Duodenal ulcer: the villain unmasked?Eradicating Helicobacter pylon will cure most patientsThe observation "no acid, no ulcer" has dominated the medical and surgical treatment of duodenal ulcer disease and has strongly influenced research.'Though patients with duodenal ulcer do, as a group, have a high acid output, individual values show considerable overlap with those of many people with normal acid secretion.2Furthermore, carbenoxolone, deglycyrrhisinised liquorice, colloidal bismuth subcitrate, and sucralfate all heal ulcers without affecting acidity, through stimulating mucosal healing or enhancing cytoprotective mechanisms in some way.These observations imply that gastric acid is only one of several factors responsible for ulcer genesis.Recently the mechanisms that protect gastric and duodenal epithelia from acid attack and other types of injury have been the subject of much research.Several have been identified, including the mucus layer, the ability of gastric and duodenal epithelia to secrete bicarbonate,3 the hydrophobic properties of gastroduodenal mucosa,4 the ability of mucosal cells to regenerate rapidly after insult, and the abundant blood supply of the upper gastrointestinal tract.These protective factors seem to be enhanced by prostaglandins.Until now the only clearly understood cause of duodenal ulcer has been the Zollinger-Ellison syndrome, in which hypergastrinaemia induced by tumours causes a continuous high output of acid.Taking non-steroidal anti-inflammatory drugs, which interfere with prostaglandin synthesis, probably represents another pathogenic mechanism.These mechan- isms, however, account for only a tiny proportion of duodenal ulcers, and the underlying cause of most remains unknown.The rediscovery of Helicobacter pylon in 1983,5 its isolation in pure culture,6 and subsequent research have convinced many gastroenterologists that this organism plays an important part in the pathogenesis of duodenal ulcers.5A recent working party convened by the World Congresses of Gastro- enterology concluded that H pylori was the major factor in the multifactorial disease that is peptic ulcer.7 On what evidence was this conclusion based?Since the turn of the century several reports have drawn attention to curved and spiral organisms colonising the mammalian stomach, but these organisms have usually been regarded as commensals.H pylon is specifically adapted to life in the mucus that overlies gastric epithelial cells in humans and some primates.It cannot colonise other epithelial cells and so is found only in the stomach, in ectopic gastric mucosa, or in duodenal or intestinal mucosa that has undergone gastric metaplasia.
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Andrew Axon (1991) studied this question.
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