Abstract
Long-term infection with Helicobacter pylori could potentially lead to asymptomatic chronic gastritis, chronic dyspepsia, duodenal ulcer disease, gastric ulcer disease, or gastric malignancy, including both adenocarcinoma and B-cell lymphoma. Currently, the two most important indications for eradication of this bacterium are proven H. pylori-associated duodenal or gastric ulcer disease. Many studies have shown that successful eradication of H. pylori dramatically reduces the rate of duodenal ulcer relapse, and long-term follow-up data appear to support the claim 'no H. pylori, no gastritis; no gastritis, no ulcer', which follows on from the old, but certainly valid, dictum 'no acid, no ulcer'. Furthermore, absence of relapse parallels the marked improvement in gastric histology (e.g. regression of gastritis). Whether there is concomitant regression of gastric metaplasia in the duodenal bulb is, however, controversial. Despite the rather limited data for H. pylori-associated gastric ulcer, successful eradication of the organism has been equated with cure of peptic ulcer disease. Again, eradication parallels a substantial improvement in gastric histology. Although eradication of H. pylori is not currently recommended in asymptomatic individuals or dyspeptics, it has been well documented in previous studies that successful eradication improves the gastric histology in patients with H. pylori-associated dyspepsia. From these studies, it appears that the disappearance of polymorphs from the inflammatory infiltrate occurs rather rapidly after eradication, although regression of the mononuclear component of the inflammatory reaction is more prolonged.
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