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The effect of fulminant hepatic failure on protein C antigen and activity
1Liver Unit, King's College Hospital, London, UK.
Insights
Fulminant hepatic failure (FHF) significantly reduces protein C levels, a key coagulation inhibitor. Low protein C in FHF may increase susceptibility to disseminated intravascular coagulation.
Area of Science:
- Hepatology
- Hematology
- Coagulation Science
Background:
- Fulminant hepatic failure (FHF) is a severe clinical syndrome.
- Patients with FHF often exhibit coagulopathy.
- Protein C is a crucial endogenous anticoagulant and fibrinolytic protein.
Purpose of the Study:
- To investigate protein C levels in patients with FHF.
- To explore the relationship between protein C and coagulation parameters in FHF.
Main Methods:
- Assessed protein C antigen and activity in 18 patients with grade III or IV FHF coma.
- Correlated protein C levels with prothrombin time and fibrinogen levels.
Main Results:
- Protein C antigen and activity were significantly decreased in FHF patients.
- Protein C levels showed significant positive correlation with fibrinogen.
- Protein C levels were inversely correlated with prothrombin time.
Conclusions:
- Reduced protein C synthesis by the damaged liver is likely responsible for low levels in FHF.
- Low protein C may predispose FHF patients to disseminated intravascular coagulation.
- Disseminated intravascular coagulation can further deplete protein C levels.
Abstract:
In eighteen patients with fulminant hepatic failure (FHF), in grade III or IV coma, both protein C antigen and activity were significantly decreased (0.35 +/- 0.03 u/ml and 0.35 +/- 0.03 u/ml respectively). There was a significant correlation between protein C antigen and activity (r = 0.61, p less than 0.01). Protein C antigen levels were inversely correlated with prothrombin time (r = -0.57, p less than 0.05) as were protein C activity levels (r = -0.57, p less than 0.05). There was also significant correlations between fibrinogen and protein C antigen (r = 0.69, p less than 0.01) and protein C activity (r = 0.61, p less than 0.01). These results demonstrate that the naturally occurring inhibitor of coagulation, protein C, is present at low levels in FHF and this is probably due to the lack of synthesis of the protein in the damaged liver. The low levels of protein C may make these patients more susceptible to the disseminated intravascular coagulation which is known to occur in FHF and this in turn will lead to a further reduction in protein C levels.