Helicobacter pylori (H. pylori), a long term colonizer of human stomach is known to infect a half of mankind. Gastric and duodenal ulcer, gastric adenocarcinoma and MALT lymphoma develop in a subset of infected individuals. Pathogenesis of H. pylori infection is based on the long-term host to bacterial interaction and affected by the virulence factors of the bacterium, environmental and host factors (age, sex, blood type). Mucosal inflammation is the basic principle mechanism underlying the disease development in which tissue destruction may be initiated and maintained by both the bacterial toxins (CagA, VacA, LPS) and immune responses by the host. Immune evasion with bacterial modulation of host response affects the long-term host colonization. Colonization is also affected by urease and/or motility of the bacterium, presence of lipopolysaccharide (LPS) and various bacterial enzymes. Gastric mucosal atrophy and intestinal metaplasia can develop during the course of H. pylori infection predisposing to carcinogenesis. Host cytokine gene polymorphism would be the one explanation for host susceptibility to peptic ulcer or gastric cancer. Investigation into the pathogenesis of H. pylori related diseases could provide an answer to the impact of chronic host to microbial interaction resulting human diseases.
Gastrointestinal Diseases ; Helicobacter Infections/microbiology/*physiopathology ; *Helicobacter pylori/physiology ; Humans

No abstract available
Cardiovascular Diseases/*microbiology/physiopathology ; Helicobacter Infections/*complications ; *Helicobacter pylori ; Humans

OBJECTIVE: To explore the relationship between the Helicobacter pylori (H.pylori) infection and gastric mucosa change and blood-lipid in people undergoing the physical examination in Changsha. METHODS: A total of 2 264 people undergoing physical examination were divided into an H. pyloripositive group (n=1 068) and an H. pylori-negative group (n=1 196). Gastric mucosa change was diagnosed by gastroscopy, blood-lipid and blood sugar were detected, and the statistical analysis was performed. RESULTS: The incidence rate of H.pylori infection was 47.2%. The incidence rate of gastric mucosal erosion, gastric ulcer, duodenal ulcer, gastric mucosal atrophy, gastric polyp, dyslipidemia, increase of triglyceride were (TG) and decrease of the high density lipoprotein cholesterol (HDL-C) in the H.pylori-positive group were all higher than those in the H.pylori-negative group (P<0.01 or P<0.05). In the H. pylori-positive group, the level of TG in people with gastric mucosal erosion, gastric ulcer and duodenal ulcer was higher than that in people with normal gastric mucosa or mild gastritis, and HDL-C was lower than that in people with normal gastric mucosa or mild gastritis. CONCLUSION H. pylori infection can induce the gastric mucosa injury and dyslipidemia, which may result in the occurrence and development of coronary heart disease by increasing TG and decreasing HDL-C, thus increasing the risk of atherosclerosis.
Adenomatous Polyps ; Cholesterol, HDL ; blood ; Duodenal Ulcer ; microbiology ; physiopathology ; Dyslipidemias ; microbiology ; Gastric Mucosa ; microbiology ; pathology ; Gastritis ; microbiology ; physiopathology ; Helicobacter Infections ; physiopathology ; Helicobacter pylori ; Humans ; Lipids ; blood ; Physical Examination ; Stomach Neoplasms ; Stomach Ulcer ; microbiology ; physiopathology ; Triglycerides ; blood

OBJECTIVEDuodenogastric reflux (DGR) is a reverse flow of duodenal juice into stomach through pylorus composed of bile acid, pancreatic secretion, and intestinal secretion. The increased entero-gastric reflux results in mucosal injury that may relate not only to reflux gastritis but also esophagitis, gastric ulcers, carcinoma of stomach and esophagus. However, the exact mechanisms of gastric mucosal damage caused by DGR are still unknown. The objective of the present study is to investigate the pathogenic effect of primary DGR on gastric mucosa in children, and to explore the correlation of DGR with clinical symptoms, Hp infection and intragastric acidity.

