In cirrhotic livers, increased resistance to portal blood flow is the primary factor in the pathophysiology of
portal hypertension (PH) and is caused by structural abnormalities in the hepatic vascular architecture and an
increased hepatic vascular tone. Von Willebrand factor antigen (vWF Ag) is released by activated endothelial cells (ECs)
and therefore represents an indicator of EC activation and plays a crucial role in high shear stress, depending on primary
hemostasis. The aim of this work was to evaluate the diagnostic performance of vWF-Ag to detect clinically significant PH
suggested by portal vein velocity (PVV) in patients with liver cirrhosis and to evaluate vWF-Ag levels in the prediction of
decompensation.
Patients and methods: vWF Ag was measured in thirty patients with liver cirrhosis and twenty healthy control
subjects and results were correlated with portal hypertension as suggested by portal vein velocity.
Results: Levels of vWF Ag were significantly higher in patients with cirrhosis than healthy control subjects
while levels of PVV were significantly lower. vWF Ag significantly increase in presence of ascites and shrunken liver.
Levels of vWF show significant correlation with PVV and the best diagnostic cutoff value for portal hypertension was found to be
270 U/dL.
Conclusion: Our study shows an impressive correlation between portal hypertension and vWF levels thus can be used as
noninvasive predictor of clinically significant portal hypertension (CSPH) in patients with liver cirrhosis.