الفهرس 
Physiology of HemostasisOnly 14 pages are availabe for public view
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Abstract
Liver cirrhosis is associated with extensive alterations in the hemostatic system. Thrombocytopenia, thrombasthenia, decreased thrombin generation capacity, and defects in the fibrinolytic system may all be found in these patients. However, compensatory mechanisms are also found and so patients with liver disease have rebalanced hemostasis.
Platelet abnormalities are compensated by elevated levels of vWF. The decreased production of procoaglant and profibrinolytic proteins are associated with parallel changes in anticoagulant and antifibrinolytic proteins.
Portal hypertension is a serious complication of cirrhosis. So, early diagnosis leads to adequate treatment and can significantly reduce the mortality rate of portal hypertensive related complications.
Endothelial dysfunction is involved in the pathogenesis of portal hypertension. vWF is released by activated endothelial cells and therefore represents an indicator of endothelilal cell activation.
The aim of our work was to study the relation between vWF and platelet function in cirrhotic patients and to identify the value of vWF as a predictor for the degree of cirrhosis and a predictor for the severity of portal hypertension.
This work included 90 subjects. They were divided into 2 groups: 70 patients with liver cirrhosis as the patient group and 20 healthy subjects as the control group.
The patient group was subjected to full history taking, complete physical examination, laboratory investigations, abdominal ultrasonography, portal vein duplex, upper endoscopy, and measurement of vWF Ag, vWF:RCo, and RCo/Ag ratio.
The control group was subjected to full history taking, laboratory investigations, and measurement of vWF Ag, vWF:RCo, and RCo/Ag ratio.
The results showed that vWF Ag and vWF:RCo levels were strongly elevated in cirrhotic patients while the RCo/Ag ratio which reflected the functional capacity of vWF Ag was reduced. There was also a significant positive correlation between vWF Ag and vWF:RCo. This means that the increase in vWF Ag is associated with increased platelet function (vWF: RCo) to compensate for the platelet abnormalities found in liver cirrhosis. However the functional capacity of vWF Ag is reduced (RCo/Ag ratio) because vWF:RCo rise was not proportional with the rise in vWF Ag.
Another finding, is that vWF Ag and vWF:RCo were affected by the severity of liver disease and that they increase with hepatic decompenstion as assessed by Child Pugh score and MELD score.
We also found that vWF Ag can be used as a non- invasive predictor for the severity of portal hypertension as it has the best sensitivity and specificity.