BACKGROUND: The effect of Helicobacter 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 Bangladesh. Improvement of GAO following anti- H. pylori therapy suggests a causal link between H. pylori infection and depressed GAO in this population.
BACKGROUND: The effect of Helicobacter pylori (H. pylori) infection on gastric acid secretion (GAS) is poorly defined in children. OBJECTIVE: To determine whether H. pyloriinfection 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. pyloriinfection. 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. pyloriinfection in Bangladesh. Improvement of GAO following anti- H. pylori therapy suggests a causal link between H. pyloriinfection and depressed GAO in this population.
Authors: Lucia Pacifico; John F Osborn; Valeria Tromba; Sara Romaggioli; Stefano Bascetta; Claudio Chiesa Journal: World J Gastroenterol Date: 2014-02-14 Impact factor: 5.742