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Prevalence of Helicobacter pylori infection in 160 patients with Barrett's oesophagus or Barrett's adenocarcinoma.
Aust N Z J Surg. 2000 Jan; 70(1):26-33.AN

Abstract

BACKGROUND

The role of Helicobacter pylori infection in the development of Barrett's oesophagus and its complications is uncertain. The aim of the present study was to determine the importance of H. pylori infection in this disease by comparing the frequency of oesophageal and gastric H. pylori infection in a group of patients with Barrett's oesophagus or adenocarcinoma, with the frequency of infection in a control group without Barrett's disease.

METHODS

The study group included 160 patients (123 male, 37 female; mean age: 61.2 years) who were classified (according to the highest grade pathological lesion in the oesophagus) as having Barrett's intestinal metaplasia (IM; 88 patients), Barrett's oesophagus with low-grade dysplasia (LGD; 28 patients), high-grade dysplasia (HGD; five patients), Barrett's indefinite for dysplasia (n = 4), and Barrett's adenocarcinoma (33 patients). A total of 91 of these patients had gastric antral specimens available for study. The control group consisted of 214 consecutive, prospectively enrolled symptomatic patients (122 male, 92 female; mean age: 57.2 years) who underwent upper gastrointestinal endoscopy and in whom Barrett's oesophagus or Barrett's adenocarcinoma was not found. A modified Warthin-Starry method was used to detect H. pylori infection.

RESULTS

Oesophageal H. pylori infection was found in eight of 160 (5%) patients with Barrett's oesophagus or Barrett's adenocarcinoma. Holicobacter pylori organisms in the oesophagus were found only on non-intestinalized cardiac or oxyntocardiac mucosa. All patients with oesophageal H. pylori infection and an antral biopsy available for study had antral H. pylori infection. Gastric antral H. pylori infection was significantly less prevalent in patients in the Barrett's study group (15/91, 16.5%) than in the non-Barrett's control group (67/214, 31.3%; Fisher's exact test, P = 0.01). Patients from the control group with an endoscopic diagnosis of duodenal ulcer, gastric ulcer, gastritis, or duodenitis had a significantly higher prevalence of infection compared with the Barrett's group, but there was no difference in the infection prevalence in patients in the Barrett's group and patients with reflux oesophagitis, hiatal hernia, no endoscopic abnormality, or any other diagnosis.

CONCLUSIONS

Oesophageal H. pylori infection is uncommon in patients with Barrett's IM, dysplasia, or adenocarcinoma, and may be restricted to non-intestinalized columnar epithelium. Gastric H. pylori infection may have a protective effect for the development of Barrett's oesophagus.

Authors+Show Affiliations

Department of Surgery, St. Vincent's Hospital, Sydney, New South Wales, Australia.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

10696939

Citation

Lord, R V., et al. "Prevalence of Helicobacter Pylori Infection in 160 Patients With Barrett's Oesophagus or Barrett's Adenocarcinoma." The Australian and New Zealand Journal of Surgery, vol. 70, no. 1, 2000, pp. 26-33.
Lord RV, Frommer DJ, Inder S, et al. Prevalence of Helicobacter pylori infection in 160 patients with Barrett's oesophagus or Barrett's adenocarcinoma. Aust N Z J Surg. 2000;70(1):26-33.
Lord, R. V., Frommer, D. J., Inder, S., Tran, D., & Ward, R. L. (2000). Prevalence of Helicobacter pylori infection in 160 patients with Barrett's oesophagus or Barrett's adenocarcinoma. The Australian and New Zealand Journal of Surgery, 70(1), 26-33.
Lord RV, et al. Prevalence of Helicobacter Pylori Infection in 160 Patients With Barrett's Oesophagus or Barrett's Adenocarcinoma. Aust N Z J Surg. 2000;70(1):26-33. PubMed PMID: 10696939.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prevalence of Helicobacter pylori infection in 160 patients with Barrett's oesophagus or Barrett's adenocarcinoma. AU - Lord,R V, AU - Frommer,D J, AU - Inder,S, AU - Tran,D, AU - Ward,R L, PY - 2000/3/4/pubmed PY - 2000/3/18/medline PY - 2000/3/4/entrez SP - 26 EP - 33 JF - The Australian and New Zealand journal of surgery JO - Aust N Z J Surg VL - 70 IS - 1 N2 - BACKGROUND: The role of Helicobacter pylori infection in the development of Barrett's oesophagus and its complications is uncertain. The aim of the present study was to determine the importance of H. pylori infection in this disease by comparing the frequency of oesophageal and gastric H. pylori infection in a group of patients with Barrett's oesophagus or adenocarcinoma, with the frequency of infection in a control group without Barrett's disease. METHODS: The study group included 160 patients (123 male, 37 female; mean age: 61.2 years) who were classified (according to the highest grade pathological lesion in the oesophagus) as having Barrett's intestinal metaplasia (IM; 88 patients), Barrett's oesophagus with low-grade dysplasia (LGD; 28 patients), high-grade dysplasia (HGD; five patients), Barrett's indefinite for dysplasia (n = 4), and Barrett's adenocarcinoma (33 patients). A total of 91 of these patients had gastric antral specimens available for study. The control group consisted of 214 consecutive, prospectively enrolled symptomatic patients (122 male, 92 female; mean age: 57.2 years) who underwent upper gastrointestinal endoscopy and in whom Barrett's oesophagus or Barrett's adenocarcinoma was not found. A modified Warthin-Starry method was used to detect H. pylori infection. RESULTS: Oesophageal H. pylori infection was found in eight of 160 (5%) patients with Barrett's oesophagus or Barrett's adenocarcinoma. Holicobacter pylori organisms in the oesophagus were found only on non-intestinalized cardiac or oxyntocardiac mucosa. All patients with oesophageal H. pylori infection and an antral biopsy available for study had antral H. pylori infection. Gastric antral H. pylori infection was significantly less prevalent in patients in the Barrett's study group (15/91, 16.5%) than in the non-Barrett's control group (67/214, 31.3%; Fisher's exact test, P = 0.01). Patients from the control group with an endoscopic diagnosis of duodenal ulcer, gastric ulcer, gastritis, or duodenitis had a significantly higher prevalence of infection compared with the Barrett's group, but there was no difference in the infection prevalence in patients in the Barrett's group and patients with reflux oesophagitis, hiatal hernia, no endoscopic abnormality, or any other diagnosis. CONCLUSIONS: Oesophageal H. pylori infection is uncommon in patients with Barrett's IM, dysplasia, or adenocarcinoma, and may be restricted to non-intestinalized columnar epithelium. Gastric H. pylori infection may have a protective effect for the development of Barrett's oesophagus. SN - 0004-8682 UR - https://www.unboundmedicine.com/medline/citation/10696939/Prevalence_of_Helicobacter_pylori_infection_in_160_patients_with_Barrett's_oesophagus_or_Barrett's_adenocarcinoma_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0004-8682&date=2000&volume=70&issue=1&spage=26 DB - PRIME DP - Unbound Medicine ER -