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Published 14 August 2009, doi:10.1136/bmj.b2784
Cite this as: BMJ 2009;339:b2784
Alexander C Ford, lecturer in medicine1, Nicholas J Talley, professor of medicine, visiting professor of medicine2,3
1 Department of Academic Medicine, St Jamess University Hospital, Leeds LS9 7TF, 2 Department of Medicine, Mayo Clinic Florida, Jacksonville, Florida, FL 32224, USA, 3 Department of Medicine, University of Sydney, Nepean Hospital, Sydney, Australia
Correspondence to: A C Ford alexf12399@yahoo.com
The link between duodenal ulcer and Helicobacter pylori has revolutionised treatment. Alexander Ford and Nicholas Talley argue that the association is causal, but Michael Hobsley and colleagues (doi:10.1136/bmj.b2788) believe acid secretion is the key
| The first 150 words of the full text of this article appear below. |
Helicobacter pylori infects the human stomach and is acquired predominantly in childhood.1 Infection is from person to person, and evidence points to transmission through the gastro-oral route.2 Gastric biopsy shows that all infected people have either antral or corpus predominant gastritis.3 Which of the two develops probably depends on the persons parietal cell mass at the time of infection.
Although causation can never be proved (hypotheses can only be dispelled), evidence for the causative role of H pylori in duodenal ulcer is remarkably compelling and fulfils the Bradford Hill criteria—for example, showing a strong, consistent, specific, and temporal association (box). The National Institutes of Health judged H pylori to be the main cause of the condition in 1994. A causal association between H pylori and chronic gastritis was proposed at the time of its discovery, and Kochs postulates have since been fulfilled for this histological lesion.4
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