Mechanism of action

All NSAIDs exert their clinical effects by inhibiting prostaglandin synthesis. Prostaglandins modulate components of the immune system and are involved in the control of body temperature, pain transmission, platelet aggregation and gastric protection. The primary site of action is the inhibition of the cyclooxygenase (COX) enzyme, which exists in two isoforms (Cox-1 and Cox-2). Selective inhibition of Cox-2 is associated with less gastrointestinal (GI) intolerance. It has also been hypothesised that COX-2 plays a role in the inflammation process, hence drugs that selectively inhibit COX-2 enzymes should have the beneficial anti-inflammatory activity of traditional NSAIDS without the toxicity. Experience with COX-2 inhibitors in paediatric patients is limited. COX-2 inhibitors are more expensive, and the debate over their safety and efficacy compared with traditional NSAIDs is not yet concluded. Meloxicam and celecoxib have proven to be effective and safe in children with musculoskeletal disorders in a controlled trial2

Pharmacology

After oral administration, the absorption of NSAIDs is generally rapid and complete with most occurring in the stomach and upper small intestine. NSAIDs are highly bound to plasma proteins, specifically to albumin (>90%). All NSAIDs can be found in synovial fluid after repeated dosing, and ibuprofen also has the ability to penetrate the CNS.3

Members of the class (with formulations) are listed in table 1.

Indications