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The following is a summary of “Fibrinogen dysfunction and fibrinolysis state in patients with hepatitis B-related cirrhosis,” published in the September 2024 issue of Hematology by Liu et al.      

Patients with hepatitis B-related cirrhosis experience alterations in fibrinogen function and increased bleeding or thrombotic risks.  

Researchers conducted a retrospective study to assess fibrinogen function in patients with hepatitis B-related cirrhosis.  

They analyzed medical records and laboratory data from patients with hepatitis B-related cirrhosis, categorized by Child-Pugh score (17 Child-Pugh A, 38 B, 25 C). They measured fibrinogen activity and antigen, fibrinogen-bound sialic acid (FSA), fibrinogen polymerization, fibrinolysis kinetics, thrombin-antithrombin complex (TAT), and plasmin-α2-antiplasmin complex (PAP).  

The results showed that 80 patients, 17 in Child-Pugh A, 38 in Child-Pugh B, and 25 in Child-Pugh C. Out of 17 patients experienced bleeding events, while 8 patients had thrombotic events. Fibrinogen activity and antigen levels were reduced with the severity of cirrhosis, while dysfibrinogenemia was observed in 22 patients. The FSA levels in patients with non-dysfibrinogenemia and those with dysfibrinogenemia were increased to 1.25 and 1.37 times those of HCs, respectively, and were negatively correlated with fibrinogen activity (ρ = −0.393, P=0.006). Compared to HCs, the amount of clot formation was reduced (P<0.001), polymerization was delayed (P<0.001), and the rate of fibrinolysis was reduced (P<0.001). The TAT levels were significantly increased in Child-Pugh C compared to Child-Pugh B (P=0.032), while the PAP levels were comparable among the 3 groups (P=0.361).  

They concluded that sialylation of fibrinogen contributed to dysfunction, with impaired fibrinolysis being more severe than polymerization, which may relate to thrombotic events.

Source: tandfonline.com/doi/full/10.1080/16078454.2024.2392028#abstract