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Behaviour of protein C inhibitor in intravascular coagulation and liver disease
Insights
Protein C inhibitor levels were measured in patients with disseminated intravascular coagulation (DIC) and liver disease. Reduced levels were observed in some DIC and liver disease patients, suggesting a role in hemostasis.
Area of Science:
- Biochemistry
- Hematology
- Hepatology
Background:
- Protein C inhibitor plays a role in regulating coagulation.
- Disseminated intravascular coagulation (DIC) involves widespread activation of the hemostatic system.
- Liver disease can affect coagulation factor synthesis and function.
Purpose of the Study:
- To measure protein C inhibitor levels in patients with DIC and liver disease.
- To investigate the potential role of protein C inhibitor in DIC pathogenesis.
- To determine if decreased protein C inhibitor contributes to accelerated fibrinolysis in liver disease.
Main Methods:
- Functional assay used to measure protein C inhibitor levels.
- Comparison of patient levels to normal pooled plasma.
- Analysis of protein C inhibitor levels in patients with DIC, liver cirrhosis, acute hepatic necrosis, accelerated fibrinolysis, and those on warfarin.
Main Results:
- Normal range for protein C inhibitor was established (65-121%).
- Lower-than-normal protein C inhibitor levels were found in 8/17 DIC patients and 3/19 liver cirrhosis patients.
- Levels were normal or elevated in patients with cirrhosis and accelerated fibrinolysis, and in those receiving warfarin.
Conclusions:
- Protein C inhibitor may be involved in regulating protein C activity during DIC.
- Decreased protein C inhibitor does not seem to cause accelerated fibrinolysis in liver disease.
- The liver is a potential site for protein C inhibitor synthesis.
Abstract:
We measured levels of protein C inhibitor in patients with disseminated intravascular coagulation (DIC) and liver disease using a functional assay. Levels in 24 normal subjects averaged 93% of the amount in normal pooled plasma, giving a normal range of 65 to 121%. Levels were below normal in 8 of 17 patients with DIC, in 4 of 19 patients with liver cirrhosis, and in 3 patients with acute hepatic necrosis. Levels were normal or elevated in 9 of 10 patients with cirrhosis and accelerated fibrinolysis, and in 6 patients receiving warfarin. We conclude that protein C inhibitor may be involved in regulation of protein C activity during pathologic activation of the hemostatic system (DIC). Decreased protein C inhibitor does not appear to contribute to the pathogenesis of accelerated fibrinolysis in liver disease. The liver may be the site of synthesis of protein C inhibitor.