Beneficial effects of NSAIDs in the gastrointestinal tract

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin exert irritant and toxic effects upon the organs of the gastrointestinal tract. NSAID toxicity in the gastrointestinal tract is related, at least in part, to the inhibition of the cyclo-oxygenase (COX) enzyme, leading to a reduction of 'cytoprotective' prostaglandin synthesis. In this paper, examples in which NSAIDs exert beneficial effects in the gastrointestinal tract are discussed. NSAIDs, particularly aspirin, are showing promise in the chemoprevention of colorectal, and, to a lesser degree, oesophageal cancers. The clinical value of NSAIDs in the treatment of established gastrointestinal tract cancers is also worthy of further study. There is good clinical evidence showing the value of diclofenac for the treatment of biliary colic and aspirin or ibuprofen for the prevention of gallstones. NSAIDs also have therapeutic potential against other inflammatory gastrointestinal diseases in the oesophagus and possibly pancreas and liver. To a lesser degree, there is some evidence that NSAIDs may have a therapeutic potential in certain gastrointestinal motility disorders, such as aspirin in the post-irradiation syndrome. It therefore follows that in these cancerous, inflammatory and motility pathologies, prostaglandins exert deleterious effects. The paradox of prostaglandins being 'cytoprotective' and potentially damaging can be explained by considering the enzymic origin of prostaglandins. COX-1 is expressed physiologically while inducible COX-2 is expressed in pathological situations. The beneficial clinical effects of selective COX-2-inhibiting NSAIDs in the gastrointestinal tract deserve further study. This paper challenges the concept of 'cytoprotection'.