Hepatotoxicity naltrexone

At the doses used, there is blockage of the effects of as much as 25 mg of injected heroin. Toxicity in heroin addicts is low, but some reported subtle adverse effects of naltrexone such as decreased energy (Hollister et al. 1981). Nonaddicted obese subjects have been known to develop markedly elevated transaminase levels at doses of 300 mg/day (Mitchell et al. 1987). The inference has been drawn that high doses are potentially hepatotoxic (Pfohl et al. 1986), and the drug is contraindicated in liver failure or acute hepatitis. 

Naltrexone can theoretically increase the risk of hepatotoxicity if combined with disulfiram, although in practice this... 

Naltrexone is hepatotoxic and contraindicated in patients with hepatitis or liver failure. LFTs should be monitored monthly for the first 3 months, then every 3 months. Side effects include nausea, headache, dizziness, nervousness, insomnia, and somnolence. 

Hepatotoxicity Naltrexone has the capacity to cause hepatocellular injury when given in excessive doses. 

Naltrexone is contraindicated in acute hepatitis or liver failure. Carefully consider its use in patients with active liver disease in light of its hepatotoxic effects. 

Naltrexone can induce hepatotoxicity at doses only five times the therapeutic dose and should be used with care in patients with poor hepatic function or liver damage. Side effects of the use of naltrexone are more frequently observed than following naloxone administration. Such side effects include headache, difficulty sleeping, lethargy, increased blood pressure, nausea, sneezing, delayed ejaculation, blurred vision, and increased appetite. 

Naltrexone is generally taken once a day in an oral dose of 50 mg for treatment of alcoholism. An extended-release formulation administered as an IM injection once every 4 weeks is also effective. The drug can cause dose-dependent hepatotoxicity and should be used with caution in patients with evidence of mild abnormalities in serum aminotransferase activity. The combination of naltrexone plus disulfiram should be avoided, since both drugs are potential hepatotoxins. Administration of naltrexone to patients who are physically dependent on opioids precipitates an acute withdrawal syndrome, so patients must be opioid-free before initiating naltrexone therapy. Naltrexone also blocks the therapeutic effects of usual doses of opioids. 

Attention to nutritional needs is not totally protective against organ system damage that occurs with chronic abuse of alcohol. Females are more susceptible to alcohol hepatotoxicity than males. Respiratory depression is a symptom of ethanol overdose, not withdrawal. Naltrexone, an opioid receptor antagonist, may have value in some patients to decrease the intensity of craving. The answer is (C). 

Naltrexone in the management of alcohol dependence has been reviewed [210 ]. The most common adverse reaction was nausea. Hepatotoxicity was a concern with doses of naltrexone over 50 mg/day. 

The adverse reactions associated with the use of naltrexone in patients with alcohol dependence tend to be mild gastrointestinal reactions (nausea, vomiting, and abdominal pain or discomfort) and they occur early in treatment [204 ]. Hepatotoxicity has been reported with high doses (100-300 mg/ day) and especially in obese individuals. Naltrexone can also precipitate opioid withdrawal and may not be suitable for those requiring future opioids, such as those requiring surgery. 

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