Duodenogastric reflux sustains Helicobacter pylori infection in the gastric stump

Duodenogastric reflux (DGR) and Helicobacter pylori infection have been suspected of being contributing agents to the genesis of gastritis and subsequent cancer, but compelling, conclusive data about the exact relationship have been lacking.

We investigated the effect of DGR on H. pylori infection in 95 gastrectomized subjects divided into four groups according to type of reconstruction: the jejunal pouch interposition group (JPI, n = 36); the Roux-en-Y group (RY, n = 17); the Billroth I group (B-I, n = 20); and the Billroth II group (B-II, n = 22). The following items were examined for each group: the duration of DGR; the prevalence of H. pylori infection; other bacterial identification and quantity; and the severity of gastritis.

The percent of total time of DGR was lower in the JPI (7%) and RY groups (28%) than in the B-I (59%) and B-II groups (88%) (P < 0.02). The prevalence of H. pylori infection was lower in the JPI (28%) and RY groups (29%) than in the B-I (60%) and B-II groups (73%) (P < 0.02). Inversely, the JPI and the RY groups had a higher quantity of other bacteria than the B-I group (P = 0.02). For all four groups, the stomachs infected with H. pylori were fewer than those tested negative for the organism (P < 0.0001). Inflammation scores were lower in both the JPI and RY groups than in the B-I and B-II groups (P < 0.05, respectively).

Duodenogastric reflux facilitates the survival of H. pylori in the gastric stump after a distal gastrectomy.