الفهرس 
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Abstract
PVT is a common complication in patients with advanced liver cirrhosis. Prevalence of PVT among cirrhotic patients ranges from 1% in compensated cirrhosis to 8-25% in patients waiting for liver transplantation (Francoz et al., 2005).
To date, the main pathogenic factor of PVT in liver cirrhosis is not completely understood, however, decreased portal blood flow (Zocco et al., 2009), vascular damage (Intagliata et al., 2015), hepatic carcinogenesis (Ponziani et al., 2010) and complex derangement of the hemostasis system due to liver cell damage (Amitrano and Guardascione, 2009) are pivotal contributors.
Blood coagulation process is triggered when circulating FVIIa forms a complex with TF that activates FX and subsequently clot formation. FVIIa is inhibited by AT only when it is bound to TF, which causes the accelerated dissociation of FVIIa from TF resulting in the formation of the FVIIa-AT complex (Palta et al., 2014).
This study was conducted in the Department of Internal Medicine, Minia University Hospital along the period from October 2013 to May 2016.
The aim of our study was to evaluate the role of FVIIa-AT complex and enhanced monocytic TF expression in pathogenesis and prediction of non-neoplastic PVT in Egyptian patients with HCV-related liver cirrhosis
Our study included a group of cirrhotic patients with non-neoplastic PVT (30 patients). This group of patients was compared to a group of cirrhotic patients without PVT (35 patients), a group of non-cirrhotic patients with PVT (15 patients) and a group of healthy subjects (15 subjects).