NSAIDs inhibit cyclooxygenase and reduce prostaglandin synthesis. Corticosteroids inhibit phospholipase A2 production by boosting production of lipocortin, an inhibitor protein. Relatively new drugs, known as COX-2 selective inhibitors or coxibs, are used as specific inhibitors of COX-2. The development of these drugs allowed the circumvention of the negative gastrointestinal effects while effectively reducing inflammation.
Both NSAIDs and Coxibs can raise the risk of myocardial infarction, when taken on a chronic basis for at least 18 months. One emerging hypothesis that may explain the cardiovascular effects is that coxibs create an imbalance in circulating TxA2 (thromboxane) and PGI2 (prostacyclin) levels. An increased in the ratio of TxA2/PGI2 could lead to increased platelet aggregation and dysregulation of platelet homeostasis.
- Cheng Y et al., Role of prostacyclin in the cardiovascular response to thromboxane A2. “Science” 2002;296:539-51. PMID 11964481.
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