PubMed · 6884815
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
K G Wormsley. 1983. Duodenal ulcer: does pathophysiology equal aetiology?. https://doi.org/10.1136/gut.24.9.775
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
H. pylori is now accepted as the cause of gastritis and gastritis-associated diseases, such as duodenal ulcer, gastric ulcer, gastric carcinoma, and gastric MALT lymphoma. The natural history of H. pylori gastritis includes inflammation progressing from the antrum into the adjacent corpus resulting in an atrophic front of advancing injury leading to a reduction in acid secretion and eventual loss of parietal cells and development of atrophy. Sub-typing intestinal metaplasia has no clinical value to the patient, the pathologist, or the endoscopist. The pattern, extent, and severity of atrophy, with or without intestinal metaplasia, is a far more important predictor than is intestinal metaplasia subtype. The challenge remains to identify a reliable marker that relates to pre-malignant potential.
BACKGROUND: Patients with duodenal ulcer are not at high risk although Helicobacter pylori infection is no doubt associated with gastric cancer development. However, little is known about the risk after long-term follow-up. AIMS: We investigated the incidence for gastric cancer development in peptic ulcer patients in a long term. PATIENTS AND METHODS: Between 1965 and 2004, endoscopic follow-up of more than 1 year was conducted on 1504 peptic ulcer patients in our hospital. They consisted of 978 gastric ulcer patients, 444 duodenal ulcer patients and 82 gastric and duodenal ulcer patients. Gastric and duodenal ulcer patients were excluded from the analysis because of their limited number. RESULTS: Gastric cancers developed in 32 (3.3%) of gastric ulcer patients and 3 (0.68%) of duodenal ulcer patients. Kaplan-Meier analysis showed that the incidence of gastric cancer in duodenal ulcer patients was significantly lower than that in gastric ulcer patients (log-rank test, p=0.0059). Cox's proportional hazard model denoted the relative risk for duodenal ulcer against gastric ulcer adjusted by sex and age as 0.23 (95% CI: 0.072-0.77, p=0.016). CONCLUSION: The risk for patients with duodenal ulcer to develop gastric cancer over the long term is significantly less than in those with gastric ulcer.
Explore the source record for details and available documents.