title: Effect of Helicobacter pylori infection on gastric acid secretion and meal-stimulated serum gastrin in children.
abstract: BACKGROUND
  Comparative studies of gastric acid secretion in children related to Helicobacter pylori infection are lacking. The purpose of this study was to compare acid secretion and meal-stimulated gastrin in relation to H. pylori infection among pediatric patients.
  
  
  METHODS
  Thirty-six children aged 10-17 years (17 with H. pylori infection) undergoing diagnostic endoscopy participated in the study. Diagnoses included gastritis only (n = 23), duodenal ulcer (n = 5) and normal histology (n = 8). Gastric acid output was studied using the endoscopic gastric secretion test before and 2-3 months after H. pylori eradication. Meal-stimulated serum gastrin response was assessed before and 12 months after eradication.
  
  
  RESULTS
  H. pylori gastritis was typically antrum-predominant. Acid secretion was greater in H. pylori-positive patients with duodenal ulcer than in gastritis-only patients or controls [mean +/- standard error (SE): 6.56 +/- 1.4, 3.11 +/- 0.4 and 2.65 +/- 0.2 mEq/10 minutes, respectively; p <.001]. Stimulated acid secretion was higher in H. pylori-positive boys than girls (5.0 +/- 0.8 vs. 2.51 +/- 0.4 mEq/10 minutes, respectively; p <.05). Stimulated acid secretion pre- and post-H. pylori eradication was similar (5.47 +/- 0.8 vs. 4.67 +/- 0.9 mEq/10 minutes, respectively; p =.21). Increased basal and meal-stimulated gastrin release reversed following H. pylori eradication (e.g. basal from 134 to 46 pg/ml, p <.001 and peak from 544 to 133 pg/ml, p <.05).
  
  
  CONCLUSIONS
  H. pylori infection in children is associated with a marked but reversible increase in meal-stimulated serum gastrin release. Gastric acid hypersecretion in duodenal ulcer remains after H. pylori eradication, suggesting that the host factor plays a critical role in outcome of the infection.
authors.affiliation: Department of Pediatrics, Showa Inan General Hospital, Komagane, Japan.
authors.forename: Seiichi
authors.initials: S
authors.lastname: Kato
authors.forename: Kyoko
authors.initials: K
authors.lastname: Ozawa
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Koike
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Sekine
authors.forename: Shuichi
authors.initials: S
authors.lastname: Ohara
authors.forename: Takanori
authors.initials: T
authors.lastname: Minoura
authors.forename: Kazuie
authors.initials: K
authors.lastname: Iinuma
mesh_terms: D000293:Adolescent; D001706:Biopsy; D001944:Breath Tests; D002648:Child; D004381:Duodenal Ulcer / Q000382:microbiology / Q000473:pathology; D004435:Eating; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000473:pathology; D005755:Gastrins / Q000097:blood*; D005756:Gastritis / Q000382:microbiology / Q000473:pathology; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000097:blood / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000302:isolation & purification / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D014508:Urea / Q000032:analysis; D014510:Urease / Q000032:analysis
chemical_list: D005755:Gastrins; D014508:Urea; D014510:Urease