V. Savarino et al., CIRCADIAN GASTRIC-ACIDITY IN HELICOBACTER-PYLORI POSITIVE ULCER PATIENTS WITH AND WITHOUT GASTRIC METAPLASIA IN THE DUODENUM, Gut, 39(4), 1996, pp. 508-512
Background-The presence of gastric metaplasia allows Helicobacter pylo
ri to colonise the duodenum and this condition is thought to be acquir
ed as a response to acid hypersecretion. This functional disorder, how
ever, is present only in a subgroup of duodenal ulcer patients and, in
addition, surface gastric metaplasia has been frequently found in the
proximal duodenum of normal subjects and patients with non-ulcer dysp
epsia, who cannot be certainly considered as acid hypersecretors. Aims
-To clarify the role of acid in inducing gastric type epithelium in th
e duodenum. This study aimed at assessing whether the pattern of circa
dian gastric acidity differs between H pylori positive duodenal ulcer
patients with and without duodenal gastric metaplasia. Patients-Sevent
y one patients with duodenal ulcer confirmed by endoscopy and who were
found to be positive for H pylori infection by histology on antrum bi
opsy specimens were enrolled into this study. Methods-Gastric type epi
thelium in the duodenum was found in 49 of 71 ulcer patients (69%). Co
ntinuous 24 hour gastric pH metry was performed in 50 healthy subjects
and in the two subgroups of duodenal ulcer patients with and without
gastric metaplasia in the duodenum. Gastric acidity was calculated for
24 hours (1700-1659), night (2000-0759) and daytime (0800-1959). Resu
lts-Ulcer patients without gastric metaplasia showed a significantly h
igher gastric acidity (p<0.001) than controls for every time interval
considered, while the ulcer subgroup with gastric metaplasia was more
acid than healthy subjects (p<0.001) during the whole 24 hour period a
nd the daytime. There was no difference between the two subgroups of d
uodenal ulcer patients with and without gastric metaplasia during the
various time segments analysed. Conclusions-The findings confirm that
the circadian gastric acidity of duodenal ulcer patients is higher tha
n that of controls. As there is no difference in gastric pH between du
odenal ulcer patients with and without gastric metaplasia, gastric hyp
eracidity is not specific to patients with duodenal gastric metaplasia
. It is probable that this histological change is a non-specific respo
nse to mucosal injury resulting from various factors and not exclusive
ly to acid.