Time Trends in Helicobacter pylori Infection and Atrophic Gastritis Over 40 Years in Japan.

BACKGROUND: Helicobacter pylori infection produces progressive mucosal damage that may eventually result in gastric cancer. We studied the changes that occurred in the presence and severity of atrophic gastritis and the prevalence of H. pylori infection that occurred coincident with improvements in economic and hygienic conditions in Japan since World War II. MATERIALS AND METHODS: The prevalence of H. pylori infection and histologic grades of gastric damage were retrospectively evaluated using gastric biopsy specimens obtained over a 40-year period. Gastric atrophy and intestinal metaplasia were scored using the updated Sydney classification system. RESULTS: The prevalence of H. pylori and severity of atrophy were examined in 1381 patients including 289 patients examined in the 1970s (158 men; mean age, 44.9 years), 787 in the 1990s (430 men; 44.2 years), and 305 in the 2010s (163 men; 53.2 years). Overall, the prevalence of H. pylori infection decreased significantly from 74.7% (1970s) to 53% (1990s) and 35.1% (2010s) (p < .01). The prevalence of atrophy in the antrum and corpus was significantly lower in the 2010s (33, 19%, respectively) compared to those evaluated in either the 1970s (98, 82%) (p < .001) or 1990s (80, 67%) (p < .001). The severity of atrophy and intestinal metaplasia also declined remarkably among those with H. pylori infection. CONCLUSIONS: There has been a progressive and rapid decline in the prevalence of H. pylori infection as well a fall in the rate of progression of gastric atrophy among H. pylori-infected Japanese coincident with the westernization and improvements in economic and hygienic conditions in Japan since World War II.

Does intragastric nitrite concentration reflect gastric carcinogenesis in Japanese Helicobacter pylori-infected patients?

Established risk factors for gastric cancer include a diet high in nitrate or nitrite and low in vitamin C and the presence of achlorhydria or hypochlorhydria. The aim of this study was to investigate the relationship between intragastric nitrite concentration and atrophic change of the stomach or gastric carcinogenesis in Japanese Helicobacter pylori-infected patients. Gastric juice pH, nitrite, and total vitamin C concentrations in gastric juice, serum pepsinogen I and II concentrations, and specific Helicobacter pylori antibody were analyzed. Intragastric total vitamin C concentration was decreased by Helicobacter pylori infection of the gastric mucosa and with progression of the atrophic grade. There was a significant positive correlation between atrophic grade and intragastric nitrite concentration. In conclusion, the levels of nitrite in gastric juice play a causal role in the development of cancer in Helicobacter pylori-associated atrophic gastric mucosa.

Gastric juice nitrite and vitamin C in patients with gastric cancer and atrophic gastritis: is low acidity solely responsible for cancer risk?

BACKGROUND: N-nitroso compounds are carcinogens formed from nitrite, a process that is inhibited by vitamin C in gastric juice. Helicobacter pylori infection has been reported to increase nitrite and decrease vitamin C in gastric juice. Therefore, susceptibility to gastric cancer in H. pylori-infected patients may be derived from increased N-nitroso compounds in gastric juice. However, most H. pylori-infected patients do not develop gastric cancer. OBJECTIVE: To investigate additional factors that may affect susceptibility to gastric cancer, we compared nitrite and vitamin C levels in gastric juice from H. pylori-infected patients with and without gastric cancer. METHODS: Serum and gastric juice were obtained from 95 patients undergoing diagnostic endoscopy, including those with normal findings, duodenal ulcer, gastric ulcer, atrophic gastritis and gastric cancer. Serum was analysed for H. pylori antibody, nitrate and nitrite, gastrin and pepsinogens; gastric juice was analysed for pH, nitrite and vitamin C. RESULTS: pH and nitrite levels were increased and vitamin C levels decreased in the gastric juice of patients with atrophic gastritis and gastric cancer compared with other patients. However, in patients with a similar gastric acidity (pH 5-8), nitrite concentrations in the gastric juice were significantly higher and vitamin C levels significantly lower in patients with gastric cancer than in those with atrophic gastritis. CONCLUSION: Although hypochlorhydria increases intraluminal nitrite and decreases intraluminal vitamin C, which increases the intraluminal formation of N-nitroso compounds, our results indicate that patients with gastric cancer may have additional factors that emphasize these changes.

Food deprivation enhances somatostatin and somatostatin receptor subtype expression in rat colon.

Somatostatin, a peptide distributed widely throughout the gut, inhibits a variety of gastrointestinal functions. We previously reported that fasting for 48 h increased gastric somatostatin peptide and mRNA content. Thus, somatostatin could contribute to the inhibition of gastric G cells during fasting. To investigate the effect of fasting on intestinal somatostatin, we determined tissue somatostatin concentration by radioimmunoassay, somatostatin mRNA expression by Northern analysis and reverse transcription polymerase chain reaction (RT-PCR), and mRNA expression for somatostatin receptor subtypes (sst) 1-5 by RT-PCR in ileum and colon of rats either freely fed or food-deprived for 48 h. In the colon, fasting increased somatostatin concentration, somatostatin mRNA expression, and mRNA expression for two receptor subtypes (sst2 and sst3). In the ileum, no change of somatostatin peptide concentration and receptor subtype mRNA expression was demonstrated; only somatostatin mRNA expression was augmented by fasting. These results suggest that in rat colon, fasting for 48 h increases somatostatin synthesis and receptor subtype expression. These changes may be important in maintaining homeostasis during starvation.

Is apoptosis in antral mucosa correlated with serum nitrite concentration in Japanese Helicobacter pylori-infected patients?

