Literature DB >> 11007219

CagA-positive strains of Helicobacter pylori may protect against Barrett's esophagus.

M F Vaezi1, G W Falk, R M Peek, J J Vicari, J R Goldblum, G I Perez-Perez, T W Rice, M J Blaser, J E Richter.   

Abstract

OBJECTIVE: Helicobacter pylori (H. pylori) colonization is associated with chronic gastritis, peptic ulcer disease, and adenocarcinoma of the distal stomach. However, the role of H. pylori strain variation in complicated gastroesophageal reflux disease, especially Barrett's esophagus, is unknown. Therefore, the aim of this study was to evaluate the prevalence of colonization by cagA+ and cagA- H. pylori strains in the spectrum of gastroesophageal reflux disease, including Barrett's esophagus.
METHODS: A total of 251 patients undergoing endoscopy were categorized into four groups: controls, patients with gastroesophageal reflux disease alone, and patients with short- and long-segment Barrett's esophagus. All patients underwent upper endoscopies with biopsies and serum collections. H. pylori and degree of mucosal inflammation in gastric biopsies were assessed and serological assessment made for H. pylori and cagA status.
RESULTS: The overall prevalence of H. pylori colonization in the study population was 35% (95% confidence interval = 29.5-41.4%) which did not differ significantly among the groups. However, colonization by cagA+ H. pylori strains was significantly more prevalent among controls (11/25; 44%) and patients with gastroesophageal reflux disease (13/36; 36%) than in patients with short-segment (2/10; 20%) or long-segment Barrett's esophagus (0/18; 0%). Patients with Barrett's esophagus were less likely to be colonized by cagA+ H. pylori strains than reflux patients without Barrett's esophagus (odds ratio = 0.27, 95% confidence interval = 0.11-0.67, p = 0.004).
CONCLUSIONS: Colonization by cagA+ H. pylori strains may be protective against the formation of short- and long-segment Barrett's esophagus and its malignant complications.

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Year:  2000        PMID: 11007219     DOI: 10.1111/j.1572-0241.2000.02305.x

Source DB:  PubMed          Journal:  Am J Gastroenterol        ISSN: 0002-9270            Impact factor:   10.864


  57 in total

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2.  Promoter DNA hypermethylation in gastric biopsies from subjects at high and low risk for gastric cancer.

Authors:  Barbara G Schneider; Dun-Fa Peng; M Constanza Camargo; M Blanca Piazuelo; Liviu A Sicinschi; Robertino Mera; Judith Romero-Gallo; Alberto G Delgado; Luis E Bravo; Keith T Wilson; Richard M Peek; Pelayo Correa; Wael El-Rifai
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3.  CagA in Barrett's oesophagus in Colombia, a country with a high prevalence of gastric cancer.

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Journal:  J Clin Pathol       Date:  2005-03       Impact factor: 3.411

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7.  Association between gastric Helicobacter pylori colonization and glycated hemoglobin levels.

Authors:  Yu Chen; Martin J Blaser
Journal:  J Infect Dis       Date:  2012-03-13       Impact factor: 5.226

Review 8.  Polymorphism in the Helicobacter pylori CagA and VacA toxins and disease.

Authors:  Dacie R Bridge; D Scott Merrell
Journal:  Gut Microbes       Date:  2013-02-04

9.  RELATIONSHIP BETWEEN THE PRESENCE OF HELICOBACTER PYLORI WITH INFLAMMATORY ENDOSCOPIC CHANGES IN GASTRODUODENAL MUCOSA.

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10.  H. pylori infection and genotyping in patients undergoing upper endoscopy at inner city hospitals.

Authors:  E W Straus; H Patel; J Chang; R M Gupta; V Sottile; J Scirica; G Tarabay; S Iyer; S Samuel; R D Raffaniello
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