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Fibrinogen dysfunction and fibrinolysis state in patients with hepatitis B-related cirrhosis
Yu Liu1, Yan Zhuang2, Guanqun Xu1
1Department of Laboratory Medicine, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
Insights
Hepatitis B cirrhosis impairs fibrinogen function, increasing sialylation and altering clot formation and breakdown. Impaired fibrinolysis is linked to thrombotic events in these patients.
Area of Science:
- Hepatology
- Hematology
- Biochemistry
Background:
- Hepatitis B-related cirrhosis significantly impacts liver function, potentially affecting coagulation factors like fibrinogen.
- Dysfibrinogenemia, an abnormality in fibrinogen function, is increasingly recognized in liver disease but its specific role in hepatitis B cirrhosis requires further elucidation.
Purpose of the Study:
- To evaluate fibrinogen function in patients with hepatitis B-related cirrhosis.
- To investigate the association between dysfibrinogenemia and the risk of bleeding and thrombotic events in this patient cohort.
Main Methods:
- Collected medical records and laboratory data from patients with hepatitis B-related cirrhosis, stratified by Child-Pugh score.
- Assessed fibrinogen activity, antigen levels, fibrinogen-bound sialic acid (FSA), fibrinogen polymerization and fibrinolysis kinetics, thrombin-antithrombin (TAT) complex, and plasmin-α2-antiplasmin (PAP) complex.
Main Results:
- Fibrinogen activity and antigen levels decreased with increasing cirrhosis severity (Child-Pugh score).
- Twenty-two patients (27.5%) exhibited dysfibrinogenemia, characterized by increased FSA levels negatively correlated with fibrinogen activity.
- Impaired fibrinogen polymerization and fibrinolysis were observed, with fibrinolysis dysfunction being more pronounced.
Conclusions:
- Fibrinogen sialylation is a key modification in hepatitis B-related cirrhosis, leading to impaired polymerization and fibrinolysis.
- The severity of impaired fibrinolysis function may contribute to thrombotic events in these patients.
Objective:
To assess the fibrinogen function in patients with hepatitis B-related cirrhosis and explore the relationship between dysfibrinogenemia and bleeding and thrombotic events.
Methods:
Medical records and laboratory data of the patients with hepatitis B-related cirrhosis were collected. Patients were categorized into three groups based on the Child-Pugh score. Fibrinogen activity and antigen, fibrinogen-bound sialic acid (FSA), fibrinogen polymerization and fibrinolysis kinetic analysis, thrombin-antithrombin complex (TAT) and plasmin-α2-antiplasmin complex (PAP) were detected.
Results:
Eighty patients with seventeen, thirty-eight and twenty-five in Child-Pugh A, B and C, respectively, were included. Seventeen patients experienced bleeding events and eight patients had thrombotic events. Fibrinogen activity and antigen levels were reduced with the severity of cirrhosis. Twenty-two patients exhibited dysfibrinogenemia. The FSA levels in patients with non-dysfibrinogenemia and those with dysfibrinogenemia were increased to 1.25 and 1.37 times of healthy controls, negatively correlated with fibrinogen activity (ρ = -0.393, p = 0.006). Compared to healthy controls, the amount of clot formation was reduced (p < 0.001), the polymerization was delayed (p < 0.001) and the rate of fibrinolysis was reduced (p < 0.001). The TAT levels were significantly increased in the Child-Pugh C patients compared to the Child-Pugh B patients (p = 0.032) while the PAP levels were comparable among 3 groups (p = 0.361).
Conclusion:
Sialylation of fibrinogen is one of the main causes of modifications of fibrinogen in patients with hepatitis B-related cirrhosis. The polymerization and fibrinolysis functions of fibrinogen are impaired. The degree of impaired fibrinolysis function is more severe than that of polymerization function, and may be partly related to the occurrence of thrombotic events.
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