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Pathogenesis of nonsteroidal anti-inflammatory drug-related upper gastrointestinal toxicity

  • Andrew Soll
    Correspondence
    Requests for reprints should be addressed to Andrew Soll, MD, Cure/WLAVA, 11302 Wilshire Boulevard, Building 115, Room 215, Los Angeles, California 90073
    Affiliations
    Cure/WLAVA, Los Angeles, California, USA
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      Abstract

      The mechanisms involved in the pathogenesis of ulcers associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) have not been fully elucidated. Although studies using acute mucosal injury as a surrogate for clinically relevant outcomes have provided useful information, in practice, acute mucosal injury does not necessarily provide a reliable predictor of clinical ulcers or complications. Several factors that increase the risk of NSAID-associated gastroenteropathy have been identified, and there are data to support or provide speculation for other physiologic factors that might predispose specific subsets of patients to increased mucosal injury. Since clinically significant events occur less frequently than does ulceration, it is the latter determinant, i.e., the identification of the traits that distinguish patients who develop serious NSAID-associated gastrointestinal (GI) toxicity from those who can tolerate these drugs, that may provide the clues necessary to understand the events underlying ulcer pathogenesis.
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