الفهرس 
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Abstract
Portal hypertensive gastropathy is a common complication of PHT in which there are macroscopic changes of gastric mucosa associated with mucosal, submucosal vascular ectasia and dilatation without significant inflammatory changes.
Metaplasia is defined as a potentially reversible change in which a fully differentiated cell type is replaced by another differentiated cell type, and usually represents a change to cells better able to withstand an adverse environment. Thus intestinal metaplasia represents a change from gastric epithelial phenotype to a small intestinal or large intestinal phenotype. As PHG is also a chronic cause of mucosal irritation, it is not surprising that IM may develop in the base of PHG.
This work is aiming at studying the prevalence of IM in patients with PHG, regardless the cause (i.e. cirrhotic or non–cirrhotic PHT).
The study was carried out on 90 patients referred to the Hepatology Unit, Internal Medicine Department, Alexandria University Main Hospital. The participants were further classified into 2 groups:-
Group I (n=60): Cirrhotic or non–cirrhotic PHG patients.
Group II (n=30): Healthy subjects with functional dyspepsia taken as controls.
An esophago–gastro–duodenal endoscopic examination was done to all participants. Endoscopic mucosal biopsies were taken and stained using H & E stain for histopathological examination of histological PHG which will be defined according to McCormack et al as well as inflammation, atrophy, IM and dysplasia. Giemsa stain was used to highlight the presence of Hp microorganisms in all the biopsies.
In this study, there was no male / female predominance in both studied groups. HCV was the most common cause of PHG followed by HBV. Fifty patients were due to mixed cirrhosis. The single non–cirrhotic case was due to portal vein thrombosis. Of cirrhotic patients, 19 were in Child stage A, 30 were in Child stage B and 10 were in Child stage C. In endoscopic examination of PHG group, 31 patients had mild PHG and 29 patients had severe PHG. Fifty one patients had diffuse type PHG, 6 patients had fundus dominant PHG and 3 patients had antral dominant PHG. Esophageal varices were seen in 59 patients with PHG. Esophageal varices were present in all cirrhotic patients with PHG. Seventeen patients had Grade I varices, 29 patients had grade II varices, 13 patients had grade III varices, 8 of them showed risk signs. Gastric varices were found in 15 patients with PHG. In cirrhotic patients with PHG; 9 patients had GEV1 and 5 patients had GEV2. The single non–cirrhotic patient with PHG was suffering from IGV1.
In PHG patients 14 (23.3%), 26 (43.3%), 24 (40%) and 16 (26.7%) patients had inflammatory infiltration of gastric mucosa, gastric glandular atrophy, IM and dysplasia respectively. On the other hand 16 (53.3%), 6 (20%), 5 (16.7%) and 2 (6.7%) subjects had gastric inflammatory infiltration, gastric glandular atrophy, IM and dysplasia respectively in the control group.