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Non-steroidal anti-inflammatory drugs and gastrointestinal damage—problems and solutions
Areas of the gastrointestinal tract that may be damaged by NSAIDs Oesophagus: oesophagitis, ulceration, stricture Stomach: ulcers, erosions Duodenum: ulcers, erosions Small intestine: ulcers, erosions, protein loss, strictures Colon: non-specific colitis, exacerbation of ulcerative colitis and Crohn...
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Published in: | Postgraduate Medical Journal 2001-02, Vol.77 (904), p.82-88 |
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Main Author: | |
Format: | Article |
Language: | English |
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Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Areas of the gastrointestinal tract that may be damaged by NSAIDs Oesophagus: oesophagitis, ulceration, stricture Stomach: ulcers, erosions Duodenum: ulcers, erosions Small intestine: ulcers, erosions, protein loss, strictures Colon: non-specific colitis, exacerbation of ulcerative colitis and Crohn's disease A recent necropsy study of 713 patients has been reported, of whom 244 had NSAIDs prescribed during the six months before death and 464 had not; death in all patients was unrelated to NSAID use. COX-1 and COX-2 COX-1 Constitutively expressed in most tissues: stomach, duodenum, kidneys, platelets Key role in the production of prostaglandins which regulate physiological processes: gastrointestinal protection, blood flow, adaptation, cellular recovery, maintenance of good renal function, vascular homoeostasis important "housekeeping" role COX-2 Normally undetectable in most tissues Can be induced rapidly and in large quantities in the presence of inflammation and other pathological processes Most conventional NSAIDs are non-selective in their COX inhibition, exerting their anti-inflammatory effects through the inhibition of COX-2, but having adverse effects (such as gastrointestinal mucosal damage and nephrotoxicity) primarily due to inhibition of COX-1. |
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ISSN: | 0032-5473 1469-0756 |
DOI: | 10.1136/pmj.77.904.82 |