Potential mechanism of corpus-predominant gastritis after PPI therapy in Helicobacter pylori-positive patients with GERD

Figure 1 Potential mechanism for the changes in Helicobactor pylori colonization with proton pump inhibitor therapy. A: Normal subject with intact acid production; B: Patient with gastroesophageal reflux disease (GERD) and proton pump inhibitor (PPI) therapy. These figures show the intragastric conditions. The yellow area represents the reflux of soluble bile acids, and the blue area represents gastric juice. In normal subjects, the concentration of soluble bile acids may be < 5% in the gastric contents of the pyloric antrum (A). In contrast, increased soluble bile acid reflux with decreased gastric acid secretion acts as a bactericide for Helicobacter pylori (H. pylori) in the distal stomach; the concentration of soluble bile acids in patients with GERD under PPI maintenance therapy is considerably higher than that in normal subjects with intact acid production, especially in the distal stomach (B). The colonization of H. pylori therefore changes the pattern from antral-predominant to corpus-predominant. E-C junction: Esophago-gastric junction.