Gastric pH and Helicobacter pylori Infection in Patients with Liver Cirrhosis

Korean J Hepatol > Volume 10(3); 2004 > Article

The Korean Journal of Hepatology 2004;10(3): 216-222.

Gastric pH and Helicobacter pylori Infection in Patients with Liver Cirrhosis

Yeong Jin Nam, M.D., Seong Jun Kim, M.D., Won Chang Shin, M.D., Jin Ho Lee, M.D., Won Choong Choi, M.D., Kwan Yeop Kim, M.D. and Tae Hui Han, M.D.*

Departments of Internal Medicine and Clinical Pathology*, Sanggye Paik Hospital, Inje University College of Medicine, Seoul, Korea

ABSTRACT

Background/Aims
Data from previous studies on gastric acid secretion and the prevalence of H. pylori in liver cirrhosis patients remain poorly defined. H. pylori is a potential source of NH₃, but the possible role of H. pylori in hepatic encephalopathy is not clear. The purpose of this study was to com pare gastric acid secretion, the impact of H. pylori infection, and the production of NH₃ between cirrhotic patients and healthy, matched controls. Methods: Twenty-nine patients with liver cirrhosis (HBV , n=12; Alcohol, n=12; HCV , n=5) were matched with 33 healthy persons for age and sex. N one of the patients or controls were being treated with antacids, H2-receptor blockers or proton pump inhibitors. The pH and NH₃ concentration was measured in gastric juice obtained by endoscopy. H. pylori infection was diagnosed using the rapid urease test. The level of NH₃ in venous blood was also measured. Results: The average gastric pH was significantly higher in cirrhosis patients compared to controls (3.91 vs. 2.99, P < 0.05). In addition, the prevalence of hypochlorhydria (defined as pH > 4) was significantly greater in cirrhosis patients (45 vs. 21% , P < 0.05). In contrast, the prevalence of H .pylori infection (62% vs.58% ) and gastric NH₃ concentrations (3.4 vs.3.3 mM/L ) were similar between both groups. However, venous NH₃ levels were significantly higher in cirrhotics than in controls (63.1 vs.25.2 μM/L ,P < 0.05).T he patients with H .pylori infection had significantly higher gastric NH₃ concentration (3.8 vs. 1.6 mM/L) and gastric pH (3.87 vs. 2.76, P < 0.05) than those without infection, but no significant difference in venous NH₃ levels were detected (39.6 vs. 48.1 μM/L ). In patients with cirrhosis, the presence of H. pylori infection was not correlated with either gastric or blood NH₃ levels. Conclusions: T he gastric pH of liver cirrhosis patients is higher than that of controls and a larger proportion of cirrhotic patients have hypochlorhydria. The prevalence of H. pylori in liver cirrhosis patients was similar to that in controls and no correlation was found between gastric and blood NH₃ levels. Thus, H. pylori infection does not seem to play a major role in generation of elevated NH₃ associated with hepatic encephalopathy. (Korean J Hepatol 2004;10:216-222)

KeyWords: Liver cirrhosis, Hypochlorhydria, H. pylori, NH₃, Hepatic encephalopathy