Evaluation of Helicobacter pylori in reflux oesophagitis and Barrett's oesophagus

• Published in: Gut Vol. 40; no. 1; pp. 9 - 13
• Main Authors: Newton, M, Bryan, R, Burnham, W R, Kamm, M A
• Format: Journal Article
• Language: English
• Published: London BMJ Publishing Group Ltd and British Society of Gastroenterology 01.01.1997; BMJ; BMJ Publishing Group LTD
• Subjects: Adolescent; Adult; Aged; Aged, 80 and over; Barrett Esophagus - microbiology; Biological and medical sciences; Biopsy; Case-Control Studies; Child; Esophagitis, Peptic - microbiology; Esophagus; Female; Gastroenterology. Liver. Pancreas. Abdomen; Gastroesophageal Reflux - microbiology; Helicobacter Infections - complications; Helicobacter pylori - isolation & purification; Humans; Male; Medical sciences; Middle Aged; Other diseases. Semiology; Human; Gastroesophageal reflux; Evaluation; Statistical analysis; Demography; Prevalence; Spirillales; Pathophysiology; Esophageal disease; Spirillaceae; Barrett esophagus; Infection; Histopathology; Helicobacter pylori; Etiology; Bacteriosis; Digestive diseases; Bacteria; Comparative study
• ISSN: 0017-5749; 1468-3288; 1458-3288
• DOI: 10.1136/gut.40.1.9

BACKGROUND: One of the major pathophysiological abnormalities in patients with gastro-oesophageal reflux disease is thought to involve transient lower oesophageal sphincter (LOS) relaxations. One component of the neural mechanism controlling the LOS appears to be a reflex are whose afferent limb originates in the gastric fundus. As inflammation is known to be associated with neural activation an investigation was made to determine whether gastric infection with H pylori is altered in prevalence or distribution in patients with reflux disease. METHODS: Five groups of subjects referred for endoscopy-group 1: 25 controls (asymptomatic individuals with anaemia and normal endoscopy); group 2: 36 subjects with erosive oesophagitis alone (Savary-Millar grades I-III); group 3: 16 subjects with duodenal ulcer alone; group 4: 15 subjects with oesophagitis with duodenal ulcer; group 5: 16 subjects with Barrett's oesophagus. No patients were receiving acid suppressants or antibiotics. An antral biopsy specimen was taken for a rapid urease test, and two biopsy specimens were taken from the antrum, fundus, and oesophagus (inflamed and non-inflamed) for histological evidence of inflammation and presence of H pylori using a Giemsa stain. RESULTS: Nine (36%) controls had H pylori. Patients with duodenal ulcer alone had a significantly higher incidence of colonisation by H pylori than other groups (duodenal ulcer 15 (94%); oesophagitis 13 (36%); oesophagitis+duodenal ulcer 6 (40%); Barrett's oesophagus 4 (25%)). H pylori was not more common in oesophagitis. When H pylori colonised the gastric antrum it was usually found in the gastric fundus. There was no difference in anatomical distribution of H pylori in the different patient groups. In Barrett's oesophagus H pylori was found in two of 16 in the metaplastic epithelium. CONCLUSION: H pylori is not more common and its distribution does not differ in those with oesophagitis compared with control subjects, and is therefore unlikely to be aetiologically important in these patients. H pylori, however, can colonise Barrett's epithelium.