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Disseminated intravascular coagulation in liver cirrhosis: fact or fiction?
Z Ben-Ari1, E Osman, R A Hutton
1Liver Institute, Rabin Medical Center, Beilinson Campus, Petah Tiqva, Israel.
Insights
Disseminated intravascular coagulation (DIC) is not a feature of stable liver cirrhosis. Studies show no significant differences in DIC markers between cirrhotic patients and controls, despite impaired liver synthetic function.
Area of Science:
- Hepatology
- Hematology
- Coagulation Disorders
Background:
- Cirrhosis frequently presents with hemostatic dysfunction.
- Laboratory findings in cirrhosis can mimic disseminated intravascular coagulation (DIC).
- Previous beliefs suggested DIC is integral to cirrhosis-related hemostatic failure.
Purpose of the Study:
- To investigate whether disseminated intravascular coagulation (DIC) is a component of the coagulopathy observed in stable liver cirrhosis.
- To differentiate between DIC and other hemostatic abnormalities in cirrhosis using specific quantitative tests.
Main Methods:
- Quantitative analysis of prothrombin fragment 1 + 2, antithrombin III, thrombin-antithrombin complex, and fibrinogen degradation products (XDP).
- Thrombelastography was used to assess the Clot Lysis Index.
- Comparison of 52 stable cirrhotic patients with an age- and gender-matched control group.
Main Results:
- No significant differences in thrombin generation markers (thrombin-antithrombin complexes, XDP, prothrombin fragments 1 + 2) between cirrhotic patients and controls.
- Significantly reduced levels of albumin, Factor V, fibrinogen, antithrombin III, and alpha2-antiplasmin in cirrhotic patients, indicating impaired synthetic function.
- Mild hyperfibrinolysis detected by an abnormal Clot Lysis Index, but no correlation between impaired synthesis and DIC indices.
Conclusions:
- Disseminated intravascular coagulation (DIC) is not a characteristic feature of stable liver cirrhosis in the absence of recent complications.
- The hemostatic dysfunction in cirrhosis is primarily due to reduced synthetic function and possibly hyperfibrinolysis, not DIC.
Objective:
Cirrhosis is commonly associated with haemostatic dysfunction. The similarities of laboratory tests of disseminated intravascular coagulation (DIC) to those found in cirrhosis has led to the belief that DIC is a feature of the haemostatic failure of cirrhosis.
Methods:
The aim of this study was to determine whether DIC is part of the coagulopathy of cirrhosis by applying quantitative tests for prothrombin fragment 1 + 2, antithrombin III, thrombin-antithrombin complex, and specific fribrinogen degradation products levels (XDP), as well as the thrombelastograph for detecting the Clot Lysis Index.
Results:
Fifty-two stable cirrhotic patients (33 men, 19 women; mean age, 58.8 yr; range, 24-72 yr) with differing etiologies were studied. On tests of thrombin generation: thrombin-antithrombin complexes, fibrin(ogen) degradation products, and prothrombin fragments 1 + 2 were not found to be significantly different from an age- and gender-matched control group (p = 0.18, 0.3, and 0.67, respectively), whereas albumin, Factor V, fibrinogen, antithrombin III, and alpha2-antiplasmin were all significantly low (p = 0.0004, 0.002, 0.06, 0.004, and 0.004, respectively), reflecting reduced synthetic function and correlation in ascitic and non-ascitic patients. There was no correlation between impaired synthesis (antithrombin III and alpha2-antiplasmin) and indices of DIC (prothrombin fragment 1 + 2, thrombin-antithrombin complexes, and XDP) (p = not significant). The percentage of patients with high prothrombin fragments 1 + 2 and thrombin antithrombin levels in each Child grade group was similar. Thrombin time was significantly elevated in the cirrhotic group (a manifestation of low fibrinogen levels). The Clot Lysis Index as measured by thrombelastography was significantly abnormal, indicating mild hyperfibrinolysis.
Conclusion:
We conclude that DIC is not part of the coagulopathy in stable liver cirrhosis without recent complications.
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