8 years. In their study, gastric cancer developed in persons infected with H. pylori but not in the uninfected persons, which is a conclusive evidence that H. pylori has a crucial role in the development of gastric cancer. In Japan,

intestinal type mucosal gastric cancer without concomitant lymph node metastasis is usually treated with endoscopic resection,[4] which removes the tumor and surrounding mucosa such that metachronous gastric cancer could develop at sites other than that of the endoscopic resection. Fukase et al.[5] investigated the prophylactic effect of H. pylori eradication on the development of metachronous gastric carcinoma after endoscopic resection for early gastric cancer. After endoscopic treatment, they randomly assigned patients to receive H. pylori eradication regimen or not. The cumulative incidence selleck chemicals of gastric cancer was significantly higher in the non-eradication therapy group than in the group undergoing eradication treatment. They concluded BI6727 that prophylactic eradication of H. pylori after endoscopic resection of early gastric cancer should be performed to prevent the development of metachronous gastric carcinoma. As to the gastric remnant, the effect of H. pylori eradication on the development of metachronous gastric carcinoma has not been clearly determined.

Evaluation of the risk of cancer in the intact stomach mucosa requires monitoring of atrophic or intestinal metaplastic changes. In the remnant stomach, however, evaluation can be confounded by H. pylori infection and by reflux of bile, intestinal juice or pancreatic juice, both of which are important risk factors for secondary carcinogenesis in the remnant stomach mucosa.[6, 7] It has been reported that H. pylori infection plays a major role in gastritis of the remnant stomach after Billroth I anastomosis, whereas 上海皓元 bile reflux is the major cause after the Billroth II procedure.[8] The remnant stomach after Billroth II anastomosis is a complicated circumstance because it is affected by H. pylori infection and bile reflux. Kato et al.[9] measured

the gastric juice pH of the patients who had undergone distal gastrectomy and H. pylori eradication therapy. pH levels in these patients were normalized after eradication in the remnant stomach, and they predicted that this effect may reduce the risk of secondary stomach carcinogenesis. Our hypothesis is that H. pylori infection triggers the development of histological inflammation in the remnant stomach after Billroth I anastomosis, which increases the risk of gastric carcinogenesis. The aim of this study was to clarify whether eradicating the bacteria results in normalization of the histological abnormalities, which may consequently reduce the risk of cancer in the remnant stomach. To more clearly understand the role of H. pylori rather than bile acid in the development of metachronous gastric carcinoma, we focused on patients with a remnant stomach after Billroth I anastomosis.