Haemostatic Imbalance in Patients With Chronic Liver Disease

Overview

To assess the level of protein C, S ,antithrombin in patients with liver cirrhosis To correlate the level of these parameters with the degree of liver cirrhosis To correlate the level of procoagulants with the level of anticoagulant proteins in liver cirrhosis

The liver has a cardinal role in the haemostatic system. Liver has the major role in synthesizing all clotting factors and coagulation inhibitors. Under the physiological conditions the balanced levels of procoagulant and anticoagulants determine the risk of hemorrhage and thrombosis. In chronic liver disease due to chronic hepatitis and underlying cirrhosis, this haemostatic imbalance leads to hypercoagulability which favors thrombosis despite the longer coagulation times of their plasma, compared with that of healthy individuals. The end stage cirrhosis is however predominately associated with bleeding tendency. Protein C (PC) and protein S (PS) are vitamin K-dependent glycoproteins, that act as natural anticoagulants. Antithrombin III (AT III) is a natural anticoagulant that is synthesized exclusively in parenchymal cells of the liver The cause of hypercoagulability in chronic liver disease is the reduced level of protein C and increased level of factor VIIIa .As a consequence of hypercoagulability, the deep vein thrombosis, pulmonary embolism, hepatic and portal vein thrombosis may occur. Varnika et al 2017 found a significantly low protein C value in both chronic hepatitis and cirrhosis group when compared with control group. Acquired deficiency of АТ III can be caused by decreased synthesis due to damage to hepatic cells Patients with CLD were (and are still) subjected to laboratory screening with the prothrombin and activated partial thromboplastin times (PT and APTT), and those with abnormal values were (are) treated with plasma or procoagulant agents to correct the abnormalities and to prevent haemorrhage during invasive procedures or to stop bleeding from the gastrointestinal tract. Saja et al., and Saray et al 2009 found significantly low protein C value in both chronic hepatitis and cirrhosis group when compared with control group. This was a sign of reduced hepatocyte synthetic capacity in chronic hepatitis. Zocco et al 2009 showed that in CLD reduction in plasma levels of PC correlate with a higher Model For End-Stage Liver Disease (MELD) score. These findings, including the present one, confirm that levels of PC are sensitive markers . Determination of the levels of AT III and aminotransferase activity in patients with liver disease may be used for differential diagnoses and the monitoring of disease progression. Little attention had been paid to the fact that, similar to procoagulant factors, their anticoagulant counterparts (namely protein C \[PC\] and antithrombin) are also reduced to the same extent in this setting.

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