الفهرس 
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Abstract
Portal hypertensive gastropathy (PHG) is a common finding in patients with cirrhosis and portal hypertension .
Lesions of gastric mucosa observed during endoscopy in patients with cirrhosis are very common, occurring in between 7% and 98% of cases, according to different series .
VEGF is a secreted,46 kDa dimeric protein, active as direct and specific mitogen for vascular endothelial cells thus a well known mediator of angiogenesis in physiological and pathological conditions.
VEGF participates in regulation of angiogenesis in gastric wall in portal hypertension .
High levels of vascular endothelial growth factor (VEGF) in mesentery suggested their contribution in portal hypertension secondary to liver cirrhosis.
The current study was carried on fifty seven patients with liver cirrhosis and portal hypertensive gastropathy attending or admitted to Hepatology, Gastroenterology and Infectious Diseases Department ,Benha University Hospital, within, as well as eleven patients with liver cirrhosis without portal hypertensive gastropathy and another twenty one persons served as control group during the period from October 2011 to March 2012 .
We aimed at evaluating the serum concentration of VEGF and mucosal gene expression of VEGF and its possible association with PHG and prognosis in patients with cirrhosis. They were clinically assessed and had laboratory investigations including CBC, liver biochemical profile, viral markers and serum VEGF. All cirrhotic patients were diagnosed by ultrasonography and the presence of PHG were diagnosed by Esophagogastroduodendoscopy.
We found that cirrhotic patients with PHG tends to be more common in males than females, with a male to female ratio 1.6 : 1 and the mean age was ( 53.5) years with a range between ( 32-72 ) years old.
Our patients presented by findings that are common in liver cirrhosis. PT and serum creatinine were the only liver biochemical parameter higher in cirrhotic with non PHG cases than in cirrhotic with PHG cases. Otherwise, conventional tests of hepatic function did not distinguish the two groups.
HCV infection was found in 98.2% of our patients . Most of our patients presented at Child B grade, and a relatively higher MELD score.
By ultrasonography, spleen size and PV diameter was more in cirrhotic with non PHG cases than in cirrhotic with PHG cases. Otherwise, other ultasonographic parameters did not distinguish the two groups.
Regarding endoscopy there was no statistically significant difference between cirrhotic patients with PHG and cirrhotic patients with non PHG, but cirrhotic patients with PHG was associated with large varices in ( 61.4% ) of patients and small varices in ( 31.6 % ) of patients.
Concerning VEGF value in our study, it was significantly increased in cirrhotic patients with PHG as it ranges between ( 34-234.1 ) pg/ml with mean (65.3) pg/ml and also in cirrhotic patients with non PHG as it ranges between (38.8-99.5) pg/ml with mean (62.7) pg/ml compared to control group as it ranges between ( 24.4-37.5 ) pg/ml with mean ( 28.3 ) pg/ml , but the There was no statistically significant difference between cirrhotic patients with PHG and cirrhotic patients with non PHG.
According to VEGF gene expression in gastric mucosa, it was highly significantly expressed in patients with liver cirrhosis with PHG than patients with liver cirrhosis with non PHG and control group.
There was no significant correlation between VEGF and severity of liver disease (Child, MELD and uMELD), varices grade, number of varices or PHG grade.
There was no statistically significant difference between patients with varices & patients without varices as regards VEGF.