THE ROLE OF HELICOBACTER-PYLORI INFECTION IN THE PATHOPHYSIOLOGY OF DUODENAL-ULCER DISEASE

The discovery of H. pylori infection and the recognition of its effect s on gastric physiology has significantly advanced our understanding o f the pathophysiology of ulcer disease, In DU patients H. pylori gastr itis is mainly confined to the antral mucosa. It stimulates increased release of gastrin by the antral mucosa and this is accompanied by hig h acid output by the oxyntic mucosa. This high acid response to gastri n stimulation by the oxyntic mucosa in DU patients is due to the combi nation of a high parietal cell mass and the fact that the function of these parietal cells is not impaired by any body gastritis. The increa sed acid secretion results in an increased duodenal acid load with the development of gastric metaplasia within the duodenal bulb and then a ctual ulceration. The reason why only some subjects develop this antra l predominant pattern of H. pylori gastritis and associated acid hyper secretion is unclear but may be explained by a premorbid high acid out put protecting the oxyntic mucosa form H. pylori gastritis.