ASYMPTOMATIC HELICOBACTER-PYLORI INFECTION IMPAIRS PH INHIBITION OF GASTRIN AND ACID-SECRETION DURING 2ND HOUR OF PEPTONE MEAL STIMULATION

Citation
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
Citations number
25
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
01632116
Volume
38
Issue
9
Year of publication
1993
Pages
1681 - 1687
Database
ISI
SICI code
0163-2116(1993)38:9<1681:AHIIPI>2.0.ZU;2-8
Abstract
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.