A reduced daily maintenance dose of bupropion; naltrexone is recommended in patients with hepatic impairment. The pharmacokinetics of bupropion; naltrexone have not been evaluated in patients with hepatic disease. However, based on information available for the individual constituents, systemic exposure is significantly higher for bupropion and metabolites (2 to 3-fold), and naltrexone and its metabolites (up to 10-fold higher) in subjects with moderate-to-severe hepatic impairment. Cases of hepatotoxicity and clinically significant liver dysfunction were observed in association with naltrexone exposure during clinical trials and postmarketing reports for naltrexone. Transient, asymptomatic hepatic transaminase elevations were also observed. When patients presented with elevated transaminases, there were often other potential causative or contributory etiologies identified, including pre-existing alcoholic liver disease, hepatitis B and/or C infection, and concomitant usage of other potentially hepatotoxic drugs. Although clinically significant liver dysfunction is not typically recognized as a manifestation of opioid withdrawal, opioid withdrawal that is precipitated abruptly may lead to systemic sequelae, including acute liver injury. Warn patients of the risk of hepatic injury and advise them to seek medical attention if they experience symptoms of acute hepatitis. Discontinue treatment in the event of symptoms and/or signs of acute hepatitis. In bupropion; naltrexone clinical trials, there were no cases of elevated transaminases greater than 3 times the upper limit of normal (ULN) in conjunction with an increase in bilirubin greater than 2 times ULN.