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To cast light on tumorigenesis in the remnant stomach after distal gastrectomy for peptic ulcer or gastric cancer, 45 cases in gastroduodenostomy (Billroth I, 17 cases) and gastrojejunostomy (Billroth II, 28 cases) groups were compared for a series of parameters. Cancers in Billroth II were significantly more predominant in the anastomosis area and more frequently associated with Epstein-Barr virus infection. Active gastritis, accelerated epithelial cell turnover (as assessed by measurements of apoptosis and cell proliferation), DNA damage, and foveolar cell hyperplasia were all greater in anastomotic areas after Billroth II than in proximal areas after Billroth II or either area after Billroth I. K-ras mutations were rare, but Epstein-Barr virus infection in cancers was seen frequently in anastomosis cases. In conclusion, active gastritis, possibly induced by enterogastric reflux, is linked to tumorigenesis in anastomosis sites in Billroth II cases.

The relationship of gastric secretion in response to a single injection of insulin and in response to a histamine infusion, before and after partial gastrectomy, was analysed in 58 patients. The aspirated gastric juice was corrected for gastric outlet loss and enterogastric reflux. Gastrectomy drastically reduced the stimulated gastric secretion by a similar proportion for the two secretagogues, thereby implying that antral gastrin plays no greater part in one than in the other. Gastric outlet losses were also reduced after gastrectomy, but as a fraction of gastric contents, both gastric outlet loss and enterogastric reflux more than doubled; the possible relationship of these findings to the aetiology of gastric ulcer is discussed.