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.

Pietroiusti, A., Luzzi, I., Gomez, M., Magrini, A., Bergamaschi, A., Forlini, A., et al. (2005). Helicobacter pylori duodenal colonization is a strong risk factor for the development of duodenal ulcer. ALIMENTARY PHARMACOLOGY & THERAPEUTICS, 21(7), 909-915 [10.1111/j.1365-2036.2005.02423.x].

Helicobacter pylori duodenal colonization is a strong risk factor for the development of duodenal ulcer

PIETROIUSTI, ANTONIO;MAGRINI, ANDREA;FORLINI, ANTONIO;GALANTE, ALBERTO
2005-01-01

Abstract

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.
2005
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/44 - MEDICINA DEL LAVORO
English
Con Impact Factor ISI
CagA protein; urease; adult; article; bacterial colonization; bacterium culture; controlled study; duodenum ulcer; dyspepsia; endoscopy; female; follow up; Helicobacter pylori; high risk patient; histology; human; human tissue; incidence; male; nonhuman; polymerase chain reaction; prevalence; priority journal; risk factor; Duodenal Ulcer; Duodenum; Female; Follow-Up Studies; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Risk Factors
Pietroiusti, A., Luzzi, I., Gomez, M., Magrini, A., Bergamaschi, A., Forlini, A., et al. (2005). Helicobacter pylori duodenal colonization is a strong risk factor for the development of duodenal ulcer. ALIMENTARY PHARMACOLOGY & THERAPEUTICS, 21(7), 909-915 [10.1111/j.1365-2036.2005.02423.x].
Pietroiusti, A; Luzzi, I; Gomez, M; Magrini, A; Bergamaschi, A; Forlini, A; Galante, A
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/34102
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