High adhesion. (11) At the same time,

High vWF levels in cirrhosis could be
explained in many aspects. It’s well established that vWF-antigen (vWF-Ag) is
released by activated endothelial cells (ECs) and therefore represents an
indicator of ECs activation. In PHT, endothelial cell dysfunction is a major
participant in hemodynamic changes, so it could be a result of PHT. In
addition, enhanced synthesis of vWF-Ag by cirrhotic liver, diminished clearance
of vWF-Ag resulting from decreased expression or activity of ADAMTS13 (vWF-Ag
cleaving protease) may further increase vWF-Ag levels.(11,12) On the other hand, high vWF,
which enhance platelet adhesion and microthrombi formation, may be a
participant in formation of PHT through thrombotic vascular obliteration and
augmentation of vascular resistance.(4,19,20)

We found in current study that vWF
correlated negatively with platelet counts. In liver cirrhosis, variable degree
of thrombocytopenia is present. High vWF in these patients is considered a
compensatory mechanism through increasing platelet adhesion. (11) At the same time, its established
that thrombocytopenia correlates with PHT and gastroesophageal varices and this
could explain this inverse correlation we found.(21)

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In the current work, when applying
the VITRO score, it could predict variceal bleeding with high sensitivity but
moderate specificity. In accordance to our results, Maieron and colleagues (22) concluded that VITRO score could
predict degree of fibrosis with high performance. Also, VITRO score was
correlated with worsening HVPG categories (P


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