EFFECT OF HELICOBACTER-PYLORI ERADICATION ON GASTRIC HISTOLOGY, SERUMGASTRIN AND PEPSINOGEN-I LEVELS, AND GASTRIC-EMPTYING IN PATIENTS WITH GASTRIC-ULCER
G. Maconi et al., EFFECT OF HELICOBACTER-PYLORI ERADICATION ON GASTRIC HISTOLOGY, SERUMGASTRIN AND PEPSINOGEN-I LEVELS, AND GASTRIC-EMPTYING IN PATIENTS WITH GASTRIC-ULCER, The American journal of gastroenterology, 92(10), 1997, pp. 1844-1848
Objective: The evolution of gastritis and the behavior of basal and me
al-stimulated gastrin release, pepsinogen levels? and gastric emptying
of solids mere studied in a series of consecutive patients with Helic
obacter pylori-positive, uncomplicated, non-NSAID-related type I gastr
ic ulcer over a follow-up period of 3 months after eradication therapy
was begun. Methods: Before starting treatment (consisting of omeprazo
le 40 mg a day for 1 month and amoxycillin 1 g three times daily for 1
4 days), and for 3 months after ulcer healing, 16 patients had a serie
s of functional examinations, including basal and meal-stimulated seru
m gastrin concentration, serum pepsinogen I levels, evaluation of gast
ric emptying of solids by means of serial ultrasonographic measurement
of the gastric antrum area, and histological assessment of antral and
corpus gastritis. Results: Double therapy resulted in the successful
eradication of H. pylori in eight of 16 evaluable patients. In the gro
up of H. pylori-eradicated patients, the mean scores of gastritis acti
vity and inflammation in the antrum and corpus had fallen, 3 months af
ter eradication. No significant changes in mean gastritis scores were
observed in the case and control group with regard to intestinal metap
lasia and atrophy in the antrum and corpus. In H. pylori-eradicated pa
tients, the integrated gastrin response to meal, but not fasting gastr
in concentration, fell significantly during follow-up, and serum pepsi
nogen I levels significantly decreased, compared with baseline. In con
trast, the fasting and maximal antral area and the gastric emptying of
solids remained unchanged over time. In the control group (but not th
e H. pylori-eradicated group), no significant modifications of any of
the above-mentioned parameters mere observed during follow-up. Conclus
ion: Our findings suggest that in non-NSAID-related type I gastric ulc
ers, the eradication of H. pylori significantly reduces gastritis acti
vity and inflammatory scores, but not atrophy and intestinal metaplasi
a, and modifies gastrin and pepsinogen I release in a short follow-up
period. In contrast, H. pylori eradication does not significantly affe
ct gastric emptying of solids, at least within a period of 3 months fr
om therapy.