Conceivable mechanisms by which Helicobacter pylori provokes duodenal ulcer disease.
A conceivable concept for the development of duodenal ulcers in Helicobacter pylori (H. pylori) infected subjects is presented in this chapter. The concept includes an explanation of the fact that only a minority of all H. pylori-infected subjects will develop a duodenal ulcer. Helicobacter pylori infection of the antrum induces a hypersecretion of gastric acid secretion, giving rise to gastric metaplasia in the duodenal bulb. This gastric metaplasia is a prerequisite for H. pylori colonization of the bulb. These events are common to all H. pylori-infected subjects. However, a much higher density of H. pylori bacteria and colonization with virulent organisms has been found in the bulb of duodenal ulcer patients, resulting in a much stronger inflammatory reaction with active duodenitis and an impaired bicarbonate secretion. These characteristics, together with acid hypersecretion, seem to be the important factors in evoking a duodenal ulcer.
Olbe
L
L
Department of Surgery, Sahlgren Hospital, Göteborg, Sweden.
Fändriks
L
L
Hamlet
A
A
Svennerholm
A M
AM
D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000378:metabolism; D001639:Bicarbonates / Q000378:metabolism; D004381:Duodenal Ulcer / Q000382:microbiology*; D004382:Duodenitis / Q000382:microbiology; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori; D006801:Humans; D008679:Metaplasia
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D001639:Bicarbonates; C080866:cagA protein, Helicobacter pylori