[Is the only good Helicobacter a dead Helicobacter?].

The discovery of Helicobacter pylori (H. pylori) has revolutionised the pathophysiological and clinical approach to gastric and duodenal ulcer. Since the first paper identifying H. pylori was published only 19-20 years ago, it has been found out that this bacterium causes probably the commonest human infection. Like other revolutions in history, the original directions of the H. pylori story have changed in response to conflicting ideologies, observation, and practices. It is known that once H. pylori is acquired, colonisation continues for life unless the organism is eliminated by antimicrobial treatment or by the usually late-in-life development of the atrophic gastritis. If any recent achievement in the world of medicine is to be called revolutionary, then it is the discovery of the role of this spiral bacterium in the etiopathogenesis of gastritis, gastric ulcer, duodenal ulcer, gastric adenocarcinomas and gastric mucosa-associated lymphoid type (MALT) B-cell lymphomas. Essentially everyone who carries the organism in the gastric mucous layer has evidence of tissue reaction (termed chronic active gastritis), but most colonised persons remain asymptomatic for life. In the absence of treatment, the presence of H. pylori can be determined with a high degree of confidence by endoscopy (with culture, histologic examination, or urease testing of gastric biopsy specimens), by serologic testing, or by urea breath tests. After successful treatment, specific antibody levels decrease so slowly that serologic testing cannot be used to document success for at least 6 months. In most patients, elimination of H. pylori changes the natural history of peptic ulcer disease and of gastric MALT lymphomas. It is now recommended that these patients have to be treated to eliminate H. pylori because the benefits seem to substantially outweigh the risks and costs. Currently, enthusiasts, drug companies, and the lay press are putting pressure on physicians to eliminate H. pylori from all patients, symptomatic or not, in whom it is detected. There is little evidence that this is appropriate, and management will continue to change as new knowledge emerges and socioeconomic environments change in ways that are relevant to H. pylori and clinical medicine.