title: Implications of corpus gastritis, atrophy and cyclooxygenase in the development of gastric erosions after curing Helicobacter pylori infection.
abstract: BACKGROUND
  Helicobacter pylori eradication decreases recurrence of peptic ulcers with marked improvement in histological inflammation, but gastric mucosal injuries may be developed even after eradication.
  
  
  OBJECTIVE
  To investigate the mechanisms responsible for the development of gastric erosions after eradication, we analysed the relationship between clinicopathological risk factors and the occurrence of gastric erosion after curing H. pylori infection.
  
  
  METHODS
  Sixty patients underwent endoscopy before, and 3, 6 and 12 months after the completion of H. pylori eradication.
  
  
  METHODS
  Risk factors associated with the development of gastric erosions after eradication were assessed by multivariate analysis, and cyclooxygenase-1 and -2 immunoreactivity was histologically examined in the gastric mucosa before and after eradication.
  
  
  RESULTS
  The cumulative prevalence of gastric erosions after H. pylori eradication was 38.3% within 1 year. Using multivariate analysis, corpus gastritis scores (inflammation score+activity score), corpus atrophy scores and an age of more than 50 years were found to be independent factors associated with the development of gastric erosion after eradication with odds ratios of 7.39, 0.13 and 5.00, respectively. Cyclooxygenase-2 immunoreactivity of the corpus was decreased for the non-erosion group after eradication, but not for the erosion group.
  
  
  CONCLUSIONS
  Severe gastritis or less severe atrophy in oxyntic glands but not in pyloric glands before eradication may be involved in the development of gastric erosions after curing H. pylori infection.
authors.affiliation: Third Department of Internal Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan. km366@nms.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Miyake
authors.forename: A
authors.initials: A
authors.lastname: Tatsuguchi
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: N
authors.initials: N
authors.lastname: Ueki
authors.forename: Y
authors.initials: Y
authors.lastname: Shinji
authors.forename: M
authors.initials: M
authors.lastname: Kusunoki
authors.forename: T
authors.initials: T
authors.lastname: Iizumi
authors.forename: T
authors.initials: T
authors.lastname: Hiratsuka
authors.forename: H
authors.initials: H
authors.lastname: Nishigaki
authors.forename: S
authors.initials: S
authors.lastname: Futagami
authors.forename: K
authors.initials: K
authors.lastname: Wada
authors.forename: T
authors.initials: T
authors.lastname: Tsukui
authors.forename: C
authors.initials: C
authors.lastname: Sakamoto
mesh_terms: D000367:Age Factors; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D001284:Atrophy; D051545:Cyclooxygenase 1; D004359:Drug Therapy, Combination; D005260:Female; D005753:Gastric Mucosa / Q000201:enzymology / Q000473:pathology*; D005756:Gastritis / Q000188:drug therapy / Q000382:microbiology / Q000473:pathology*; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000188:drug therapy*; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D015999:Multivariate Analysis; D010437:Peptic Ulcer / Q000188:drug therapy / Q000382:microbiology; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D012307:Risk Factors
chemical_list: D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D008565:Membrane Proteins; D051545:Cyclooxygenase 1; C496511:PTGS1 protein, human; D011451:Prostaglandin-Endoperoxide Synthases