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SSRIs and codeine – a poorly understood drug interaction
Codeine is a widely prescribed opioid agent most commonly used for the management of moderate to severe pain. Codeine is often prescribed in compound products such as those which contain a combination of paracetamol with codeine. Codeine is in fact relatively in active as an analgesic and largely relies upon metabolic conversion of codeine to small amounts of morphine for its clinical pain-relieving properties. This conversion is facilitated through metabolism of codeine via the cytochrome P450 2D6 isoenzyme. There is a degree of variability in the activity of the 2D6 enzyme, which may account for the variability in clinical response to codeine. From a pharmacodynamic viewpoint if an individual has a low activity of CYP 2D6 then the metabolic conversion of codeine to morphine will be less efficient and therefore the analgesic effects will be diminished.
It is not widely appreciated that several of the SSRI antidepressants are potent inhibitors of the 2D6 isoenzyme, whilst exert a milder inhibition of this activity. Paroxetine, fluoxetine and to a lesser extent sertraline are the SSRIs which inhibit the isoenzyme most significantly. The coadministration of these drugs with codeine will be likely to reduce or eliminate the analgesic effect of the opioid. As a clinical marker, the presence of constipation as an adverse effect associated with codeine tends to suggest that metabolic activation to morphine is taking place efficiently. In the absence of constipation it may be that the therapeutic benefit of codeine is being blocked by the co-administration of the SSRI. Pharmacogenomic analysis is simple and easy to arrange and can be undertaken using non-invasive means (buccal swab) that can be quickly completed in the pharmacy. For more information contact the pharmacy to arrange a detailed discussion.
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