Objective: To study the clinical relations of portal hypertensive gastropathy (PHG) of hepatitis B cirrhosis to other factors.
Methods: Three groups of subjects were studied prospectively at our hospital from March 2000 to March 2001: 159 hepatitis B cirrhotic patients with portal hypertension, 114 hepatitis B cirrhotic patients without portal hypertension, and 97 control subjects. Free portal vein pressure (FPP) was measured during surgery. Liver function was assessed by Pugh’s modification of Child’s criteria. The area of liver collagen fibrin was studied using color image analysis system. Esophageal varices were identified by Dagradi grading. Gastric varices were identified according to Northern Italian Endoscopic Council (NIEC) grading. Hypersplenism was assessed with the reduction of WBC, HGB and PLT. Hepatitis B virus in the gastric mucosa was detected by immunizing histochemistry. Helicobacter pylori (H. pylori) organisms were identified by rapid urease testing and/or examination of the stained biopsy specimens (haematoxylin and eosin). To analyze the correlation between these endoscopic signs at the gastric level and other factors.
Results: The differences of FPP among the three groups (patients with grade Ⅰ, Ⅱ, and Ⅲ gastropathy) were not significant. There was no correlation between Child-Pugh classification grading and the severity of gastropathy (P=0.153). The differences of the area of liver collagen fibrin among the three grade gastropathy were not statistically significant (P=0.801). There was a significant difference in the prevalence of severe PHG among grade Ⅰ, Ⅱ, Ⅲ, Ⅳ and Ⅴ esophageal varices (P<0.001). PHG was present in a similar percentage of patients with gastric varices compared with those without gastric varices (P=0.209). There was a significant difference in the severity between PHG and hypersplenism (P=0.003). Seven patients with PHG had no microscopic evidence of hepatitis B virus infection in the gastric wall. There was no correlation between Child-Pugh classification grading and infection of H. pylori (P=0.7491).
Conclusions: The most important element causing PHG is the increased portal pressure as a prerequisite. In addition, other factors may contribute to the development of PHG. PHG often occurs in patients with the presence of esophageal varices. There is a marked correlation between the severity of PHG and hypersplenism. Hepatitis B virus and H. pylori infection are unlikely to be involved in the pathogenesis of PHG. The development of PHG is less influenced either by the severity of liver disease (Child-Pugh grade) and cirrhosis or by the presence or non presence of gastric varices.