title: Treatment with a proton pump inhibitor promotes corpus gastritis in patients with Helicobacter pylori-infected antrum-predominant gastritis.
abstract: BACKGROUND
  Proton pump inhibitors have been reported to modify the level of Helicobacter pylori gastritis.
  
  
  OBJECTIVE
  To quantitatively investigate the effect of a proton pump inhibitor on the mucosal neutrophil reaction.
  
  
  METHODS
  Forty-six H. pylori-infected patients (17 duodenal ulcer, 29 gastric ulcer) were enrolled. During endoscopic examination, biopsy samples were obtained from the antrum and the corpus. The tissue content of neutrophil myeloperoxidase was measured by enzyme-linked immunoabsorbent assay, and H. pylori infection was histologically assessed. A proton pump inhibitor was administered orally for 8 weeks.
  
  
  RESULTS
  In the patients as a whole, antral myeloperoxidase decreased significantly after proton pump inhibitor treatment, but corpus myeloperoxidase remained largely unchanged. In duodenal ulcer patients, myeloperoxidase significantly decreased in the antrum, but increased in the corpus. In gastric ulcer patients, a significant reduction was observed in antral myeloperoxidase, but corpus myeloperoxidase remained unchanged. In the antral myeloperoxidase > corpus myeloperoxidase subgroup (n=24), antral myeloperoxidase significantly decreased, whereas corpus myeloperoxidase increased. No changes were observed at either site in the corpus myeloperoxidase > antral myeloperoxidase subgroup. Histology showed that the antral bacterial load of H. pylori decreased in all subgroups, but that it was mostly unchanged in the corpus.
  
  
  CONCLUSIONS
  Proton pump inhibitor treatment stimulated the neutrophil reaction in the corpus mucosa of duodenal ulcer patients and of patients in whom antral neutrophil accumulation was more predominant than that of the corpus. This phenomenon may not be caused by increased bacterial density.
authors.affiliation: Division of Gastroenterology, National Tokyo Medical Center, Tokyo, Japan. msuzuki@ntmc.hosp.go.jp
authors.forename: M
authors.initials: M
authors.lastname: Suzuki
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: T
authors.initials: T
authors.lastname: Kitahora
authors.forename: M
authors.initials: M
authors.lastname: Miyazawa
authors.forename: S
authors.initials: S
authors.lastname: Nagahashi
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: H
authors.initials: H
authors.lastname: Ishii
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000284:Administration, Oral; D000328:Adult; D000368:Aged; D001562:Benzimidazoles / Q000494:pharmacology; D001706:Biopsy; D004381:Duodenal Ulcer / Q000188:drug therapy / Q000382:microbiology; D016099:Endoscopy, Gastrointestinal; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D005756:Gastritis / Q000209:etiology* / Q000382:microbiology; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy*; D016480:Helicobacter pylori / Q000187:drug effects / Q000472:pathogenicity; D006801:Humans; D064747:Lansoprazole; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D009853:Omeprazole / Q000031:analogs & derivatives* / Q000494:pharmacology; D009195:Peroxidase / Q000378:metabolism*; D054328:Proton Pump Inhibitors; D011706:Pyloric Antrum / Q000382:microbiology / Q000473:pathology; D064750:Rabeprazole; D013276:Stomach Ulcer / Q000188:drug therapy / Q000382:microbiology
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D001562:Benzimidazoles; D004791:Enzyme Inhibitors; D054328:Proton Pump Inhibitors; D064747:Lansoprazole; D064750:Rabeprazole; D009195:Peroxidase; D009853:Omeprazole