrombin index, reduced fibrinogen levels, prolonged aPTT, and the presence of fibrin degradation products, including fibrinogen B and D-dimer.