A Case of Valproate Induced Hyperammonemic Encephalopathy

A 36-years-old man on phenytoin, levetiracetam, and sodium valproate presented with acute confusion. Routine investigations including serum valproate and phenytoin concentration were normal. His serum ammonia concentration was raised. His valproate was held and 2 days later he recovered with concord...

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Main Authors: Surjit Tarafdar, Mark Slee, Faisal Ameer, Matt Doogue
Format: Article
Language:English
Published: Hindawi Limited 2011-01-01
Series:Case Reports in Medicine
Online Access:http://dx.doi.org/10.1155/2011/969505
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spelling doaj-5c7d00bc867f4f9390f86d1b3db8c5ca2020-11-24T21:46:35ZengHindawi LimitedCase Reports in Medicine1687-96271687-96352011-01-01201110.1155/2011/969505969505A Case of Valproate Induced Hyperammonemic EncephalopathySurjit Tarafdar0Mark Slee1Faisal Ameer2Matt Doogue3Nephrology, Flinders Medical Centre, Bedford Park, SA 5042, AustraliaNeurology, Flinders Medical Centre, Bedford Park, SA 5042, AustraliaGeneral Medicine, John Hunter Hospital, Newcastle, NSW 2305, AustraliaEndocrinology/Clinical Pharmacology, Flinders Medical Centre, Bedford Park, SA 5042, AustraliaA 36-years-old man on phenytoin, levetiracetam, and sodium valproate presented with acute confusion. Routine investigations including serum valproate and phenytoin concentration were normal. His serum ammonia concentration was raised. His valproate was held and 2 days later he recovered with concordant normalisation of serum ammonia concentration. Urea acid cycle disorder was ruled out, and a diagnosis of valproate induced hyperammonemic encephalopathy (VHE) was made. Asymptomatic hyperammonemia occurs in 15–50% of valproate-treated patients, and while the true incidence of VHE is not known, it is a recognized complication of sodium valproate treatment. VHE typically presents acutely with impaired consciousness, lethargy, and vomiting. Valproate concentrations may be in the therapeutic range, and liver function tests are typically “normal.” Treatment for VHE consists of ceasing valproate and providing supportive care. Some have advocated carnitine replacement.http://dx.doi.org/10.1155/2011/969505
collection DOAJ
language English
format Article
sources DOAJ
author Surjit Tarafdar
Mark Slee
Faisal Ameer
Matt Doogue
spellingShingle Surjit Tarafdar
Mark Slee
Faisal Ameer
Matt Doogue
A Case of Valproate Induced Hyperammonemic Encephalopathy
Case Reports in Medicine
author_facet Surjit Tarafdar
Mark Slee
Faisal Ameer
Matt Doogue
author_sort Surjit Tarafdar
title A Case of Valproate Induced Hyperammonemic Encephalopathy
title_short A Case of Valproate Induced Hyperammonemic Encephalopathy
title_full A Case of Valproate Induced Hyperammonemic Encephalopathy
title_fullStr A Case of Valproate Induced Hyperammonemic Encephalopathy
title_full_unstemmed A Case of Valproate Induced Hyperammonemic Encephalopathy
title_sort case of valproate induced hyperammonemic encephalopathy
publisher Hindawi Limited
series Case Reports in Medicine
issn 1687-9627
1687-9635
publishDate 2011-01-01
description A 36-years-old man on phenytoin, levetiracetam, and sodium valproate presented with acute confusion. Routine investigations including serum valproate and phenytoin concentration were normal. His serum ammonia concentration was raised. His valproate was held and 2 days later he recovered with concordant normalisation of serum ammonia concentration. Urea acid cycle disorder was ruled out, and a diagnosis of valproate induced hyperammonemic encephalopathy (VHE) was made. Asymptomatic hyperammonemia occurs in 15–50% of valproate-treated patients, and while the true incidence of VHE is not known, it is a recognized complication of sodium valproate treatment. VHE typically presents acutely with impaired consciousness, lethargy, and vomiting. Valproate concentrations may be in the therapeutic range, and liver function tests are typically “normal.” Treatment for VHE consists of ceasing valproate and providing supportive care. Some have advocated carnitine replacement.
url http://dx.doi.org/10.1155/2011/969505
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