Objective: To study the clinical relations of portal hy- pertensive gastropathy (PHG) of hepatitis B cirrho- sis to other factors. Methods: Three groups of subjects were studied pro- spectively at our hospital from Ma...Objective: To study the clinical relations of portal hy- pertensive gastropathy (PHG) of hepatitis B cirrho- sis to other factors. Methods: Three groups of subjects were studied pro- spectively at our hospital from March 2000 to March 2001: 159 hepatitis B cirrhotic patients with portal hypertension, 114 hepatitis B cirrhotic patients with- out portal hypertension, and 97 control subjects. Free portal vein pressure (FPP) was measured dur- ing 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 Dagra- di grading. Gastric varices were identified according to Northern Italian Endoscopic Council (NIEC) grading. Hypersplenism was assessed with the reduc- tion of WBC, HGB and PLT. Hepatitis B virus in the gastric mucosa was detected by immunizing histo- chemistry. Helicobacter pylori (H. pylori) organisms were identified by rapid urease testing and/or exami- nation of the stained biopsy specimens (haematoxylin and eosin). To analyze the correlation between these endoscopic signs at the gastric level and other fac- tors. Results: The differences of FPP among the three groups (patients with grade Ⅰ, Ⅱ, and Ⅲ gastropa- thy) were not significant. There was no correlation between Child-Pugh classification grading and the se- verity 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 gas- tric varices compared with those without gastric vari- ces (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 prerequi- site. 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 infec- tion are unlikely to be involved in the pathogenesis of PHG. The development of PHG is less influenced ei- ther by the severity of liver disease (Child-Pugh grade) and cirrhosis or by the presence or non pre- sence of gastric varices.展开更多
文摘Objective: To study the clinical relations of portal hy- pertensive gastropathy (PHG) of hepatitis B cirrho- sis to other factors. Methods: Three groups of subjects were studied pro- spectively at our hospital from March 2000 to March 2001: 159 hepatitis B cirrhotic patients with portal hypertension, 114 hepatitis B cirrhotic patients with- out portal hypertension, and 97 control subjects. Free portal vein pressure (FPP) was measured dur- ing 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 Dagra- di grading. Gastric varices were identified according to Northern Italian Endoscopic Council (NIEC) grading. Hypersplenism was assessed with the reduc- tion of WBC, HGB and PLT. Hepatitis B virus in the gastric mucosa was detected by immunizing histo- chemistry. Helicobacter pylori (H. pylori) organisms were identified by rapid urease testing and/or exami- nation of the stained biopsy specimens (haematoxylin and eosin). To analyze the correlation between these endoscopic signs at the gastric level and other fac- tors. Results: The differences of FPP among the three groups (patients with grade Ⅰ, Ⅱ, and Ⅲ gastropa- thy) were not significant. There was no correlation between Child-Pugh classification grading and the se- verity 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 gas- tric varices compared with those without gastric vari- ces (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 prerequi- site. 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 infec- tion are unlikely to be involved in the pathogenesis of PHG. The development of PHG is less influenced ei- ther by the severity of liver disease (Child-Pugh grade) and cirrhosis or by the presence or non pre- sence of gastric varices.
