Incidence

  • Hospitalizations for UGIB increasing
  • Due to increased NSAID use
    • Risk of bleeding and perforation proportional to daily dose of NSAID
  • Also increases with
    • Age > 60
    • Prior GI event
    • Concurrent use of NSAIDs and steroids or anticoagulants
    • 2-10 x increased risk of GI complications

Pathophysiology

  • NSAIDs absorbed through stomach and small intestine
  • Action of NSAIDs
    • Systemic inhibition of cyclo-oxygenase enzymes
    • COX form rate limiting step in prostaglandin synthesis in GIT
    • Prostaglandins promote gastric and duodenal mucosal protection via numerous mechanisms
    • Risk of mucosal injury and ulceration is proportional to anti-inflammatory effect of each NSAID
  • Ulcers usually
    • Found in stomach (H. pylori higher in duodenum)
    • Not associated with gastritis (only 25%, c.f. H. pylori)
    • Heal when NSAID discontinued, and do not recur