PURPOSE: The risk factors for secondary stomach carcinogenesis after distal gastrectomy have not been evaluated in detail. METHODS: Using gastrointestinal endoscopy, we examined 112 patients who had undergone gastrectomy. Biopsy specimens were taken from the stoma and the upper corpus mucosa in the remnant stomach to examine the associations among Helicobacter pylori (H.pylori) infection, bile reflux, and the expressions of interleukin-8 (IL-8), cyclo-oxygenase-2 (COX-2), and trefoil factor family 1 (TFF1) genes in the stomach mucosa. RESULTS: The IL-8 levels in the corpus mucosa were significantly higher in the H.pylori-positive patients than in the H.pylori-negative patients (P = 0.015). The IL-8 levels were significantly higher in the stomal mucosa than in the corpus mucosa in the H.pylori-positive patients (P = 0.047). The COX-2 levels in the corpus mucosa tended to be higher in the H.pylori-positive patients, but these levels were not significantly different in the stoma mucosa. The COX-2 levels in the corpus were significantly higher after Billroth II (BII) anastomosis than after Billroth I (BI) anastomosis (P = 0.041). TFF1 expression in the stoma was higher in the H.pylori-positive patients than in the H.pylori-negative patients, but the difference was not significant. CONCLUSIONS: Both H.pylori infection and bile reflux increased IL-8 levels after BI anastomosis. Furthermore, COX-2 levels were higher after BII than after BI anastomosis. These indicators will become useful not only as biomarkers to predict the degree of inflammation in the stomach mucosa, but also as surrogate biomarkers to predict the risk of secondary stomach carcinogenesis in the remnant stomach mucosa.
PURPOSE: The risk factors for secondary stomach carcinogenesis after distal gastrectomy have not been evaluated in detail. METHODS: Using gastrointestinal endoscopy, we examined 112 patients who had undergone gastrectomy. Biopsy specimens were taken from the stoma and the upper corpus mucosa in the remnant stomach to examine the associations among Helicobacter pylori (H.pylori) infection, bile reflux, and the expressions of interleukin-8 (IL-8), cyclo-oxygenase-2 (COX-2), and trefoil factor family 1 (TFF1) genes in the stomach mucosa. RESULTS: The IL-8 levels in the corpus mucosa were significantly higher in the H.pylori-positive patients than in the H.pylori-negative patients (P = 0.015). The IL-8 levels were significantly higher in the stomal mucosa than in the corpus mucosa in the H.pylori-positive patients (P = 0.047). The COX-2 levels in the corpus mucosa tended to be higher in the H.pylori-positive patients, but these levels were not significantly different in the stoma mucosa. The COX-2 levels in the corpus were significantly higher after Billroth II (BII) anastomosis than after Billroth I (BI) anastomosis (P = 0.041). TFF1 expression in the stoma was higher in the H.pylori-positive patients than in the H.pylori-negative patients, but the difference was not significant. CONCLUSIONS: Both H.pyloriinfection and bile reflux increased IL-8 levels after BI anastomosis. Furthermore, COX-2 levels were higher after BII than after BI anastomosis. These indicators will become useful not only as biomarkers to predict the degree of inflammation in the stomach mucosa, but also as surrogate biomarkers to predict the risk of secondary stomach carcinogenesis in the remnant stomach mucosa.