Duodenal Helicobacter pylori infection differs in cagA genotype between asymptomatic subjects and patients with duodenal ulcers

A Hamlet, AC Thoreson, O Nilsson, AM Svennerholm… - Gastroenterology, 1999 - Elsevier
A Hamlet, AC Thoreson, O Nilsson, AM Svennerholm, L Olbe
Gastroenterology, 1999Elsevier
Background & Aims: It is unclear why only a minority of subjects infected by Helicobacter
pylori develop duodenal ulcers (DU). The aim of this study was to investigate whether the
number and type of H. pylori strains in the duodenum of patients with DU may play a critical
role. Methods: Twenty-one patients with DU and 20 asymptomatic subjects with antral H.
pylori infection were studied. Paired biopsy specimens were taken from the antrum and from
each quadrant of the duodenal bulb. Analyses included extent of duodenal gastric …
Background & Aims
It is unclear why only a minority of subjects infected by Helicobacter pylori develop duodenal ulcers (DU). The aim of this study was to investigate whether the number and type of H. pylori strains in the duodenum of patients with DU may play a critical role.
Methods
Twenty-one patients with DU and 20 asymptomatic subjects with antral H. pylori infection were studied. Paired biopsy specimens were taken from the antrum and from each quadrant of the duodenal bulb. Analyses included extent of duodenal gastric metaplasia, severity of duodenitis, bacterial density, presence of the cagA gene, and vacuolating cytotoxin activity.
Results
H. pylori was cultured from duodenal biopsy specimens in 95% of patients with DU and 80% of asymptomatic subjects. Both groups had a similar bacterial density and proportion of cagA-positive strains in the antrum (86% vs. 75%), but patients with DU had a 20-fold higher density of H. pylori and a higher proportion of cagA-positive strains in the duodenal bulb (81% vs. 30%). Active duodenitis was present only in patients with DU infected by cagA positive strains in the duodenum.
Conclusions
The results suggest that a high density of cagA-positive strains in the duodenum with severe duodenitis are important determinants of DU disease. GASTROENTEROLOGY 1999;116:259-268
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