ERADICATION OF HELICOBACTER-PYLORI INFECTION IN PATIENTS WITH NONULCER DYSPEPSIA - EFFECTS ON BASAL AND BOMBESIN-STIMULATED SERUM GASTRIN AND GASTRIC-ACID SECRETION
Ml. Verhulst et al., ERADICATION OF HELICOBACTER-PYLORI INFECTION IN PATIENTS WITH NONULCER DYSPEPSIA - EFFECTS ON BASAL AND BOMBESIN-STIMULATED SERUM GASTRIN AND GASTRIC-ACID SECRETION, Scandinavian journal of gastroenterology, 30(10), 1995, pp. 968-973
Background: This study evaluates the effect of eradicating Helicobacte
r pylori on basal and bombesin-stimulated gastric acid secretion and s
erum gastrin in non-ulcer dyspepsia. Methods: Before and 1 month after
an attempt to eradicate H. pylori basal and bombesin-stimulated gastr
ic acid outputs were measured in 23 patients. H. pylori was eradicated
in 15 patients (group A) but not in the other 8 (group B). Incrementa
l gastric acid output was calculated by subtracting basal from bombesi
n-stimulated values. Results: Basal acid output increased significantl
y (p=0.01) after therapy in group A (Delta 1.6 +/- 0.6 mmol/h) but not
in group B (Delta 0.2 +/- 0.5 mmol/h). Incremental gastric acid outpu
t decreased distinctly (Delta-3.9 +/- 1.4 mmol/h) after therapy in gro
up A (p = 0.02) but not in group B (Delta-2.2 +/- 1.7 mmol/h). Basal s
erum gastrin decreased significantly (p < 0.005) after therapy in grou
p A (Delta-9 +/- 4 pM) but not in group B (Delta-1 +/- 2 pM). Integrat
ed serum gastrin responses to bombesin decreased markedly (p < 0.001)
after therapy in group A (Delta-5.0 +/- 1.6 nM60 min) but slightly in
group B (Delta-0.9 +/- 1.3 nM60 min) (p < 0.05). Conclusions: In pat
ients with non-ulcer dyspepsia basal serum gastrin concentrations decr
ease but basal gastric acid outputs increase after eradication of H. p
ylori. Bombesin-induced increments in gastric acid output, however, de
crease in parallel with gastrin release.