title: Characteristics of gastritis in patients with Helicobacter pylori-positive reflux esophagitis.
abstract: OBJECTIVE
  The influence of Helicobacter pylori on gastric acid secretion differs with the status of gastritis. The histological characteristics of gastritis in H. pylori-positive patients with reflux esophagitis have not been fully investigated. We therefore studied the pattern of endoscopic gastric mucosal atrophy and degree of histological gastritis in such patients.
  
  
  METHODS
  Subjects comprised 41 H. pylori-positive patients with reflux esophagitis, 41 age- and sex-matched patients with duodenal ulcer, and 41 patients with early gastric cancer. The endoscopic pattern of gastric mucosal atrophy was reviewed, and the degree of histological gastritis in biopsy specimens from the antrum and corpus was assessed in accordance with the updated Sydney system.
  
  
  RESULTS
  The grade of endoscopic and histological gastric mucosal atrophy in patients with reflux esophagitis was significantly lower than that in patients with gastric cancer, and the histological scores for antral atrophy and metaplasia in patients with reflux esophagitis tended to be lower than those in patients with duodenal ulcer. In patients with reflux esophagitis and duodenal ulcer, the scores for antral inflammation and activity tended to be higher than those for the corpus. Conversely, the inflammation and activity score in patients with early gastric cancer showed a corpus-predominant gastritis pattern.
  
  
  CONCLUSIONS
  In H. pylori-positive patients with reflux esophagitis, the degree of endoscopic gastric mucosal atrophy is low and histologically there is an antral-predominant gastritis pattern. Therefore, gastric acid secretion in H. pylori-positive patients with reflux esophagitis may be augmented by H. pylori infection.
authors.affiliation: Department of Gastroenterology and Hepatology, Shimane University, School of Medicine, Izumo, Japan.
authors.forename: Takafumi
authors.initials: T
authors.lastname: Mihara
authors.forename: Kyoichi
authors.initials: K
authors.lastname: Adachi
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Komazawa
authors.forename: Manabu
authors.initials: M
authors.lastname: Yoshida
authors.forename: Asuka
authors.initials: A
authors.lastname: Araki
authors.forename: Riruke
authors.initials: R
authors.lastname: Maruyama
authors.forename: Kenji
authors.initials: K
authors.lastname: Furuta
authors.forename: Shunji
authors.initials: S
authors.lastname: Ishihara
authors.forename: Yuji
authors.initials: Y
authors.lastname: Amano
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Kinoshita
mesh_terms: D016022:Case-Control Studies; D004381:Duodenal Ulcer / Q000473:pathology; D004942:Esophagitis, Peptic / Q000473:pathology*; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology*; D005757:Gastritis, Atrophic / Q000382:microbiology / Q000473:pathology*; D016481:Helicobacter Infections / Q000473:pathology*; D016480:Helicobacter pylori; D006551:Hernia, Hiatal / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011706:Pyloric Antrum / Q000473:pathology*; D012720:Severity of Illness Index; D013274:Stomach Neoplasms / Q000473:pathology