patients with liver cirrhosis, most of them somewhat higher than our study7, 8, 12, 14, 17, 18). Moreover, the prevalence of H. pylori infection in cirrhotic patients in our study was significantly lower than that in the control and reference groups, a finding that was different from that found by many groups6, 7, 13-18, 23, 24). It was consistent with the results of others19, 20). This relatively low prevalence of H. pylori infection in cirrhotic patients in our study can be explained by the enrollment of more than 50% of Child-Pugh B and C cirrhotic patients in our study. Although those who took antibiotics within 2 weeks before entry were excluded, those who had a history of extensive but remote use of antibiotics were included. Therefore, inclusion of decompensated cirrhotic patients with a history of extensive but remote use of antibiotics due to various reasons might affect the prevalence of H. pylori. The relatively low prevalence of H. pylori infection in cirrhotic patients in our study can also be partially explained by the difference in the diagnostic methods used in the setting of H. pylori infection. In general, studies that use serologic tests (IgG to H. pylori) report higher prevalence than the studies that use the rapid urease test, histology, or urea breath test for detection of H. pylori infection (76.2～89% vs. 39～59.7%). If H. pylori infection and liver cirrhosis have the same risk factors, but H. pylori infection cannot easily persist in the stomach of cirrhotic patients, serologic determination of H. pylori infection may lead to confounding results. The 2007 Maastricht Consensus Report on H. pylori diagnosis and treatment does not recommend serological determination of H. pylori infection in routine clinical practice. It also recommends that the primary diagnosis of H. pylori infection should be established by rapid urease test and/or histology25-28). The accuracy of gastric mucosal biopsy may be affected by various factors: the presence of bacteria other than H. pylori that produce urease, the patch distribution of H. pylori in gastric mucosa, and the histologic overestimation of H. pylori due to the presence of confounding bacteria. Thus, primary diagnosis by gastric mucosa biopsy urease testing and/or histology has some limitations19). So the accuracy of diagnostic methods use to detect H. pylori infection in our study may affect the result of low prevalence of H. pylori infection. The concordance of rapid urease test and histology for the diagnosis of H. pylori infection in our study was 255 out of 288 in cirrhotic patients and 293 out of 339 in peptic ulcer patients without chronic liver disease. The prevalence of H. pylori infection in the control group of the present study (62.4%) was slightly lower than the seroprevalence (66.9%) in asymptomatic Korean adults29). This discrepancy may be due to the different study groups and diagnostic methods. H. pylori infection in the general population correlates with age, social class, education level, overcrowding, bed-sharing, and economic level during childhood13). Thus, a Dong Joon Kim, et al : H. pylori and Peptic Ulcer in Cirrhosis 19 valid comparison of the prevalence of H. pylori infection in patients with cirrhosis and the general population, a control group matched by prognostic variables (age, socioeconomic status, ethanol intake, etc.) would be required. Although our study used age- and sex-matched control and reference groups, socioeconomic status and ethanol intake were not matched. Consequently, out study may not provide definitive data. Besides H. pylori, other factors may contribute to the increased risk of peptic ulcer in cirrhotic patients30, 31). Reduced prostaglandins, decreased gastric acid secretion, elevated serum gastrin concentration, impaired mucus secretion, a reduction in potential difference of the gastric mucosa, and portal hypertensive gastropathy may all play a role in the pathogenesis of peptic ulcer disease in cirrhotic patients1-3). Several studies have been previously performed regarding the relationship between the prevalence of H. pylori infection and peptic ulcer disease according to the etiology and severity of liver cirrhosis. The present study demonstrated an interesting finding in that the prevalence of H. pylori infection in patients with liver cirrhosis varied according to the etiology of cirrhosis (viral vs. alcoholic = 42.5 vs. 22.0%, p <0.001). In Korea, HBV infection is still the leading cause of liver cirrhosis (53%), followed by alcohol (31%) and HCV infection (10%)32). Since our study included a relatively small proportion of cirrhotic patients with HCV infection, the fact that the prevalence of H. pylori infection in virus-related liver cirrhosis was higher than that in alcohol-related cirrhosis patients may not be generalizable in other countries where the major cause of liver cirrhosis is HCV infection. It is of interest to note that the prevalence of H. pylori infection was related inversely to Child-Pugh classification. Although this observation is consistent with a previous report, which suggested that the prevalence of H. pylori infection among cirrhotic patients might be inversely related to the severity of liver cirrhosis, many previous data have noted no relationship between H. pylori infection and severity of liver cirrhosis8, 10, 11, 33, 34). Several factors, such as diagnostic methods, etiology of liver cirrhosis, proportion of decompensated cirrhosis, and geographic and racial differences in H. pylori prevalence, may explain the discrepancy. Based on our study, we hypothesize that the environment of the stomach in cirrhotic patients may not be suitable for the growth of H. pylori, and the progression of liver disease may lead to a more hostile milieu to H. pylori. Many studies have argued for the relationship between H. pylori and peptic ulcer in cirrhotic patients, but the 'statistically high' (which is at most 2 times higher than control) prevalence of H. pylori in cirrhotic patients in those studies cannot explain completely the 'vividly and absolutely high' (which is at least 10 times higher than control) prevalence of peptic ulcer in cirrhotic patients. Our study showed that even though H. pylori infection