Carbamazepine

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Reactions 930 - 30 Nov 2002 Carbamazepine Vanishing bile duct syndrome: case report A 26-year-old man developed reversible vanishing bile duct syndrome while receiving carbamazepine to control seizures. The man had been receiving carbamazepine 1200 mg/day for 2 years when an elevated γ-glutamyl transferase level of 348 UI/ml (normal 11–50) was first noted. Carbamazepine had been tapered and, 6 months later, completely discontinued; his seizures had been controlled with phenobarbital thereafter. His γ-glutamyl transferase level had continued to rise and, 11 months after the detection of liver dysfunction, a liver biopsy had revealed the absence of interlobular bile ducts in all 30 portal tracts represented in the sample. His γ-glutamyl transferase level remained elevated. 18 months after carbamazepine withdrawal, a second liver biopsy had revealed the presence of 8 interlobular bile ducts in the 14 portal tracts represented. The bile ducts showed epithelial regenerative activity and distortion as well as bile ductular proliferation. The man received ursodeoxycholic acid and, at last follow-up, was asymptomatic, but his γ-glutamyl transferase levels remained slightly elevated (129 UI/ml). Author comment: ‘Other causes of hepatic disease were ruled out, and investigation was performed to show that carbamazepine was involved in the findings.’ Ramos AMO, et al. Reversible vanishing bile duct syndrome induced by carbamazepine. European Journal of Gastroenterology and Hepatology 14: 1019-1022, Sep 2002 - Brazil 800920505 1 Reactions 30 Nov 2002 No. 930 0114-9954/10/0930-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved

Transcript of Carbamazepine

Page 1: Carbamazepine

Reactions 930 - 30 Nov 2002

Carbamazepine

Vanishing bile duct syndrome: case reportA 26-year-old man developed reversible vanishing bile duct

syndrome while receiving carbamazepine to control seizures.The man had been receiving carbamazepine 1200 mg/day

for 2 years when an elevated γ-glutamyl transferase level of348 UI/ml (normal 11–50) was first noted. Carbamazepine hadbeen tapered and, 6 months later, completely discontinued;his seizures had been controlled with phenobarbital thereafter.His γ-glutamyl transferase level had continued to rise and, 11months after the detection of liver dysfunction, a liver biopsyhad revealed the absence of interlobular bile ducts in all 30portal tracts represented in the sample. His γ-glutamyltransferase level remained elevated.

18 months after carbamazepine withdrawal, a second liverbiopsy had revealed the presence of 8 interlobular bile ducts inthe 14 portal tracts represented. The bile ducts showedepithelial regenerative activity and distortion as well as bileductular proliferation. The man received ursodeoxycholic acidand, at last follow-up, was asymptomatic, but his γ-glutamyltransferase levels remained slightly elevated (129 UI/ml).

Author comment: ‘Other causes of hepatic disease wereruled out, and investigation was performed to show thatcarbamazepine was involved in the findings.’Ramos AMO, et al. Reversible vanishing bile duct syndrome induced bycarbamazepine. European Journal of Gastroenterology and Hepatology 14:1019-1022, Sep 2002 - Brazil 800920505

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Reactions 30 Nov 2002 No. 9300114-9954/10/0930-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved