Carbamazepine
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Reactions 1174 - 20 Oct 2007 S Carbamazepine Liver injury in a patient with hepatitis B: case report A 16-year-old boy with chronic hepatitis B developed liver injury during treatment with carbamazepine for epilepsy. After receiving carbamazepine 400–600 mg/day for almost 3 years, the boy was hospitalised with a carbamazepine blood level of 19.96 mg/L, and was diagnosed with mild carbamazepine poisoning. Two months later he was referred to a toxicology ward because of jaundice and biochemical symptoms of acute liver injury; he had received treatment in another ward for the previous 5 days, where his bilirubin level had increased to 445 µmol/L. On admission to the toxicology ward, he reported fatigue, and was noted to have a yellowing of his skin and a rash on his chest and face. Laboratory examination showed a total bilirubin level of 355.5 µmol/L, an AST level of 648 U/L, an ALT level of 1497 U/L, a PA [not defined] of 312 U/L and a gamma-glutamyl transpeptidase level of 85 U/L. He was also noted to have an albumin level of 30 g/L, an INR of 1.59, a prothrombin time of 20.1 seconds, a prothrombin index of 62.8%, and a blood ammonia level of 60.9 µmol/L. Carbamazepine was discontinued. The boy was treated with ornithine aspartate, lactulose and neomycin, in addition to dietary and symptomatic therapy. Initially there was a slight rise in his hyperbilirubinaemia, before it decreased gradually to 152 µmol/L on discharge. Also by this time, his prothrombin index and prothrombin time had normalised, with less active transminases and obstructive enzymes. Only maintenance therapy was administered. After 2 weeks he was assessed as being in a good condition and discharged. Author comment: Taking into consideration the whole clinical picture and information gathered during consultation, it was established that the most probable cause of liver damage was long-term carbamazepine administration. In the case of this patient a chronic inflammation caused by viruses was a factor. The influence of this on the metabolism of carbamazepine or the formation of free radicals cannot be excluded. Gawlikowski T, et al. Carbamazepine hepatotoxicity - a case report. Przeglad Lekarski 64: 318-319, No. 4-5, 2007 [Translated from Polish] - Poland 801093380 1 Reactions 20 Oct 2007 No. 1174 0114-9954/10/1174-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
Transcript of Carbamazepine
Reactions 1174 - 20 Oct 2007
SCarbamazepine
Liver injury in a patient with hepatitis B: case reportA 16-year-old boy with chronic hepatitis B developed liver
injury during treatment with carbamazepine for epilepsy.After receiving carbamazepine 400–600 mg/day for almost
3 years, the boy was hospitalised with a carbamazepine bloodlevel of 19.96 mg/L, and was diagnosed with mildcarbamazepine poisoning. Two months later he was referredto a toxicology ward because of jaundice and biochemicalsymptoms of acute liver injury; he had received treatment inanother ward for the previous 5 days, where his bilirubin levelhad increased to 445 µmol/L. On admission to the toxicologyward, he reported fatigue, and was noted to have a yellowingof his skin and a rash on his chest and face. Laboratoryexamination showed a total bilirubin level of 355.5 µmol/L, anAST level of 648 U/L, an ALT level of 1497 U/L, a PA [notdefined] of 312 U/L and a gamma-glutamyl transpeptidaselevel of 85 U/L. He was also noted to have an albumin level of30 g/L, an INR of 1.59, a prothrombin time of 20.1 seconds, aprothrombin index of 62.8%, and a blood ammonia level of60.9 µmol/L.
Carbamazepine was discontinued. The boy was treated withornithine aspartate, lactulose and neomycin, in addition todietary and symptomatic therapy. Initially there was a slightrise in his hyperbilirubinaemia, before it decreased gradually to152 µmol/L on discharge. Also by this time, his prothrombinindex and prothrombin time had normalised, with less activetransminases and obstructive enzymes. Only maintenancetherapy was administered. After 2 weeks he was assessed asbeing in a good condition and discharged.
Author comment: Taking into consideration the wholeclinical picture and information gathered during consultation,it was established that the most probable cause of liverdamage was long-term carbamazepine administration. In thecase of this patient a chronic inflammation caused by viruseswas a factor. The influence of this on the metabolism ofcarbamazepine or the formation of free radicals cannot beexcluded.Gawlikowski T, et al. Carbamazepine hepatotoxicity - a case report. PrzegladLekarski 64: 318-319, No. 4-5, 2007 [Translated from Polish] -Poland 801093380
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Reactions 20 Oct 2007 No. 11740114-9954/10/1174-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
