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Helicobacter pylori duodenal colonization is a strong risk factor for the development of duodenal ulcer.
Alimentary Pharmacology & Therapeutics 2005 April 1
AIM: To test the hypothesis that duodenal colonization represents the final crucial step in the development of Helicobacter pylori related duodenal ulcer.
METHODS: Patients with non-ulcer dyspepsia who had gastric colonization by H. pylori were included in the study. At baseline endoscopy, we evaluated the prevalence of duodenal colonization (culture, urease testing and histology), and cytotoxin-associated gene A status (polymerase chain reaction). No patients received eradication during 1 year follow-up. At this time, endoscopy was repeated and the incidence of duodenal ulcer was assessed.
RESULTS: Among 181 patients completing follow-up, 53 (29%) had duodenal colonization: 72% of them were cytotoxin-associated gene A positive, versus 37% patients without duodenal colonization (P < 0.001). Duodenal ulcer developed in 12 (22.6%) patients with duodenal colonization and in two (1.6%) without duodenal colonization (odds ratio for duodenal ulcer: 6.29, 95% confidence intervals 2.44-17.45). The incidence of duodenal ulcer was similar among cytotoxin-associated gene A positive and cytotoxin-associated gene A negative subjects with duodenal colonization: 21.05% versus 26.6%.
CONCLUSIONS: The assessment of duodenal colonization by H. pylori in patients with non-ulcer dyspepsia is strongly predictive for the subsequent development of duodenal ulcer and may help to stratify patients at risk for this disease.
METHODS: Patients with non-ulcer dyspepsia who had gastric colonization by H. pylori were included in the study. At baseline endoscopy, we evaluated the prevalence of duodenal colonization (culture, urease testing and histology), and cytotoxin-associated gene A status (polymerase chain reaction). No patients received eradication during 1 year follow-up. At this time, endoscopy was repeated and the incidence of duodenal ulcer was assessed.
RESULTS: Among 181 patients completing follow-up, 53 (29%) had duodenal colonization: 72% of them were cytotoxin-associated gene A positive, versus 37% patients without duodenal colonization (P < 0.001). Duodenal ulcer developed in 12 (22.6%) patients with duodenal colonization and in two (1.6%) without duodenal colonization (odds ratio for duodenal ulcer: 6.29, 95% confidence intervals 2.44-17.45). The incidence of duodenal ulcer was similar among cytotoxin-associated gene A positive and cytotoxin-associated gene A negative subjects with duodenal colonization: 21.05% versus 26.6%.
CONCLUSIONS: The assessment of duodenal colonization by H. pylori in patients with non-ulcer dyspepsia is strongly predictive for the subsequent development of duodenal ulcer and may help to stratify patients at risk for this disease.
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