Peptic ulcer and Helicobacter pylori: eradication and relapse

All duodenal ulcers and the vast majority of gastric ulcers are the consequence of Helicobacter pylori-associated inflammation. In duodenal ulcer disease, the inflammation is maximally intense in the antrum and is associated with gastric metaplasia in the bulb. H. pylori is presumably more virulent in duodenal ulcer disease. Gastrin homeostasis is disturbed and there is robust acid secretion. In gastric ulcers, there is pangastritis with a degree of atrophy. Acid secretion is normal or low.

Analysis of the literature data is performed concerning ulcer relapse rates after cure of the infection.

Successful eradication of the infection cures both the duodenal ulcer and gastric ulcer diathesis. Amalgamated figures for ulcer relapse/year in H. pylori +ve duodenal ulcer is 58% compared to 2.6% for H. pylori -ve duodenal ulcer patients. The corresponding figures for gastric ulcers are > 50% for H. pylori +ve and 2.0% for H. pylori -ve patients. Many of the recurrent ulcers in H. pylori -ve patients occurred in individuals consuming aspirin or NSAID. This striking difference persists over at least 7 years, as the reinfection rate in the developed world is < 1%/year. Moreover, recurrent bleeding in bleeding-prone duodenal ulcer patients is abolished after cure of the infection.

The decreased relapse rate after cure of the infection is the most compelling argument in favour of the infectious etiology of peptic ulcer disease.