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Disseminated intravascular coagulation in liver cirrhosis
C M Bakker1, E A Knot, J Stibbe
1Department of Internal Medicine, University Hospital, Rotterdam, The Netherlands.
Insights
Disseminated intravascular coagulation (DIC) in liver cirrhosis is linked to low antithrombin-III (AT-III) levels. When AT-III is deficient, thrombin formation increases, leading to DIC markers like soluble fibrin and D-dimer.
Area of Science:
- Hepatology
- Hematology
- Coagulation Disorders
Background:
- Liver cirrhosis is associated with hemostatic abnormalities.
- The presence and diagnostic markers of disseminated intravascular coagulation (DIC) in liver cirrhosis require further elucidation.
- Thrombin-antithrombin III complex (TAT), soluble fibrin (SF), and D-dimer are potential indicators of coagulation activation.
Purpose of the Study:
- To investigate the utility of TAT, SF, and D-dimer levels in diagnosing DIC in patients with liver cirrhosis.
- To explore the relationship between these markers and antithrombin-III (AT-III) levels in liver cirrhosis.
Main Methods:
- Measurement of TAT, SF, D-dimer, and AT-III levels in 51 liver cirrhosis patients and a reference group.
- Statistical analysis to determine correlations between coagulation markers and AT-III levels.
- Comparison of marker levels between patient and control groups.
Main Results:
- Elevated TAT and SF levels were observed in liver cirrhosis patients compared to controls.
- A significant inverse correlation was found between SF levels and AT-III concentration (r = 0.60, p < 0.001).
- SF levels were markedly increased in patients with AT-III levels below 0.30 U/ml.
Conclusions:
- Increased thrombin formation, indicated by elevated TAT, occurs in liver cirrhosis.
- Plasma AT-III concentration is crucial in the development of DIC in liver cirrhosis.
- DIC is evident in severe liver cirrhosis when AT-III levels fall below 0.30 U/ml.
Unlabelled:
We measured thrombin-antithrombin III complex (TAT), soluble fibrin (SF) and D-dimer levels in 51 patients with liver cirrhosis to determine whether these tests provide new evidence for the presence of disseminated intravascular coagulation (DIC) in liver cirrhosis. TAT levels (median, range) were increased in the patient group (4.2 micrograms/l, 1.8-60.0) compared to the reference group (2.0 micrograms/l, range 1.5-7.6 micrograms/l). SF levels (0 nmol/l, range 0-80 nmol/l) were also increased in the patients as compared to the controls (0 nmol/l, 0), but there was no correlation between TAT and SF levels (r = 0.23, p less than 0.98). TAT levels did not correlate with AT-III levels (r = -0.36, p less than 0.49), but there was an inverse correlation between SF and AT-III (r = 0.60, p less than 0.001). If AT-III levels were above 0.30 U/ml, SF levels remained low, whereas SF levels were increased in patients with AT-III levels below 0.30 U/ml. These findings suggest that if sufficient AT-III is present, thrombin formation is adequately controlled, whereas at low levels of AT-III, thrombin escapes inactivation by AT-III and may act upon fibrinogen, leading to the formation of SF and a low-grade DIC. SF levels correlated well with D-dimer levels (r = 0.55, p less than 0.001), which is consistent with DIC and secondary fibrinolysis.
In Conclusion:
(1) thrombin formation is increased in liver cirrhosis, as indicated by increased TAT levels in 21 of 51 patients; (2) the plasma concentration of AT-III appears to be of major importance for the development of DIC. The present study provides evidence for DIC in severe liver cirrhosis when AT-III levels are less than 0.30 U/ml.