title: Enhanced somatostatin secretion into the gastric juice with recovery of basal acid output after Helicobacter pylori eradication in gastric ulcers.
abstract: OBJECTIVE
  Antral somatostatin interacts with gastric acid secretion. We aimed to investigate the effect of eradication on gastric acid, somatostatin secretion and mucosal histology in gastric ulcer patients with Helicobacter pylori (H. pylori) infection.
  
  
  METHODS
  Twenty-eight patients (21 male, 7 female) with H. pylori-positive gastric ulcer were treated with dual therapy. Before and 4-8 weeks after the therapy, the histology of biopsy specimens, basal acid output (BAO) and maximal acid output (MAO) after stimulation with tetragastrin were assessed. Somatostatin concentration in the gastric juice was measured by radioimmunoassay, and somatostatin output during either the basal or gastrin-stimulated period was also examined.
  
  
  RESULTS
  Eradication was successful in 22 patients. Before treatment, the acid and somatostatin output were inversely related to the severity of neutrophil infiltration in the corpus and antrum, respectively. After successful eradication, improvement of histological inflammation and an increase in BAO, basal and gastrin-stimulated somatostatin output were observed. Eradication had no effect on atrophy and MAO. There was a positive correlation between gastric acid and somatostatin output in the basal or stimulated condition, irrespective of H. pylori infection.
  
  
  CONCLUSIONS
  The present results suggest that recovery of gastric BAO may be caused by an improvement in corpus neutrophil infiltration, but not by an increase in parietal cell volume or a change in atrophy. Also, there was an increase in basal and gastrin-stimulated somatostatin-containing cell activity accompanied by improved antral neutrophil infiltration in the early phase after H. pylori eradication in gastric ulcers.
authors.affiliation: Department of Internal Medicine, Aichi Medical University School of Medicine, Aichi Cancer Center Hospital, Japan.
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Hayakawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kaneko
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Konagaya
authors.forename: Kaori
authors.initials: K
authors.lastname: Shinozaki
authors.forename: Akihito
authors.initials: A
authors.lastname: Kasahara
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Funaki
authors.forename: Shozaburo
authors.initials: S
authors.lastname: Mori
authors.forename: Takio
authors.initials: T
authors.lastname: Yokoi
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Hirooka
authors.forename: Kazuo
authors.initials: K
authors.lastname: Kusugami
authors.forename: Shinichi
authors.initials: S
authors.lastname: Kakumu
mesh_terms: D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005745:Gastric Acidity Determination; D005750:Gastric Juice / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000378:metabolism / Q000382:microbiology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008875:Middle Aged; D013004:Somatostatin / Q000378:metabolism*; D013276:Stomach Ulcer / Q000188:drug therapy* / Q000378:metabolism / Q000382:microbiology
chemical_list: D000897:Anti-Ulcer Agents; D013004:Somatostatin