The phenotype of gastric mucosa coexisting with Barrett's oesophagus

Citation
M. Rugge et al., The phenotype of gastric mucosa coexisting with Barrett's oesophagus, J CLIN PATH, 54(6), 2001, pp. 456-460
Citations number
51
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF CLINICAL PATHOLOGY
ISSN journal
00219746 → ACNP
Volume
54
Issue
6
Year of publication
2001
Pages
456 - 460
Database
ISI
SICI code
0021-9746(200106)54:6<456:TPOGMC>2.0.ZU;2-Y
Abstract
Background/Aims-Barrett's oesophagus complicates the gastro-oesophageal aci d reflux. Helicobacter pylori infection, particularly with cagA positive st rains, induces inflammatory/atrophic lesions of the gastric mucosa, which m ay impair acid output. No systematic study has investigated the phenotype o f the gastric mucosa coexisting with Barrett's oesophagus. This study was d esigned to identify the phenotype of gastric mucosa associated with Barrett 's oesophagus. Methods-In this retrospective case control study, the phenotype of the gast ric mucosa was histologically characterised in 53 consecutive patients with Barrett's oesophagus and in 53 (sex and age matched) non-ulcer dyspeptic c ontrols. Both patients and controls underwent extensive sampling of the gas tric mucosa (two antral, one incisural, and two oxyntic biopsies). Intestin al metaplasia (IM) was categorised (type I, complete IM; types II and III, incomplete IM) by the high iron diamine stain; cagA status was ascertained by genotyping. Results-Helicobacter pylori was present in 19 of the 53 patients with Barre tt's oesophagus and in 30 of the 53 controls (p < 0.02); eight of the 19 pa tients with Barrett's oesophagus and 28 of the 35 controls harboured cagA p ositive H pylori (p < 0.03). The histological severity of nonatrophic gastr itis detected in the controls was significantly higher than that detected i n the patients with Barrett's oesophagus (p < 0.8001). Multifocal atrophic gastritis was present in 4% of the patients with Barrett's oesophagus and i n 23% of controls (p < 0.01). The odds ratio for the association between mu ltifocal atrophic gastritis and Barrett's oesophagus was 0.20 (95% confiden ce interval, 0.006 to 0.60). Gastric IM was detected in 13.2% of the patien ts with Barrett's oesophagus and in 30.1% of the controls (p < 0.03). Type III IM at the gastric mucosa was only detected among controls. Conclusions-Barrett's oesophagus is associated with a low prevalence of H p ylori cagA positive infection and multifocal atrophic gastritis. This patho biological pattern is considered to be associated with a low risk of distal gastric cancer.