THE BIOCHEMICAL BASIS OF NONSTEROIDAL ANTIINFLAMMATORY DRUG-INDUCED DAMAGE TO THE GASTROINTESTINAL-TRACT - A REVIEW AND A HYPOTHESIS

Non-steroidal anti-inflammatory drugs (NSAIDs) are amongst the most successful group of drugs ever marketed, which demonstrates their overall efficacy. They are not, however, without side effects (1). The gastrointestinal tract bears the brunt of NSAID-related toxicity (2-5). The gastro-duodenal side effects have attracted most attention because of the frequency, severity, and ease of documentation of the damage. Point prevalence studies suggest that 10-30% of patients on NSAIDs have gastroduodenal ulcers (6-10), but the clinical implications of these findings have been played down by suggestions that definitions of ulcer in these studies included a substantial number of large erosions (called endoscopic ulcers; purported to account for up to 50% of "ulcers" in these studies) of little clinical consequence as opposed to clinically significant ulcers (pre-excising diathesis; implying NSAID-associated rather than NSAID-induced ulcers), which have increased potential to perforate or bleed because of NSAIDs (11). There are, on the other hand, ample experimental data demonstrating NSAID-induced ulcers in all of the intestinal tract of animals and some erosions may be transitory lesions in the development of ulcers in man and hence markers of unacceptable mucosal damage (12). © 1995 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.