New classification of aspirin-like drugs

The discovery of two distinct isoforms of cyclooxygenase (COX) has promoted a better understanding of the anti-inflammatory and toxicity profiles of non-steroidal anti-inflammatory drugs (NSAIDs). Prostanoids that are derived from the COX-1 pathway regulate platelet aggregation via thromboxane A2 (TXA2), the function and integrity of the gut mucosa, and kidney function via prostaglandin E2 (PGE2) and prostacyclin. COX-2 is expressed in various cell types, including monocytes, fibroblasts and synovial cells, in response to inflammatory stimuli (e.g. cytokines and endotoxin). Consequently, COX-1 inhibition by NSAIDs is associated with gastrointestinal and renal toxicity, whereas, COX-2 inhibition limits the formation of pro-inflammatory and nociceptive prostanoids at the site of the inflammatory response.