Buprenorphine is a partial agonist at mu opioid receptors and an antagonist at delta and kappa receptors. It is typically used for analgesia (in low-dose patch formulation) and in ORT, where oral and sublingual formulations are usually used.
There is limited evidence regarding buprenorphine for CNCP due to a lack of high-quality randomised controlled trials (RCTs).101
However, transdermal buprenorphine for osteoarthritis has been shown to be effective and well tolerated, with analgesic effects similar to tramadol.102
Case reports suggest that buprenorphine is effective in peripheral103,104
and central neuropathic pain in the clinical setting.105
However, large trials are lacking and currently there is not enough evidence to support or dispute efficacy of buprenorphine in any neuropathic pain condition.106
Buprenorphine is listed for use in ORT (as Section100 [S100]).
Buprenorphine is PBS listed for chronic severe pain and ORT.
Transdermal patches (used for pain, not ORT) generally provide a week of analgesia. Occasionally, patients complain that there is release of the drug from the transdermal patch for only six, or rarely five, days. In these instances, the patches may need to be changed more frequently than weekly.
Buprenorphine can be safely used in patients with renal impairment and has less immunosuppressive effect than pure mu opioid agonists.107
As long as sedative medication is not given concurrently, the risk of respiratory depression with buprenorphine is low compared to morphine, methadone, hydromorphone and fentanyl.108 There is a ceiling effect for respiratory depression but not for analgesia.109 If buprenorphine-induced respiratory depression occurs it may be completely reversed with naloxone,107 although higher than usual doses and a longer duration infusion of naloxone are required.110
Withdrawal symptoms may occur if buprenorphine is ceased after long-term treatment; however, these symptoms are milder and more delayed in onset (≥72 hours) compared with other opioids.108
Buprenorphine binds strongly to the mu receptor site, but does not fully activate it.111 Therefore, if buprenorphine is combined with pure mu agonists (eg morphine, fentanyl), interactions may occur. For example, if a pure mu agonist is given to a person on maintenance buprenorphine it may be less effective. Conversely, buprenorphine could theoretically cause a withdrawal reaction if given to a patient taking longer-term opioid (mu) therapy.111
Antagonism of response to pure mu agonists (precipitated withdrawal) can occur with buprenorphine but it has only been demonstrated at buprenorphine doses exceeding the ranges used for analgesia (eg at dosages for ORT). In practice, these drug interactions are unlikely.