BACKGROUND: Infection with Helicobacter pylori (H. pylori) has been associated with an increased risk for developing gastric cancer. This risk is further enhanced with CagA positive H. pylori strains. Increased epithelial cell proliferation is associated with an increased risk for gastric cancer. The aim of the study was to investigate whether the gastric epithelial cell proliferation was related to the expression of CagA and VacA in H. pylori infection. METHODS: The subjects were 77 patients who had undergone diagnostic esophagogastroduodenoscopy with biopsy; 18 gastritis, 18 gastric ulcer, 17 duodenal ulcer and 24 gastric cancer. The expression of cytotoxic genes was determined indirectly by assaying serum IgG antibodies to specific antigens of H. pylori. Gastric epithelial cell proliferation was assessed using immunohistochemical method using Ki-67 monoclonal antibody. Acute and chronic inflammation, intestinal metaplasia and glandular atrophy were scored according to the updated Sydney system. RESULTS: Ki-67 labeling index, acute and chronic inflammation were significantly higher in H. pylori infected persons (n=70, 90.9%) than in uninfected persons (n=7, 9.1%) (p< 0.05), but the difference in intestinal metaplasia and glandular atrophy between the two groups was not statistically significant. Ki-67 labeling indices in persons infected with CagA positive strains (n=56, 80.0%) were significantly higher than in persons infected with CagA negative strains (n=14, 20%) (0.55+/-0.13 vs 0.37+/-0.17, p< 0.05), but the differences in acute and chronic inflammation, intestinal metaplasia and glandular atrophy between the two groups were not statistically significant. No significant difference was found in Ki-67 labeling index, acute and chronic inflammation, intestinal metaplasia and glandular atrophy according to expression of VacA. CONCLUSION: Gastric mucosal cell proliferation, which might be closely involved in the pathogenesis of gastric carcinoma, was significantly higher in CagA positive H. pylori infected persons.
Antibodies ; Atrophy ; Biopsy ; Cell Proliferation ; Duodenal Ulcer ; Endoscopy, Digestive System ; Epithelial Cells* ; Gastritis ; Helicobacter pylori* ; Helicobacter* ; Humans ; Immunoglobulin G ; Inflammation ; Metaplasia ; Stomach Neoplasms ; Stomach Ulcer

BACKGROUND: Propofol can be used to provide general anesthesia or sedation. The objectives of this study were to assess propofol as sedative agents for outpatient GI endoscopy, amnestic effects, hemodynamic state and oxygenation during the procedure. METHODS: From April and June 2000, 50 patients scheduled outpatient gastrointestinal endoscopy were enrolled in this study. 30 healthy outpatients requesting sedation at diagnostic gastroscopy were received a bolus dose of propofol 2.5 mg/kg and compared with 20 patients with non-sedation. Pulse rate, blood-pressure and arterial oxygen saturation was monitored. RESULTS: Statistically significant decrease in arterial oxygen saturation were observed since 5 min after endoscopy in patients receiving propofol (p=0.006). Patients receiving sedative endoscopy, pulse rate during endoscopy was significantly increased compared with propofol group (p=0.009). Patients receiving propofol are more tolerable than patients with non-sedative endoscopy (p=0.001), therefore all patients receiving propofol wanted the same sedative endoscopy in their next endoscopy. CONCLUSION: Propofol is believed to be a useful, safe sedative agent for upper gastrointestinal endoscopy with satisfactory sedation and conditions. However, due to its untoward effect of hypoxia, careful monitoring is recommended.
Anesthesia, General ; Anoxia ; Conscious Sedation* ; Endoscopy ; Endoscopy, Gastrointestinal* ; Gastroscopy ; Heart Rate ; Hemodynamics ; Humans ; Outpatients ; Oxygen ; Propofol*