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A Case of Valproate-Induced Hyperammonemic Encephalopathy

A 56-year-old Caucasian male with a history of seizure disorder on long-term prophylaxis with valproate presented with altered mental status, aggressive behavior, decreased oral intake, and frequent myoclonic jerking movements. Electrolyte and other basic metabolic lab testing, liver function testin...

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Detalles Bibliográficos
Autores principales: Zafar, Faraaz, Billadeau, Beau M, Ahmed, Ahsen U
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7417127/
https://www.ncbi.nlm.nih.gov/pubmed/32789057
http://dx.doi.org/10.7759/cureus.9114
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author Zafar, Faraaz
Billadeau, Beau M
Ahmed, Ahsen U
author_facet Zafar, Faraaz
Billadeau, Beau M
Ahmed, Ahsen U
author_sort Zafar, Faraaz
collection PubMed
description A 56-year-old Caucasian male with a history of seizure disorder on long-term prophylaxis with valproate presented with altered mental status, aggressive behavior, decreased oral intake, and frequent myoclonic jerking movements. Electrolyte and other basic metabolic lab testing, liver function testing, and imaging studies were negative for acute abnormalities or infection, though ammonia levels returned markedly elevated, and he also had a macrocytic anemia despite having normal folate and B12 levels. Following discussions with neurology, his valproate was felt to be the inducing factor for his hyperammonemic encephalopathy. After discontinuation of valproate and changing to a new anti-seizure medication, he soon returned to his neurologic baseline. This case report evaluates his presentation and current literature on hyperammonemic encephalopathy induced by valproate.
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spelling pubmed-74171272020-08-11 A Case of Valproate-Induced Hyperammonemic Encephalopathy Zafar, Faraaz Billadeau, Beau M Ahmed, Ahsen U Cureus Internal Medicine A 56-year-old Caucasian male with a history of seizure disorder on long-term prophylaxis with valproate presented with altered mental status, aggressive behavior, decreased oral intake, and frequent myoclonic jerking movements. Electrolyte and other basic metabolic lab testing, liver function testing, and imaging studies were negative for acute abnormalities or infection, though ammonia levels returned markedly elevated, and he also had a macrocytic anemia despite having normal folate and B12 levels. Following discussions with neurology, his valproate was felt to be the inducing factor for his hyperammonemic encephalopathy. After discontinuation of valproate and changing to a new anti-seizure medication, he soon returned to his neurologic baseline. This case report evaluates his presentation and current literature on hyperammonemic encephalopathy induced by valproate. Cureus 2020-07-10 /pmc/articles/PMC7417127/ /pubmed/32789057 http://dx.doi.org/10.7759/cureus.9114 Text en Copyright © 2020, Zafar et al. http://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Internal Medicine
Zafar, Faraaz
Billadeau, Beau M
Ahmed, Ahsen U
A Case of Valproate-Induced Hyperammonemic Encephalopathy
title 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_short A Case of Valproate-Induced Hyperammonemic Encephalopathy
title_sort case of valproate-induced hyperammonemic encephalopathy
topic Internal Medicine
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7417127/
https://www.ncbi.nlm.nih.gov/pubmed/32789057
http://dx.doi.org/10.7759/cureus.9114
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