A Case of Valproate Induced Hyperammonemic Encephalopathy

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: Tarafdar, Surjit, Slee, Mark, Ameer, Faisal, Doogue, Matt
Format: Online
Language:English
Published: Hindawi Publishing Corporation 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099231/
id pubmed-3099231
recordtype oai_dc
spelling pubmed-30992312011-05-31 A Case of Valproate Induced Hyperammonemic Encephalopathy Tarafdar, Surjit Slee, Mark Ameer, Faisal Doogue, Matt Case Report 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. Hindawi Publishing Corporation 2011 2011-05-04 /pmc/articles/PMC3099231/ /pubmed/21629819 http://dx.doi.org/10.1155/2011/969505 Text en Copyright © 2011 Surjit Tarafdar et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Tarafdar, Surjit
Slee, Mark
Ameer, Faisal
Doogue, Matt
spellingShingle Tarafdar, Surjit
Slee, Mark
Ameer, Faisal
Doogue, Matt
A Case of Valproate Induced Hyperammonemic Encephalopathy
author_facet Tarafdar, Surjit
Slee, Mark
Ameer, Faisal
Doogue, Matt
author_sort Tarafdar, Surjit
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
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.
publisher Hindawi Publishing Corporation
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099231/
_version_ 1611455030970286080

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