PubMed · 669448
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I L Horovitz, I Baier. 1978. [Highly selective vagotomy].. https://pubmed.ncbi.nlm.nih.gov/669448/
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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.
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Reports from countries with a high prevalence of Helicobacter pylori (H pylori) infection do not show a proportionately high prevalence of duodenal ulceration, suggesting the possibility that H pylori cannot be a primary cause of duodenal ulceration. It has been mooted that this discrepancy might be explained by variations in the prevalence of virulence factors in different populations. The aim of this paper is to determine whether the published literature gives support to this possibility. The relevant literature was reviewed and analyzed separately for countries with a high and low prevalence of H pylori infection and virulence factors. Although virulent strains of H pylori were significantly more often present in patients with duodenal ulcer than without the disease in countries with a low prevalence of H pylori infection in the population, there was no difference in the prevalence of virulence factors between duodenal ulcer, non - ulcer dyspepsia or normal subjects in many countries, where the prevalence of both H pylori infection and of virulence factors was high. In these countries, the presence of virulence factors was not predictive the clinical outcome. To explain the association between virulence factors and duodenal ulcer in countries where H pylori prevalence is low, only two papers were found that give little support to the usual model proposed, namely that organisms with the virulence factors are more likely than those without them to initiate a duodenal ulcer. We offer an alternative hypothesis that suggests virulence factors are more likely to interfere with the healing of a previously produced ulcer. The presence of virulence factors only correlates with the prevalence of duodenal ulcer in countries where the prevalence of H pylori is low. There is very little evidence that virulence factors initiate duodenal ulceration, but they may be related to failure of the ulcer to heal.