NSAID-related gastrointestinal complications

Clin Cornerstone. 1999;1(5):42-56. doi: 10.1016/s1098-3597(99)90088-1.


Despite the common induction of gastrointestinal (GI) complications by nonsteroidal anti-inflammatory drugs (NSAIDs), many aspects of pathogenesis and management remain controversial. The most important complications are bleeding and perforation arising in the esophagus, stomach, and duodenum due to NSAID effects on platelets and on a variety of mucosal lesions. Complications arise from preexisting peptic ulcer, NSAID-induced ulcers and erosions, and other lesions (not caused by NSAIDs) caused to bleed by NSAID-induced platelet dysfunction. Much confusion has arisen from the umbrella term "NSAID gastropathy" used to embrace a variety of pathogenetically distinct mucosal lesions. Failure to discriminate among the different forms of NSAID injury has hampered clinical investigation. This article offers general guidelines for prevention of NSAID complications, but there remain many unresolved issues, including the role of Helicobacter pylori infection. The best approach to management is to remove or reduce exposure to NSAIDs whenever possible. The newer NSAIDs (e.g., cyclo-oxygenase [COX]-2-selective inhibitors) have a much lower risk of endoscopic ulcers and minimal platelet effects, which are likely to translate into lower risk of GI complications. However, this benefit on clinical outcome remains to be established.

Publication types

  • Review

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage
  • Anti-Inflammatory Agents, Non-Steroidal / adverse effects*
  • Endoscopy, Gastrointestinal
  • Gastrointestinal Diseases / chemically induced*
  • Gastrointestinal Diseases / pathology
  • Gastrointestinal Diseases / prevention & control*
  • Helicobacter Infections / complications
  • Helicobacter Infections / drug therapy
  • Helicobacter pylori
  • Humans
  • Peptic Ulcer / chemically induced
  • Peptic Ulcer / diagnosis
  • Peptic Ulcer / prevention & control*
  • Prostaglandins / biosynthesis
  • Risk Factors


  • Anti-Inflammatory Agents, Non-Steroidal
  • Prostaglandins