Detalhes bibliográficos
| Resumo: | Valproic acid (VPA; 2-n-propylpentanoic acid) is widely used as a major drug in the treatment of epilepsy and in the control of several types of seizures. Being a simple fatty acid, VPA is a substrate for the fatty acid P-oxidation (FAO) pathway, which takes place primarily in mitochondria. The toxicity of valproate has long been considered to be due primarily to its interference with mitochondrial P-oxidation. The metabolism of the drug, its effects on enzymes of FAO and their cofactors such as CoA and/or carnitine will be reviewed. The cumulative consequences of VPA therapy in inborn errors of metabolism (IEMs) and the importance of recognizing an underlying IEM in cases of VPA-induced steatosis and acute liver toxicity are two different concepts that will be emphasized. |
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| Autores principais: | Silva, M. F. B. |
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| Outros Autores: | Aires, C. C. P.; Luis, P. B. M.; Ruiter, J. P. N.; IJist, L.; Duran, M.; Wanders, R. J. A.; de Almeida, I. Tavares |
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| Assunto: | Endocrinology & Metabolism Genetics & Heredity |
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| Ano: | 2008 |
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| País: | Portugal |
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| Tipo de documento: | artigo |
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| Tipo de acesso: | acesso a metadados |
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| Instituição associada: | Universidade de Lisboa |
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| Idioma: | inglês |
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| Origem: | Repositório da Universidade de Lisboa |
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