Ibuprofen
First line non-steroidal anti-inflammatory drug (NSAID)
Mechanism of action: A propionic acid derivative non-steroidal anti-inflammatory drug (NSAID). It is a non-selective inhibitor of cyclooxygenases COX-1 and COX-2, thus results in a decrease in the synthesis of prostaglandins which are involved in pain and inflammatory processes.
Presentation: tablet, oral suspension, topical gel 5%. Capsule & cream not available in OUH.
Suggested dose: 400mg three times a day for adults over 50kg with normal hepatic and renal function. 400mg four times a day is acceptable for short durations (e.g., 3 days)
Co-prescribe proton pump inhibitor (PPI) cover.
Oral absorption: Very high bioavailability. Peak serum concentrations attained in 1-2 hours after oral administration.
Protein binding: 99%
Metabolism: Ibuprofen is administered as a racemic mixture of R and S enantiomers, with S-ibuprofen primarily responsible for its pharmacological activity. Around 50-65% of R-ibuprofen undergoes conversion in the liver to theS enantiomer. Ibuprofen is almost completely metabolized in the liver to inactive metabolites by cytochrome P450 enzymes.
Elimination: 90% excreted in urine as metabolites or their conjugates.
Half-life: approx. 2 hours
Significant interactions (see the BNF for more interactions):
- Aspirin: NSAIDs competitively inhibit aspirin binding to platelets so antagonise the cardioprotective effect of low-dose aspirin
- Lithium: NSAIDs increase the serum lithium level and reduce lithium clearance, risking acute lithium intoxication
- Anti-hypertensives: NSAIDs compromise the efficacy of anti-hypertensive drugs such as ß-adrenergic blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and diuretics.
Further prescribing information (side effects, contraindications, interactions):