[Cardiovascular events: a class effect by COX-2 inhibitors].

Non-steroidal anti-inflamatories (NSAIDs) are widely used in the treatment of post-surgery pain1, osteoarthritis2, rheumatoid arthritis3 and muscle-skeletal pain4,5, in different conditions. Major effects are: anti-inflammatory, analgesic, and antipyretic6. Generally speaking, such effects are associated to the inhibition of the enzyme cyclooxygenase (COX). COX catalyzes the transformation of arachidonic acid into different lipid mediators called prostaglandins and thromboxanes2. Those substances play a relevant hemostatic role in protecting gastric mucosa, renal physiology, and platelet aggregation, in addition to having their production induced under conditions such as inflammation and cancer7. Two isozymes – or forms of the COX enzyme – have been characterized: cyclooxygenase-1 (COX-1) and cycloxygenase-2(COX-2)2. COX-1 has shown to be constitutive in all body tissues8. It is the only isozyme found in platelets, leading to the formation of TXA2. It is found in gastric mucosa, among other tissues, where it catalyzes the biosynthesis of cytoprotective prostaglandins in vascular endotelium and in renal tissue. Finally, it is believed that COX-1 also plays a role in pathologic conditions such as inflammation7. On the other hand, COX-2 is shown to be increased in inflammatory and cell transformation processes particularly9-12, although its constitutive expression has been demonstrated in some CNS and kidney tissues7.