imipramine

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Reactions 607 - 29 Jun 1996 S Imipramine Liver failure: case report Subfulminant liver failure occurred in a 48-year-old man following treatment with imipramine 25 mg/day for panic attacks. Approximately 4 months after the initiation of imipramine therapy, the man experienced nausea and fatigue, and jaundice was noted. Imipramine was stopped 2 weeks later; however, his condition deteriorated and he was hospitalised after a further week. His bilirubin, ALT and AST levels were 520 µmol/l (normal 17), 3998U (53) and 4340U (60), respectively. His γ-glutamyl transpeptidase and alkaline phophatase levels were 416U (normal 80) and 250U (130), respectively. The man’s condition deteriorated further with the appearance of grade I hepatic encephalopathy and he had elevated ammonia levels, fatigue, ascites and coagulopathy. A liver biopsy showed massive liver necrosis with hepatic architecture disturbances and portal areas that contained lymphocytes and a significant amount of eosinophyles. He was given supportive treatment and his condition improved gradually. Within 3 months there was no evidence of liver disease. Author comment: ‘The liver biopsy, the absence of any other etiological factor, and the complete recovery upon stopping the drug support the hypothesis that it was an imipramine-mediated liver condition.’ Ilan Y, et al. Hepatic failure associated with imipramine therapy. Pharmacopsychiatry 29: 79-80, Mar 1996 - Israel 800448889 1 Reactions 29 Jun 1996 No. 607 0114-9954/10/0607-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved

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Page 1: Imipramine

Reactions 607 - 29 Jun 1996

SImipramine

Liver failure: case reportSubfulminant liver failure occurred in a 48-year-old man

following treatment with imipramine 25 mg/day for panicattacks.

Approximately 4 months after the initiation of imipraminetherapy, the man experienced nausea and fatigue, andjaundice was noted. Imipramine was stopped 2 weeks later;however, his condition deteriorated and he was hospitalisedafter a further week. His bilirubin, ALT and AST levels were 520µmol/l (normal ≤ 17), 3998U (≤ 53) and 4340U (≤ 60),respectively. His γ-glutamyl transpeptidase and alkalinephophatase levels were 416U (normal ≤ 80) and 250U (≤ 130),respectively.

The man’s condition deteriorated further with theappearance of grade I hepatic encephalopathy and he hadelevated ammonia levels, fatigue, ascites and coagulopathy. Aliver biopsy showed massive liver necrosis with hepaticarchitecture disturbances and portal areas that containedlymphocytes and a significant amount of eosinophyles. He wasgiven supportive treatment and his condition improvedgradually. Within 3 months there was no evidence of liverdisease.

Author comment: ‘The liver biopsy, the absence of anyother etiological factor, and the complete recovery uponstopping the drug support the hypothesis that it was animipramine-mediated liver condition.’Ilan Y, et al. Hepatic failure associated with imipramine therapy.Pharmacopsychiatry 29: 79-80, Mar 1996 - Israel 800448889

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Reactions 29 Jun 1996 No. 6070114-9954/10/0607-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved