Abstract
BackgroundHCV infection is a major worldwide cause of chronic liver diseases. Esophageal and gastric varices are common in cirrhotic patients due to concomitant portal hypertension. Variceal hemorrhage is a major decompensating event with high morbidity and mortality. Endothelial dysfunction, occurring in cirrhosis, facilitates the development of liver cirrhosis, portal hypertension and contributes to increased intrahepatic vascular resistance..VEGF family members are major regulators of blood vessel development and function.ResultsThe study was conducted on 90 subjects admitted to Tropical Medicine Department, Alexandria Main University Hospital: 30 cirrhotic patients with endoscopically proven varices (group A), 30 cirrhotic patients without varices (group B), and 30 healthy controls (group C). All patients was subjected to detailed history taking and thorough clinical examination, laboratory investigations, ultrasound abdomen, upper gastrointestinal endoscopy, and genotyping for VEGF C(+405)G (rs2010963) by 5′ nuclease assay. The VEGF C(+405)G (rs2010963) GG genotype was associated with higher prevalence of esophageal and gastric varices and higher bleeding risk.ConclusionVEGF C(+405)G (rs2010963) is an important genetic determinant of esophageal varices, gastric varices, and correlates with variceal bleeding risk. Genetic testing of this SNP would be useful in prediction of esophageal and gastric varices and bleeding risk.
Highlights
Hepatitis C virus (HCV) infection is a major worldwide cause of chronic liver diseases
HCV infection is a worldwide cause of chronic liver diseases [1]
The hepatic pathology progress from minimal histological alterations up to extensive hepatocellular necrosis, fibrosis, and cirrhosis that could be complicated by hepatocellular carcinoma (HCC) [2]
Summary
HCV infection is a major worldwide cause of chronic liver diseases. Esophageal and gastric varices are common in cirrhotic patients due to concomitant portal hypertension. Endothelial dysfunction, occurring in cirrhosis, facilitates the develop‐ ment of liver cirrhosis, portal hypertension and contributes to increased intrahepatic vascular resistance..VEGF family members are major regulators of blood vessel development and function. HCV infection is a worldwide cause of chronic liver diseases [1]. Cirrhosis is the common end-result for chronic liver injury regardless of the etiology. It is characterized by diffuse hepatocellular necrosis and diffuse nodular regeneration surrounded by dense fibrotic septa causing pronounced distortion of hepatic vascular architecture causing increased resistance to portal blood flow and in portal hypertension [4]
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