title: Does eradication of Helicobacter pylori impair healing of nonsteroidal anti-inflammatory drug associated bleeding peptic ulcers? A prospective randomized study.
abstract: BACKGROUND
  Despite the widely accepted view that Helicobacter pylori is the most important cause of peptic ulcer disease, recent studies have suggested that the microbe protects against nonsteroidal anti-inflammatory drug (NSAID)-associated gastroduodenal lesions and promotes ulcer healing. We investigated the effects of H. pylori eradication on the healing of NSAID-associated bleeding peptic ulcers.
  
  
  METHODS
  Chronic NSAID users presenting with peptic ulcer haemorrhage underwent endoscopy to secure haemostasis and to document H. pylori infection by rapid urease test and culture. They were prospectively randomized to receive either omeprazole (20 mg once daily) for 8 weeks or a 1-week course of triple therapy (bismuth subcitrate 120 mg, tetracycline 500 mg, metronidazole 400 mg, all given four times daily) plus omeprazole (20 mg once daily) for 8 weeks. Endoscopy was repeated after 8 weeks. Final H. pylori status was determined by a 13C-urea breath test that was performed at least 4 weeks after discontinuation of omeprazole.
  
  
  RESULTS
  195 H. pylori-infected NSAID users, complicated by bleeding ulcers, were randomized to receive omeprazole alone (102) or triple therapy plus omeprazole (93). 174 patients returned for second endoscopy at 8 weeks (91 in the omeprazole group, 83 in the triple therapy group). Urea breath test was negative in 14% in the omeprazole group vs. 92% in the triple therapy group (P < 0.001). Complete ulcer healing was achieved in 88 (97%) patients in the omeprazole group and 77 (93%) in the triple therapy group (P=0. 31). On intention-to-treat analysis, ulcers were healed in 86% of the omeprazole group and 83% of the triple therapy group (P=0.50). There was no significant difference in the healing rates of gastric or duodenal ulcers between the two groups.
  
  
  CONCLUSIONS
  Eradication of H. pylori did not impair the healing of NSAID-associated bleeding peptic ulcers.
authors.affiliation: Department of Medicine & Therapeutics, Prince of Wales Hospital, Chinese University of Hong Kong, Shatin. fklchan@cuhk.edu.hk
authors.forename: F K
authors.initials: FK
authors.lastname: Chan
authors.forename: J J
authors.initials: JJ
authors.lastname: Sung
authors.forename: R
authors.initials: R
authors.lastname: Suen
authors.forename: Y T
authors.initials: YT
authors.lastname: Lee
authors.forename: J C
authors.initials: JC
authors.lastname: Wu
authors.forename: W K
authors.initials: WK
authors.lastname: Leung
authors.forename: H L
authors.initials: HL
authors.lastname: Chan
authors.forename: A C
authors.initials: AC
authors.lastname: Lai
authors.forename: J Y
authors.initials: JY
authors.lastname: Lau
authors.forename: E K
authors.initials: EK
authors.lastname: Ng
authors.forename: S C
authors.initials: SC
authors.lastname: Chung
mesh_terms: D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D004359:Drug Therapy, Combination / Q000627:therapeutic use*; D005260:Female; D016481:Helicobacter Infections / Q000188:drug therapy*; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D008297:Male; D008795:Metronidazole / Q000627:therapeutic use; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use*; D009942:Organometallic Compounds / Q000627:therapeutic use; D010438:Peptic Ulcer Hemorrhage / Q000188:drug therapy*; D013752:Tetracycline / Q000627:therapeutic use
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000897:Anti-Ulcer Agents; D009942:Organometallic Compounds; D008795:Metronidazole; D013752:Tetracycline; C002791:bismuth tripotassium dicitrate; D009853:Omeprazole