The transient lower oesophageal sphincter relaxations which allow reflux ma
y be due to altered afferent pathways from the fundus. We aimed to determin
e whether fundal inflammation is the underlying cause. Two endoscopic biops
ies were taken from each of the gastric antrum and fundus in 25 asymptomati
c controls with a normal endoscopy (median age 54 range 13-83 years), and 3
3 patients with erosive oesophagitis (median age 52, 11-78 years). No patie
nt had taken acid suppression therapy or antibiotics for at least 1 month.
Sections were stained with haematoxylin and eosin and Giemsa stain and exam
ined in a blinded fashion by one pathologist for the presence of gastritis
(Sydney classification) and Helicobacter pylori. Chronic gastritis was comm
on in both groups, but was usually mild. In Helicobacter pylori-negative su
bjects, there was significantly less chronic gastritis in the antrum and th
e fundus in oesophagitis patients than in controls (p < 0.05). When present
, gastric atrophy was usually antral and mild in severity. There was no dif
ference in the incidence of gastric atrophy in patients with oesophagitis c
ompared with controls (24% compared with 40%; p > 0.05). Chronic gastritis
is not more common in patients with oesophagitis, and is unlikely to play a
part in the pathogenesis of this disease.