Carbamazepine
1
Reactions 1278 - 14 Nov 2009 S Carbamazepine Hyperammonaemia: case report A 26-year-old man, who had a history of hyperammonaemia during treatment with valproic acid and, later, carbamazepine, developed symptomatic hyperammonaemia while receiving carbamazepine for bipolar disorder. The man had a history of seizure disorder secondary to brain trauma, multiple sclerosis, unilateral blindness and mild mental retardation, and lived in a group home. He started receiving oral carbamazepine 200mg three times daily in addition to his existing regimen (topiramate, olanzapine, quetiapine, guanfacine and desmopressin), and developed worsening agitation 3 weeks later. One month after initiation of carbamazepine therapy, he was hospitalised after becoming physically aggressive and assaultive. On admission, he was agitated and fearful, exhibited labile affect, and was laughing inappropriately and yelling. He was only oriented to his name and staff members at his group home, and was incapable of participating in cognitive test; judgement and insight were impaired. Laboratory investigations were only notable for a serum ammonia level of 127 µg/dL; his carbamazepine concentration was within the therapeutic range. Carbamazepine was discontinued on admission, the man received lactulose, and his topiramate dosage was decreased on day 2. His serum ammonia level decreased to 56 µg/dL by day 4. Due to the possibility of a carnitine deficiency or urea cycle disorder, he also received levocarnitine for 3 days, and carnitine levels were normal on day 4. His hospital course was uneventful, and he was discharged after 4 days. At that time, fearfulness and aggression had resolved, but his judgement and insight remained impaired. Review of his history revealed that he had also developed hyperammonaemia with identical clinical symptoms while receiving carbamazepine 1 year earlier [details not stated]; additionally, he had developed encephalopathy due to hyperammonaemia while receiving valproic acid 3 years before the current presentation. Author comment: "In the case of our patient, the Naranjo et al. adverse-drug-reaction probability scale indicated a probable correlation between the patient’s hyperammonemia and carbamazepine therapy (score = 8). The fact that this patient had previously experienced hyperammonemia with carbamazepine corroborated the association." Adams EN, et al. Carbamazepine-induced hyperammonemia. American Journal of Health-System Pharmacy 66: 1468-1470, No. 16, 15 Aug 2009 - USA 801154526 1 Reactions 14 Nov 2009 No. 1278 0114-9954/10/1278-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
Transcript of Carbamazepine
Reactions 1278 - 14 Nov 2009
SCarbamazepine
Hyperammonaemia: case reportA 26-year-old man, who had a history of
hyperammonaemia during treatment with valproic acidand, later, carbamazepine, developed symptomatichyperammonaemia while receiving carbamazepine forbipolar disorder.
The man had a history of seizure disorder secondary tobrain trauma, multiple sclerosis, unilateral blindness andmild mental retardation, and lived in a group home. Hestarted receiving oral carbamazepine 200mg three timesdaily in addition to his existing regimen (topiramate,olanzapine, quetiapine, guanfacine and desmopressin), anddeveloped worsening agitation 3 weeks later. One monthafter initiation of carbamazepine therapy, he washospitalised after becoming physically aggressive andassaultive. On admission, he was agitated and fearful,exhibited labile affect, and was laughing inappropriatelyand yelling. He was only oriented to his name and staffmembers at his group home, and was incapable ofparticipating in cognitive test; judgement and insight wereimpaired. Laboratory investigations were only notable for aserum ammonia level of 127 µg/dL; his carbamazepineconcentration was within the therapeutic range.
Carbamazepine was discontinued on admission, theman received lactulose, and his topiramate dosage wasdecreased on day 2. His serum ammonia level decreased to56 µg/dL by day 4. Due to the possibility of a carnitinedeficiency or urea cycle disorder, he also receivedlevocarnitine for 3 days, and carnitine levels were normalon day 4. His hospital course was uneventful, and he wasdischarged after 4 days. At that time, fearfulness andaggression had resolved, but his judgement and insightremained impaired. Review of his history revealed that hehad also developed hyperammonaemia with identicalclinical symptoms while receiving carbamazepine 1 yearearlier [details not stated]; additionally, he had developedencephalopathy due to hyperammonaemia while receivingvalproic acid 3 years before the current presentation.
Author comment: "In the case of our patient, the Naranjoet al. adverse-drug-reaction probability scale indicated aprobable correlation between the patient’s hyperammonemiaand carbamazepine therapy (score = 8). The fact that thispatient had previously experienced hyperammonemia withcarbamazepine corroborated the association."Adams EN, et al. Carbamazepine-induced hyperammonemia. American Journal ofHealth-System Pharmacy 66: 1468-1470, No. 16, 15 Aug 2009 - USA 801154526
1
Reactions 14 Nov 2009 No. 12780114-9954/10/1278-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
