| Naltrexone |
Naltrexone is an opioid antagonist used in the prevention of relapse in alcohol and opioid dependence. It is thought that alcohol ingestion causes the release of endogenous opioids, reinforcing the drinking behaviour. By blocking central opioid receptors, naltrexone prevents the reinforcing effects of alcohol and continued use inhibits the craving for alcohol. In opioid dependence, blockade of opioid receptors markedly weakens or completely blocks the euphoria and other effects of opioids. It is important that naltrexone is only used as an adjunct to psychological and social treatments.
Naltrexone is almost completely absorbed after oral administration, and reaches peak plasma concentrations within 1 hour. Bioavailability ranges from 5% to 40% because of extensive first-pass hepatic metabolism. The major active metabolite, 6-beta-naltrexol, reaches peak plasma concentrations 2 to 10 times higher than naltrexone, which probably contributes to the long duration of action. Naltrexone should not be used in patients with hepatitis or liver failure.
Patients should be warned that naltrexone can accelerate the loss of tolerance that occurs with abstinence from opioids. As a result, use of opioid agonists after cessation of naltrexone administration can place the person at high risk of fatal overdose.
Administration of naltrexone to an opioid-dependent person precipitates withdrawal within minutes. This persists for up to 48 hours, and is difficult to reverse. Nausea, vomiting, severe diarrhoea, confusion, irritability and hallucinations may occur. Therefore, naltrexone should not be administered until the withdrawal process is complete and the person has remained opioid-free for 7 to 10 days, or longer if a longer-acting opioid such as methadone has been used.
The most commonly reported adverse effects are nausea and headache.
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