BACKGROUND AND AIM: Helicobacter pylori infection in gastric mucosa is a form of chronic active gastritis that leads to expression of inducible nitric oxide synthase in host macrophages and polymorphonuclear leukocytes. Nitric oxide produced by these cells infiltrating the gastric mucosa could damage DNA. We correlated apoptosis in H. pylori-infected antral tissue from peptic ulcer patients with serum nitrate-plus-nitrite. METHODS: Biopsy specimens were obtained endoscopically from antrum and fundus in 17 peptic ulcer patients before and after H. pylori eradication. Tissue samples were subjected to rapid urease testing and histopathological scoring (updated Sydney system), as well as immunohistochemical detection of single-stranded DNA indicating apoptotic cells. Fasting serum samples were analyzed for combined nitrate and nitrite content. RESULTS: In all cases atrophy was absent to mild in antral mucosa and H. pylori was eradicated successfully. A strong positive correlation was present between apoptosis and both inflammation and activity scores in infected antral mucosa. A significant positive correlation also was noted between apoptosis and H. pylori density. Serum nitrite concentrations were decreased significantly by successful eradication of H. pylori, and showed a strong positive correlation with H. pylori density. Serum nitrite concentrations showed a significant positive correlation with numbers of single-stranded DNA-positive cells. CONCLUSIONS: High H. pylori density was associated with elevated serum nitrate-plus-nitrite (a marker of nitric oxide production in gastric mucosa). Increased apoptosis and abnormal gastric cell turnover are likely results.

Helicobacter pylori infection increases serum nitrate and nitrite more prominently than serum pepsinogens.

BACKGROUND: Helicobacter pylori infection causes chronic gastritis and results in increased serum concentrations of pepsinogens I and II as well as gastrin, while the ratio of pepsinogen I to II (I : II) is decreased. Inducible nitric oxide synthase (iNOS) is induced in H. pylori-associated gastritis and may modulate inflammation. However serum nitrate and nitrite (NOx) concentrations in patients with H. pylori-induced chronic gastritis have not been reported. We examined differences in serum NOx between H. pylori-negative and positive volunteers relative to differences in pepsinogens and gastrin. MATERIALS AND METHODS: Sera from 80 healthy asymptomatic volunteers younger than 36 years were analyzed for anti-H. pylori antibody, NOx, gastrin and pepsinogens. RESULTS: In H. pylori antibody-positive subjects serum NOx concentrations were higher than in negative subjects (p < .005). In H. pylori-negative subjects, NOx correlated with pepsinogen II (r = .405, p < .05). In subjects with low pepsinogen I or II, NOx was higher in H. pylori-positive than negative subjects (p < .001). In subjects with high pepsinogen I : II (6 or higher), serum NOx was higher in H. pylori-positive than in negative subjects. CONCLUSIONS: H. pylori-induced gastritis increases serum NOx concentrations more prominently than those of pepsinogen. In H. pylori-negative subjects, serum correlates with serum pepsinogen II.

The effects of rabeprazole on parietal cells and enterochromaffin-like cells in rats: a comparison with omeprazole.

BACKGROUND: We investigated the effects of rabeprazole compared with those of omeprazole on enterochromaffin-like cells and parietal cells in rats. METHODS: Rabeprazole or omeprazole was administered for 7 days by intraperitoneal injection (100 mg/kg or 20mg/kg once a day) and the serum gastrin concentration, the antral density of G cells and D cells, fundic histamine content, fundic H+, K+-ATPase mRNA level, and parietal cell morphology were determined. RESULTS: Both rabeprazole and omeprazole inhibited gastric acid secretion and increased the intragastric pH to over 6.5, as well as causing a marked increase in the serum gastrin concentration. The serum gastrin level was lower with rabeprazole treatment than with omeprazole treatment at both doses. Also, the antral G-cell density was higher with omeprazole than with rabeprazole, while the increase in both the histamine content and the H+, K-ATPase mRNA level in the fundic mucosa was higher with omeprazole treatment at both doses, with the difference being significant at 100 mg/kg. Ultrastructural examination indicated that the stimulation of parietal cells by omeprazole was stronger than that by rabeprazole. CONCLUSIONS: Rabeprazole treatment does not drive enterochromaffin-like cells and parietal cells as strongly as omeprazole treatment despite its potent acid suppressive effect, suggesting that it represents a new generation of proton pump inhibitors.

Does serum nitrite concentration reflect gastric carcinogenesis in Japanese Helicobacter pylori-infected patients?

This study investigated whether the serum nitrite concentration reflects Helicobacter pylori-induced inflammation and atrophic changes of gastric mucosa. Ninety-seven patients underwent biopsy of both antrum and fundus. Samples were analyzed by the rapid urease test and histopathological examination according to the updated Sydney system. Fasting serum samples from each subject were analyzed for specific IgG Helicobacter pylori antibodies, pepsinogen I and II concentrations, and NO2-/NO3- content. Eleven patients had H. pylori eradicated with proton pump-based triple therapy. There was a strong positive correlation between the Helicobacter pylori density in the gastric mucosa and the serum nitrite concentration, but a negative correlation existed between the atrophic grade of the gastric mucosa and both serum nitrite concentration and Helicobacter pylori density in the gastric mucosa. Serum nitrite concentrations decreased significantly after successful eradication of Helicobacter pylori. Therefore, serum nitrite concentration may be a useful marker for oxidative DNA damage and apoptosis associated with Helicobacter pylori infection.

Comparative report on endoscopic and surgical treatment for early gastric cancer in elderly patients

Dois casos de pacientes idosos com câncer gástrico precoce similares, foram submetidos a tratamento endoscópico e cirúrgico e säo apresentados como exemplos. Considerando os pacientes idosos como um grupo distinto no processo da decisäo terapêutica, discute-se os prós e contras de cada abordagem, tendo em vista a eficácia, efeitos colaterais e qualidade de vida