Peptic ulcer and gastric cancer

About 15% of infected individuals will develop peptic ulcer (duodenal or gastric) or gastric cancer as a long term consequence of infection. The outcome of infection depends mainly on the severity and topography of histological gastritis, which may be determined by the age at which infection is acquired. Infection in infancy is thought to lead to pangastritis, whereas acquisition in later childhood may lead to a predominantly antral gastritis only.

With antral gastritis there is loss of regulatory feedback (but with an intact and undamaged acid secreting gastric corpus), and the high acid load reaching the duodenum leads to the development of duodenal gastric metaplasia. The islands of gastric metaplasia are subsequently colonised by Hpylori, leading to duodenitis and a high risk of duodenal ulcer.

In contrast, pangastritis, with an inflamed corpus, is associated with the loss of acid secreting cells, which leads to an increased risk of gastric ulcer and gastric cancer—similar to that seen with autoimmune gastritis in pernicious anaemia.

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