Pr. Tarnasky et al., ASYMPTOMATIC HELICOBACTER-PYLORI INFECTION IMPAIRS PH INHIBITION OF GASTRIN AND ACID-SECRETION DURING 2ND HOUR OF PEPTONE MEAL STIMULATION, Digestive diseases and sciences, 38(9), 1993, pp. 1681-1687
H. pylori infection is associated with acid-peptic disease, although i
ts role in the pathogenesis is unclear. The purpose of this study was
to determine if chronic infection in asymptomatic subjects impairs the
inhibition Of meal-stimulated gastrin and acid secretion that is obse
rved normally at low intragastric pH. Presence of infection was determ
ined by both C-14 urea breath test and serology. Acid secretion was me
asured under basal conditions and in response to peptone meal stimulat
ion and pentagastrin. Plasma gastrin concentrations were determined by
radioimmunoassay under basal conditions and during peptone meal stimu
lation. Intragastric titration with 1% peptone during the first hour,
and 8% peptone during the second hour, was performed at both pH 7.0 an
d 2.5 on different days to compare the inhibition of gastrin and acid
secretion. Compared to noninfected subjects, asymptomatic individuals
infected with H. pylori had significantly increased: (1) basal gastrin
values (P < 0.005); (2) 8% peptone-stimulated gastrin responses at bo
th pH 7.0 and 2.5 (P < 0.05); and (3) 8% peptone-stimulated acid outpu
t at pH 2.5 (P = 0.01). During the second hour of peptone-stimulation,
subjects infected with H. pylori had significantly decreased inhibiti
on of gastrin (52% vs 95%) (P = 0.002) and acid (30% vs 81%) (P = 0.01
) secretion from pH 7. 0 to 2.5. Thus, chronic infection with H. pylor
i results in impaired inhibition of gastrin and acid secretion at low
intragastric pH during the second hour of peptone meal stimulation. Th
ese defects may be unrelated to the pathogenesis of acid-peptic diseas
e, since they occur in asymptomatic subjects infected with H. pylori.