NSAIDs represent one of the most commonly used therapeutic drug groups worldwide. 1.5percent of the world population is estimated as taking NSAIDs. However, their use is not risk free and gastrointestinal (GI) lesions do appear, which is indeed the main reason for their toxicity. Frequently (50percent) NSAID-induced GI-Lesions are asymptomatic, 71percent of GI perforations and 50percent of upper gastric hemorrhages (UGH) are associated with taking NSAIDs How frequent GI lesions appear is directly related to whether the patient is in a risk group or not. Factors increasing the risk of GI lesions occurring are the following: being older than 60, using corticoids or other NSAIDs concomitantly, having a history of duodenal ulcer, alcohol consumption, smoking or taking oral anticoagulants. As the toxicity and how frequent the lesions appear depend on which drug is used, there is a need for research into new drugs which are both clinically effective and safer to use. GI toxicity of NSAIDs is mediated by two mechanisms, direct toxicity and prostaglandin synthesis inhibition or sistemic mechanism. Due to the relatively recent discoveries concerning the physiopathology of inflammation and gastric physiology, research into new NSAID derivatives is taking place. Such derivatives are prodrugs, galenic buffer forms, selective COX-2 inhibitors, isomeric compounds, NO-donors, and as a future possibility, phosphodiesterase inhibitors.
Keywords: Antiinflamatory Agents Less, Gastrointestinal Tract, COX-2 inhibitors, cyclooxygenase-2 COX-2, Polymorphouuclear leukocyte, PMN-endothelial cell, Intercellular adhesion molecular 1 ICAM, Water immersion restraint WIR, Oxidative Metabolism
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