title: Effect of acid suppression therapy on development of gastric erosions after cure of Helicobacter pylori infection.
abstract: BACKGROUND
  Helicobacter pylori eradication markedly improves histological inflammation and decreases peptic ulcer recurrence, but little is known about the subsequent development of gastric mucosal injury.
  
  
  OBJECTIVE
  To investigate whether acid suppression treatment after eradication influences the development of gastric erosions.
  
  
  METHODS
  Eighty-one patients (gastritis or peptic ulcer) after successful H. pylori eradication were divided into two groups: 40 received an H2-blocker for 6 months (H2-blocker-positive) and 41 received no treatment (H2-blocker-negative). Endoscopy was performed before, and at 3 and 6 months after completion of eradication.
  
  
  RESULTS
  Cumulative prevalence of gastric erosions in the H2-blocker-positive group was significantly lower than in the H2-blocker-negative group, 25% vs. 42%, respectively. In the H2-blocker-negative group but not the H2-blocker-positive group, the cumulative prevalence of gastric erosions after eradication was higher in patients with less severe corpus atrophy or more severe corpus gastritis.
  
  
  CONCLUSIONS
  Development of gastric erosions after H. pylori eradication may be controlled by acid suppression treatment. Less severe atrophy or more severe gastritis in oxyntic glands before eradication may be involved in the development of gastric erosions. These results support the idea that recovery of acid secretion may be one of factors for development of gastric mucosal erosions after successful eradication.
authors.affiliation: Third Department of Internal Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Miyake
authors.forename: T
authors.initials: T
authors.lastname: Tsukui
authors.forename: S
authors.initials: S
authors.lastname: Futagami
authors.forename: A
authors.initials: A
authors.lastname: Tatsuguchi
authors.forename: K
authors.initials: K
authors.lastname: Shinoki
authors.forename: T
authors.initials: T
authors.lastname: Hiratsuka
authors.forename: T
authors.initials: T
authors.lastname: Iizumi
authors.forename: K
authors.initials: K
authors.lastname: Nagata
authors.forename: Y
authors.initials: Y
authors.lastname: Shinji
authors.forename: K
authors.initials: K
authors.lastname: Wada
authors.forename: N
authors.initials: N
authors.lastname: Yamada
authors.forename: M
authors.initials: M
authors.lastname: Kobayashi
authors.forename: C
authors.initials: C
authors.lastname: Sakamoto
mesh_terms: D001706:Biopsy; D016099:Endoscopy, Gastrointestinal; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000473:pathology; D005756:Gastritis / Q000209:etiology*; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy / Q000382:microbiology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006635:Histamine H2 Antagonists / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000209:etiology*; D016896:Treatment Outcome
chemical_list: D006635:Histamine H2 Antagonists