الفهرس 
PORTAL HYPERTENSION
Etiology of Prehepatic PHTOnly 14 pages are availabe for public view
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Abstract
Liver cirrhosis is a major cause of morbidity and mortality and is currently the 14th leading cause of death worldwide. Portal hypertension(PHT) is an almost unavoidable consequence of liver cirrhosis. It is a very frequent and dreadful complication of the liver cirrhosis. It leads to serious complications as variceal bleeding, hepatorenal syndrome, hepatic encephalopathy, spontaneous bacterial peritonitis and cardiopulmonary complications like porto-pulmonary hypertension and hepato-pulmonary syndrome that responsible for significant morbidity and mortality in patients with liver cirrhosis and accounts for most indications of liver transplantation. Recently, increased intrahepatic resistance is the primary factor of PHT, this is aggravated by an increased hepatic vascular tone, which results from an insufficient hepatic bioavailability of nitric oxide (NO). Nitric oxide plays a pivotal role in the pathogenesis of PHT so NO donor or drug delivery system that selectively targets liver cells (portal/septal myofibroblasts, activated hepatic stellate cells, and vascular smooth muscle cells in portal vasculature) without actions on the systemic circulation is required to reduce PHT without adverse systemic effects. So, the aim of this study was to study the portal hypertension by Doppler ultrasound in cirrhotic patients before and after receiving simvastatin and to study other Doppler parameters reflecting hepatic fibrosis in cirrhotic patients.