title: Significant upper gastrointestinal events associated with conventional NSAID versus celecoxib.
abstract: Despite their substantial clinical benefits in the management of rheumatoid arthritis, osteoarthritis, pain, and other musculoskeletal complaints, conventional nonsteroidal antiinflammatory drugs (NSAID) are associated with significant toxicities that can frequently limit their use. The most common and noteworthy adverse effects of NSAID are gastrointestinal (GI), and range from dyspeptic symptoms to ulcers and serious ulcer complications. The upper GI toxicities associated with the use of conventional NSAID led to the search for medications that were as clinically effective as these agents, but with a significantly improved GI safety profile. It is now known that the constitutively expressed isoenzyme cyclooxygenase (COX)-1 catalyzes the synthesis of prostanoids that help to regulate normal physiologic processes, including GI mucosa protection, whereas the inducible isoenzyme COX-2 leads to the generation of prostaglandins that mediate inflammation, pain, and fever. This knowledge has led to the development of new compounds that, at therapeutic concentrations, inhibit COX-2 without affecting COX-1. The first COX-2 targeted agent approved by the US Food and Drug Administration (FDA) was celecoxib. This article reviews the risks of GI complications associated with conventional NSAID use and compares these risks with that of the new COX-2 specific inhibitor celecoxib.
authors.affiliation: Department of Medicine, College of Medicine, University of Illinois at Chicago, USA.
authors.forename: J L
authors.initials: JL
authors.lastname: Goldstein
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D000068579:Celecoxib; D016861:Cyclooxygenase Inhibitors / Q000009:adverse effects*; D004064:Digestive System / Q000187:drug effects*; D006801:Humans; D009656:North America / Q000453:epidemiology; D010437:Peptic Ulcer / Q000139:chemically induced; D011720:Pyrazoles; D013276:Stomach Ulcer / Q000139:chemically induced* / Q000453:epidemiology; D013449:Sulfonamides / Q000009:adverse effects*; D006113:United Kingdom / Q000453:epidemiology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D011720:Pyrazoles; D013449:Sulfonamides; D000068579:Celecoxib