The Role of Helicobacter pylori in Cirrhotic Patients with Peptic Ulcers

Oh, Seong Wook; Kim, Kyung Chul; Hong, Chang Kweon; Park, Sung Gon; Kim, Dong Il; Oh, Jae In; Lee, June Sung; Kim, Bae Young; Hong, Sung Pyo; Hwang, Seong Gyu; Park, Pil Won; Rim, Kyu Sung

Abstract

BACKGROUND AND AIMS
The overall age-matched incidence of gastroduodenal ulcers was considerably higher in cirrhotic patients compared to the general population. There are several possible underlying mechanisms which may explain the ulcerogenic factors in cirrhotic patients. Recently, Helicobacter pylori (H. pylori) was proven as the cause of peptic ulcer disease in the general population. But the role of H. pylori infection in the pathogenesis of peptic ulcers of cirrhotic patients has not been clearly elucidated. The purpose of this study was to determine the role of H. pylori infection in cirrhotic patients with peptic ulcers.
METHODS
From 1995 to 1997, 105 patients with histologically or radiologically proven liver cirrhosis (LC) who received panendoscopic examination due to presence of any upper gastrointestinal symptoms were studied. During endoscopic examination, a CLO (campylobacter like organism) test or gastric antral mucosal biopsy was performed in all patients. The severity of LC assessed by Child's criteria revealed that 31 patients had Child's A, 26 patients Child's B, and the remain 48 patients, Child's C. Child B or C was classified as decompensated LC. An esophageal varix was present in 73 patients or absent in 32.
RESULTS
There was no statistical difference in the H. pylori prevalance between the ulcer group and non-ulcer group (67% vs 52%). In Child A group, the H. pylori prevalence was significantly higher in the ulcer group when compared with the non-ulcer group (87% vs 50%, p<0.05). In contrast, in the Child B or C group, there was no statistical difference between the ulcer group and non-ulcer group. In the abscence of esophageal varix, the ulcer group showed significantly higher prevalence of H. pylori than the non-ulcer group (87% vs 59%, p<0.05). But in the esophageal variceal group, there was no significant difference in the H. pylori prevalence between the ulcer and non-ulcer group (60% vs 40%).
CONCLUSIONS
These observations suggest that H. pylori infection may play a role in the pathogenesis of peptic ulcer in compensated cirrhotic patients. However, in cirrhotic patients with decompensation or an esophageal varix, the association between H. pylori infection and peptic ulcers was weak, so other factors (portal hypertension etc.) should be considered as more potent etiology of peptic ulcers in cases of decompensated cirrhosis.