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. 2001 Sep;49(3):341–346. doi: 10.1136/gut.49.3.341

The significance of cagA+Helicobacter pylori in reflux oesophagitis

V Warburton-Timms 1, A Charlett 1, R Valori 1, J Uff 1, N Shepherd 1, H Barr 1, C McNulty 1
PMCID: PMC1728436  PMID: 11511554

Abstract

BACKGROUND—Helicobacter pylori is a gastroduodenal pathogen associated with ulceration, dyspepsia, and adenocarcinoma. Recent preliminary studies have suggested that H pylori may be protective for oesophageal adenocarcinoma. In addition, strains of H pylori identified by the presence of the cytotoxin associated gene A (cagA) are shown to have a significant inverse association with oesophageal adenocarcinoma. Given that cagA+ H pylori may protect against oesophageal carcinoma, these strains may be protective for oesophagitis, a precursor of oesophageal carcinoma.
AIMS—The aim of this study was to investigate the association between cagA+ H pylori and endoscopically proved oesophagitis.
PATIENTS—The study group included 1486 patients attending for routine upper gastrointestinal tract endoscopy.
METHODS—At endoscopy the oesophagus was assessed for evidence of reflux disease and graded according to standard protocols. Culture and histology of gastric biopsy specimens determined H pylori status. The prevalence of cagA was identified by an antibody specific ELISA (Viva Diagnostika, Germany).
RESULTS—H pylori was present in 663/1485 (45%) patients and in 120/312 (38%) patients with oesophagitis. Anti-CagA antibody was found in 499/640 (78%) H pylori positive patients. Similarly, anti-CagA antibody was found in 422/521 (81%) patients with a normal oesophagus and in 42/60 (70%) with mild, 24/35 (69%) with moderate, and 11/24 (46%) with severe oesophagitis. The risk of severe oesophagitis was significantly decreased for patients infected with cagA+ H pylori after correction for confounding variables (odds ratio 0.57, 95% confidence interval 0.41-0.80; p=0.001).
CONCLUSIONS—These results suggest that infection by cagA+ H pylori may be protective for oesophageal disease.


Keywords: Helicobacter pylori; cagA+; gastro-oesophageal reflux disease; oesophagitis; oesophageal adenocarcinoma; hiatus hernia

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