Influence of H elicobacter pylori Infection on Gastric Acid Secretion in Pre‐School B angladeshi Children

Background The effect of H elicobacter pylori ( H . pylori ) infection on gastric acid secretion ( GAS ) is poorly defined in children. Objective To determine whether H . pylori infection is associated with abnormal GAS in children. Methods We studied 30 H . pylori ‐infected children (identified by a positive urea breath test) and 30 noninfected children of both sexes, aged 2–5 years. Gastric pH and GAS were measured before and 8 weeks after the completion of a 2‐week course of anti‐ H . pylori therapy (omeprazole, clarithromycin, and amoxicillin). Gastric acid output ( GAO ) was quantified during a 1‐h basal period ( GAO‐B ) (mmol/h) and a 1‐hour stimulated period ( GAO ‐ S ) (mmol/hour) following subcutaneous administration of pentagastrin (6 μg/kg). Results A significantly greater number of infected children had a high gastric pH (>4.0, p  = 0.03) compared with the noninfected group. GAO ‐ B and GAO ‐ S in H . pylori ‐infected children were significantly lower, around 50%, compared with children without H . pylori infection. H . pylori ‐eradication therapy resulted in a rise of both the mean GAO ‐ B (paired t ‐test before vs. after therapy; 0.28 ± 0.40 vs. 0.62 ± 1.0, p  =   0.12) and GAO ‐ S (before vs. after therapy; 2.0 ± 1.4 vs. 3.4 ± 2.5, p  =   0.001), with values reaching equivalence to those in the H . pylori ‐negative children (0.71 ± 0.56 for BAO , 3.3 ± 2.0 for SAO , p  =  NS ). Conclusion The results suggest that the gastric barrier is compromised in children with H . pylori infection in B angladesh. Improvement of GAO following anti‐ H . pylori therapy suggests a causal link between H . pylori infection and depressed GAO in this population.