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


CONCLUSIONS
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.
Newton
M
M
St Mark's Hospital, London.
Bryan
R
R
Burnham
W R
WR
Kamm
M A
MA
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001471:Barrett Esophagus / Q000382:microbiology*; D001706:Biopsy; D016022:Case-Control Studies; D002648:Child; D004942:Esophagitis, Peptic / Q000382:microbiology*; D005260:Female; D005764:Gastroesophageal Reflux / Q000382:microbiology*; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008875:Middle Aged