Gastric pH and Helicobacter pylori Infection in Patients with Liver Cirrhosis.
- Author:
Yeong Jin NAM
1
;
Seong Jun KIM
;
Won Chang SHIN
;
Jin Ho LEE
;
Won Choong CHOI
;
Kwan Yeop KIM
;
Tae Hui HAN
Author Information
1. Department of Internal Medicine, Sanggye Paik Hospital, Inje University College of Medicine, Seoul, Korea. choi829@sanggyepaik.ac.kr
- Publication Type:Original Article ; English Abstract
- Keywords:
Liver cirrhosis;
Hypochlorhydria;
H. pylori;
NH3;
Hepatic encephalopathy
- MeSH:
Achlorhydria/complications;
Ammonia/analysis;
English Abstract;
Female;
Gastric Acid/secretion;
*Gastric Acidity Determination;
Helicobacter Infections/*complications/physiopathology;
*Helicobacter pylori;
Humans;
Hydrogen-Ion Concentration;
Liver Cirrhosis/*metabolism/microbiology/physiopathology;
Male;
Middle Aged
- From:The Korean Journal of Hepatology
2004;10(3):216-222
- CountryRepublic of Korea
- Language:Korean
-
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 compare 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. None 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 micro M/L, P<0.05). The 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 micro M/L). In patients with cirrhosis, the presence of H. pylori infection was not correlated with either gastric or blood NH3 levels. CONCLUSIONS: The 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.
