Diclofenac

Third line non-steroidal anti-inflammatory drug (NSAID)

Mechanism of action:  A phenylacetic 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, suppository, solution for injection, topical gel

Suggested dose:  50mg three times a day for adults over 50kg with normal hepatic and renal function

Co-prescribe proton pump inhibitor (PPI) cover.

Oral absorption: High bioavailability, peak plasma concentration at 1.5-2 hours

Protein binding: more than 99%

Metabolism:  Diclofenac is metabolized in the liver by cytochrome P450.

Elimination:  The metabolites of diclofenac and a small amount of unchanged drug are mainly excreted in the urine (70%), with around 30% excreted in bile

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
  • Methotrexate: toxic interaction between diclofenac and methotrexate

Further prescribing information (side effects, contraindications, interactions):

BNF-Diclofenac

References

Davies NM, Anderson KE. Clinical pharmacokinetics of diclofenac. Drug Disposition. 1997; 33(3):184-213.https://doi.org/10.2165/00003088-199733030-00003.pdf