METHODTotally 81 patients with upper gastrointestinal manifestations were enrolled and they were graded according to the symptom scores and underwent endoscopic, histological examinations and 24-hour intra-gastric bilirubin was monitored with Bilitec 2000. Of the 81 cases, 51 underwent the 24-hour intra-gastric pH monitoring by ambulatory pH recorder simultaneously. The total fraction time of bile reflux was considered as a marker to evaluate the severity of DGR. The total fraction time of bile reflux was compared between the patients with positive and negative results under endoscopy and histologically, respectively. The correlations of the total fraction time of bile reflux with clinical symptom score, Hp infection, intragastric acidity were analyzed respectively.

RESULTThe total fraction time of bile reflux in the patients with hyperemia and yellow stain gastric antral mucosa under endoscopy was significantly higher than that without those changes [17.1% (0.5% approximately 53.2%) vs. 6.5% (0 approximately 58.6%), Z = -1.980, P < 0.05; 19.8% (0.5% approximately 58.6%) vs. 8.8% (0 approximately 38.0%), Z = -2.956, P < 0.01 respectively]. Histologically, the cases with intestinal metaplasia had significantly higher total fraction time of bile reflux than in the cases without intestinal metaplasia [29.0% (1.9% approximately 58.6%) vs. 14.3% (0 approximately 53.7%), Z = -2.026, P < 0.05], but no significant difference was found either between the cases with and without chronic inflammation (P > 0.05) or between the cases with and without active inflammation (P > 0.05). The severity of bile reflux was positively correlated with the score of abdominal distention (r = 0.258, P < 0.05), but no correlation with either the severity of intragastric acid (r = -0.124, P > 0.05), or Hp infection (r = 0.016, P > 0.05) was found.

CONCLUSIONPrimary DGR could cause gastric mucosal lesions manifested mainly as hyperemia and bile-stained gastric antral mucosa under endoscopy and the gastric antral intestinal metaplasia histologically in children. There was no significant correlation between DGR and gastric mucosal inflammatory infiltration. DGR had no relevance to Hp infection and intragastric acidity. We conclude that DGR is probably an independent etiological factor and might play a synergistic role in the pathogenesis of gastric mucosal lesions along with gastric acid and Hp infection.

Adolescent ; Bile Reflux ; pathology ; physiopathology ; Child ; Child, Preschool ; Duodenogastric Reflux ; microbiology ; pathology ; physiopathology ; Female ; Gastric Mucosa ; microbiology ; pathology ; Helicobacter Infections ; Helicobacter pylori ; Humans ; Hydrogen-Ion Concentration ; Male

BACKGROUND: The adhesion of H. pylori to the gastric epithelial cells may be an essential step for the pathophysiology of various H. pylori-induced gastrointestinal diseases. The purpose of this study was to investigate the ultrastructural relation of H. pylori and gastric epithelial cells in their adhesion. METHODS: Endoscopic biopsy of gastric antrum and body was performed from 15 patients (9 men, 6 women) with chronic gastritis and H. pylori infection. The specimens were processed for electron microscopy and observed with a transmission electron microscope (Hitachi H-600). RESULTS: On the basis of morphological appearances, the adhesions of H. pylori to the gastric epithelial cells were categorized into three types; filamentous connection, adhesion pedestals and membrane fusion. Coccoid and undetermined forms adhered mainly by the filamentous connection, whereas the bacillary forms adhered primarily by the adhesion pedestals and membrane fusion. CONCLUSION: Various types of adhesion were associated with H. pylori and gastric epithelium. Further studies are needed to evaluate the influence of different types of adhesion to the pathophysiology of H. pylori.
*Bacterial Adhesion ; Endoscopy, Gastrointestinal ; Female ; Gastritis/*microbiology/pathology ; Helicobacter Infections/*microbiology/pathology/physiopathology ; Helicobacter pylori/classification/physiology/*ultrastructure ; Human ; Male ; Microscopy, Electron ; Middle Age ; Stomach/*microbiology/pathology ; Support, Non-U.S. Gov't

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.
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