NSAIDs represent one of the most commonly used therapeutic drug groups worl
d wide. 1.5% of the world's population is estimated as taking NSAIDs. Howev
er, their use is not risk free and gastrointestinal (GI) lesions do appear,
which is indeed the main reason for their toxicity. Frequently (50%) NSAID
-induced Gi lesions are asymptomatic, and perforations or hemorrhages could
occur without any previous symptoms. 71% of GI perforations and 50% of upp
er gastric hemorrhages (UGH) are associated with taking NSAIDs.
How frequent GI lesions appear is directly related to whether the patient i
s in a risk group or not. Factors increasing the risk of GI lesions occurri
ng are the following: being older than 60, using corticoids or other NSAIDs
concomitantly, having a history of duodenal ulcer, alcohol consumption, sm
oking or taking oral anticoagulants. As the toxicity and how frequent the l
esions appear depend on which drug is used, there is a need for research in
to new drugs which are both clinically effective and safer to use.
GI toxicity of NSAIDs is mediated by two mechanisms, direct toxicity and pr
ostaglandin synthesis inhibition or sistemic mechanism. Due to the relative
ly recent discoveries concerning the physiopathology of inflammation and ga
stric 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, phosphodieste
rase inhibitors.