BACKGROUND: Infection of the gastric mucosa by helicobacter pylori is primarily responsible for gastritis, gastric ulcer, adenocarcinoma, and lymphoproliferative disorders. H. pylori appears to accelerate apoptosis and the proliferation of the gastric epithelium directly or indirectly. To precisely assess the proliferative and apoptotic profile of .H pylori-infected gastric mucosa, a quantitative imaging system is now required. METHODS: Fifty-two patients with H. pylori gastritis were the subjects of the study. Biopsy materials were taken from at least two sites (usually three to five sites) including the antrum and corpus. The grade of gastritis was evaluated by the updated Sydney System. The proliferative and apoptotic profile was examined by Ki-67 immunohistochemistry and by a terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling method. In addition, Ki-67-positive cells were quantitated by an image processor for analytical pathology (IPAP) system. RESULTS: H. pylori density and polymorphonuclear neutrophil activity were significantly decreased after H. pylori eradication ( P< 0.0001). Chronic inflammation (P< 0.0001) and lymphoid follicle numbers ( P < 0.0005) were also significantly decreased after the eradication. Glandular atrophy and intestinal metaplasia were slightly decreased after eradication, but the decrease did not reach the significant level. the Ki-67 labeling index was significantly decreased after the eradication P< 0.0001). The apoptosis index was also decreased after the eradication, but this decrease did not reach the significant level ( P = 0.06). CONCLUSION: our data suggest that the activation of proliferative cells and induction of apoptosis in the gastric mucosa is a response to H. pylori-induced mucosal damage. Moreover, IPAP may be a useful technology for evaluating the results of immunohistochemistry, and it could provide quantitative and reliable data for studying H. pylori gastritis.
BACKGROUND: Infection of the gastric mucosa by helicobacter pylori is primarily responsible for gastritis, gastric ulcer, adenocarcinoma, and lymphoproliferative disorders. H. pylori appears to accelerate apoptosis and the proliferation of the gastric epithelium directly or indirectly. To precisely assess the proliferative and apoptotic profile of .H pylori-infected gastric mucosa, a quantitative imaging system is now required. METHODS: Fifty-two patients with H. pylorigastritis were the subjects of the study. Biopsy materials were taken from at least two sites (usually three to five sites) including the antrum and corpus. The grade of gastritis was evaluated by the updated Sydney System. The proliferative and apoptotic profile was examined by Ki-67 immunohistochemistry and by a terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling method. In addition, Ki-67-positive cells were quantitated by an image processor for analytical pathology (IPAP) system. RESULTS:H. pylori density and polymorphonuclear neutrophil activity were significantly decreased after H. pylori eradication ( P< 0.0001). Chronic inflammation (P< 0.0001) and lymphoid follicle numbers ( P < 0.0005) were also significantly decreased after the eradication. Glandular atrophy and intestinal metaplasia were slightly decreased after eradication, but the decrease did not reach the significant level. the Ki-67 labeling index was significantly decreased after the eradication P< 0.0001). The apoptosis index was also decreased after the eradication, but this decrease did not reach the significant level ( P = 0.06). CONCLUSION: our data suggest that the activation of proliferative cells and induction of apoptosis in the gastric mucosa is a response to H. pylori-induced mucosal damage. Moreover, IPAP may be a useful technology for evaluating the results of immunohistochemistry, and it could provide quantitative and reliable data for studying H. pylorigastritis.