Codeine
First line weak opioid
Mechanism of action: mu-opioid agonist. The analgesic properties of codeine are predominantly a result of its conversion to morphine.
Presentation: tablet, oral solution. Also present in some over-the-counter combination analgesics with paracetamol
Suggested dose: 30-60mg orally four times a day for adults over 50kg with normal hepatic and renal function, reduce in frailty
Co-prescribe prn Naloxone
Oral absorption: Approx. 60%, peak plasma levels reached at 45-60 mins
Protein binding: approx. 25%
Metabolism: principally liver, although some metabolism occurs in the intestine and brain.
Approximately 50-70% of codeine is converted by UGT2B7 to codeine-6-glucuronide, which has a similar affinity to codeine for the mu opioid receptor.
Approximately 10-15% of codeine is N-demethylated by CYP3A4 to norcodeine which also has a similar affinity to codeine for the mu opioid receptor.
Between 0-15% of codeine is O-demethylated by CYP2D6 to Morphine , the most active metabolite, which has 200 fold greater affinity for the mu opioid receptor compared to codeine. As it is this conversion to morphine that provides the main analgesic activity of codeine, the genetic polymorphism of CYP2D6 has a large impact on the effectiveness of codeine as an analgesic.
Four phenotypes of CYP2D6 have been identified: ultra-rapid, extensive, intermediate and poor metabolizers. The result of this CYP2D6 polymorphism is an inter-individual altered analgesic response to codeine, with ultra-rapid metabolizers developing concentrations of codeine metabolites 45 times higher than poor metabolizers [Kirchheiner].
Elimination: excreted by the kidneys
Half-life: approx. 3 hours
Further prescribing information (side effects, contraindications, interactions):