We have previously reported that H. pylori infection prevents reflux esophagitis (RE) and Barrett’s esophagus (BE) by decreasing gastric acid secretion. Gastroesophageal (GE) junction adenocarcinoma, including Barrett’s adenocarcinoma, has been thought to be a complication of gastroesophageal reflux disease. However, the relationship between H. pylori infection, gastric acid secretion and GE junction adenocarcinoma had not yet been investigated in Japan. We demonstrated that the status of gastric acid secretion was higher in patients with GE junction adenocarcinoma than in patients with early gastric cancer (EGC), and that the level was the same in patients with RE and those with BE. We also found that the prevalence of H. pylori infection in patients with GE junction adenocarcinoma was significantly lower than that in patients with EGC, although not as low as that in patients with RE and BE, suggesting that preservation of gastric acid secretion may be important for the development of GE junction adenocarcinoma in Japanese people, regardless of the presence of H. pylori infection.
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Received 12 July 2006; revised and accepted 3 November 2006
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Koike, T., Ohara, S., Inomata, Y. et al. The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with gastroesophageal junction adenocarcinoma in Japan. Inflammopharmacol 15, 61–64 (2007). https://doi.org/10.1007/s10787-006-1549-x
- Pylorus Infection
- Early Gastric Cancer
- Gastric Acid Secretion
- Atrophic Gastritis
- Gastric Cardia