title: Famotidine for the prevention of gastric and duodenal ulcers caused by nonsteroidal antiinflammatory drugs.
abstract: BACKGROUND
  Acid suppression with famotidine, a histamine H2-receptor antagonist, provides protection against gastric injury in normal subjects receiving short courses of aspirin or naproxen. The efficacy of famotidine in preventing peptic ulcers in patients receiving long-term therapy with nonsteroidal antiinflammatory drugs (NSAIDs) is not known.
  
  
  METHODS
  We studied the efficacy of two doses of famotidine (20 mg and 40 mg, each given orally twice daily), as compared with placebo, in preventing peptic ulcers in 285 patients without peptic ulcers who were receiving long-term NSAID therapy for rheumatoid arthritis (82 percent) or osteoarthritis (18 percent). The patients were evaluated clinically and by endoscopy at base line and after 4, 12, and 24 weeks of treatment. The evaluators were unaware of the treatment assignment. The primary end point was the cumulative incidence of gastric or duodenal ulceration at 24 weeks.
  
  
  RESULTS
  The cumulative incidence of gastric ulcers was 20 percent in the placebo group, 13 percent in the group of patients receiving 20 mg of famotidine twice daily (P = 0.24 for the comparison with placebo), and 8 percent in the group receiving 40 mg of famotidine twice daily (P = 0.03 for the comparison with placebo). The proportion of patients in whom duodenal ulcers developed was significantly lower with both doses of famotidine than with placebo (13 percent in the placebo group, 4 percent in the low-dose famotidine group [P = 0.04], and 2 percent in the high-dose famotidine group [P = 0.01]). Both doses of famotidine were well tolerated.
  
  
  CONCLUSIONS
  Treatment with high-dose famotidine significantly reduces the cumulative incidence of both gastric and duodenal ulcers in patients with arthritis receiving long-term NSAID therapy.
authors.affiliation: Department of Gastroenterology, Glasgow Royal Infirmary, Scotland.
authors.forename: A S
authors.initials: AS
authors.lastname: Taha
authors.forename: N
authors.initials: N
authors.lastname: Hudson
authors.forename: C J
authors.initials: CJ
authors.lastname: Hawkey
authors.forename: A J
authors.initials: AJ
authors.lastname: Swannell
authors.forename: P N
authors.initials: PN
authors.lastname: Trye
authors.forename: J
authors.initials: J
authors.lastname: Cottrell
authors.forename: S G
authors.initials: SG
authors.lastname: Mann
authors.forename: T J
authors.initials: TJ
authors.lastname: Simon
authors.forename: R D
authors.initials: RD
authors.lastname: Sturrock
authors.forename: R I
authors.initials: RI
authors.lastname: Russell
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy; D004311:Double-Blind Method; D004381:Duodenal Ulcer / Q000139:chemically induced / Q000453:epidemiology / Q000517:prevention & control*; D015738:Famotidine / Q000627:therapeutic use*; D005260:Female; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D010003:Osteoarthritis / Q000188:drug therapy; D012307:Risk Factors; D013276:Stomach Ulcer / Q000139:chemically induced / Q000453:epidemiology / Q000517:prevention & control*; D016896:Treatment Outcome
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000897:Anti-Ulcer Agents; D006635:Histamine H2 Antagonists; D015738:Famotidine