Antralization at the edge of proximal gastric ulcers: Does Helicobacter pylori infection play a role?

Figure 1 Prevalence of antral-type mucosa at the edge of proximal gastric ulcers and non-ulcerated gastric body in H. pylori-positive patients (H. pylori⁺, n = 101) and those without H. pylori infection (H. pylori^-, n = 15).

Figure 2 Presence of antral-type mucosa at the edge of proximal gastric ulcers and non-ulcerated gastric body in patients with H. pylori eradicated (n = 28) and in those with persistent infection (n = 37) before (month 0) and 12 mo after treatment.

Figure 3 Gastric mucosa at the ulcer edge before and after eradication of H. pylori infection in the same patient. A, biopsy of the ulcer edge before H. pylori eradication showing antral-type gastric mucosa with severe active chronic inflammation; B, biopsy of the healed ulcer site after H. pylori eradication showing body-type gastric mucosa with presence of parietal and chief cells in the gastric glands and mild residual chronic inflammation. Haematoxylin & eosin (H&E) staining × 250.