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Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unveiled by valproate
Valproic acid (VPA) is widely used as an anti-epileptic drug. The primary mechanism of VPA toxicity is interference with mitochondrial beta-oxidation, and it can exacerbate an underlying mitochondrial cytopathy. We report a case of Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2013
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3783723/ https://www.ncbi.nlm.nih.gov/pubmed/24082934 http://dx.doi.org/10.4103/1817-1745.117847 |
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author | Chaudhry, Neera Patidar, Yogesh Puri, Vinod |
author_facet | Chaudhry, Neera Patidar, Yogesh Puri, Vinod |
author_sort | Chaudhry, Neera |
collection | PubMed |
description | Valproic acid (VPA) is widely used as an anti-epileptic drug. The primary mechanism of VPA toxicity is interference with mitochondrial beta-oxidation, and it can exacerbate an underlying mitochondrial cytopathy. We report a case of Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unmasked by use of Sodium Valproate in a 12-year-old boy who presented with headache and seizures. There was precipitation of encephalopathy, myopathy, lactic acidosis, and hepatic damage within two days of valproate use, after withdrawing of which there was a remarkable clinical and biochemical recovery. |
format | Online Article Text |
id | pubmed-3783723 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-37837232013-09-30 Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unveiled by valproate Chaudhry, Neera Patidar, Yogesh Puri, Vinod J Pediatr Neurosci Case Report Valproic acid (VPA) is widely used as an anti-epileptic drug. The primary mechanism of VPA toxicity is interference with mitochondrial beta-oxidation, and it can exacerbate an underlying mitochondrial cytopathy. We report a case of Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unmasked by use of Sodium Valproate in a 12-year-old boy who presented with headache and seizures. There was precipitation of encephalopathy, myopathy, lactic acidosis, and hepatic damage within two days of valproate use, after withdrawing of which there was a remarkable clinical and biochemical recovery. Medknow Publications & Media Pvt Ltd 2013 /pmc/articles/PMC3783723/ /pubmed/24082934 http://dx.doi.org/10.4103/1817-1745.117847 Text en Copyright: © Journal of Pediatric Neurosciences http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Case Report Chaudhry, Neera Patidar, Yogesh Puri, Vinod Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unveiled by valproate |
title | Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unveiled by valproate |
title_full | Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unveiled by valproate |
title_fullStr | Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unveiled by valproate |
title_full_unstemmed | Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unveiled by valproate |
title_short | Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unveiled by valproate |
title_sort | mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes unveiled by valproate |
topic | Case Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3783723/ https://www.ncbi.nlm.nih.gov/pubmed/24082934 http://dx.doi.org/10.4103/1817-1745.117847 |
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