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Antiepileptic drugs and bone metabolism

Anti-epileptic medications encompass a wide range of drugs including anticonvulsants, benzodiazepines, enzyme inducers or inhibitors, with a variety effects, including induction of cytochrome P450 and other enzyme, which may lead to catabolism of vitamin D and hypocalcemia and other effects that may...

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Detalles Bibliográficos
Autores principales: Valsamis, Helen A, Arora, Surender K, Labban, Barbara, McFarlane, Samy I
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1586194/
https://www.ncbi.nlm.nih.gov/pubmed/16956398
http://dx.doi.org/10.1186/1743-7075-3-36
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author Valsamis, Helen A
Arora, Surender K
Labban, Barbara
McFarlane, Samy I
author_facet Valsamis, Helen A
Arora, Surender K
Labban, Barbara
McFarlane, Samy I
author_sort Valsamis, Helen A
collection PubMed
description Anti-epileptic medications encompass a wide range of drugs including anticonvulsants, benzodiazepines, enzyme inducers or inhibitors, with a variety effects, including induction of cytochrome P450 and other enzyme, which may lead to catabolism of vitamin D and hypocalcemia and other effects that may significantly effect the risk for low bone mass and fractures. With the current estimates of 50 million people worldwide with epilepsy together with the rapid increase in utilization of these medications for other indications, bone disease associated with the use of anti-epileptic medications is emerging as a serious health threat for millions of people. Nevertheless, it usually goes unrecognized and untreated. In this review we discuss the pathophysiologic mechanisms of bone disease associated with anti-epileptic use, including effect of anti-epileptic agents on bone turnover and fracture risk, highlighting various strategies for prevention of bone loss and associated fractures a rapidly increasing vulnerable population.
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spelling pubmed-15861942006-10-03 Antiepileptic drugs and bone metabolism Valsamis, Helen A Arora, Surender K Labban, Barbara McFarlane, Samy I Nutr Metab (Lond) Review Anti-epileptic medications encompass a wide range of drugs including anticonvulsants, benzodiazepines, enzyme inducers or inhibitors, with a variety effects, including induction of cytochrome P450 and other enzyme, which may lead to catabolism of vitamin D and hypocalcemia and other effects that may significantly effect the risk for low bone mass and fractures. With the current estimates of 50 million people worldwide with epilepsy together with the rapid increase in utilization of these medications for other indications, bone disease associated with the use of anti-epileptic medications is emerging as a serious health threat for millions of people. Nevertheless, it usually goes unrecognized and untreated. In this review we discuss the pathophysiologic mechanisms of bone disease associated with anti-epileptic use, including effect of anti-epileptic agents on bone turnover and fracture risk, highlighting various strategies for prevention of bone loss and associated fractures a rapidly increasing vulnerable population. BioMed Central 2006-09-06 /pmc/articles/PMC1586194/ /pubmed/16956398 http://dx.doi.org/10.1186/1743-7075-3-36 Text en Copyright © 2006 Valsamis et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Valsamis, Helen A
Arora, Surender K
Labban, Barbara
McFarlane, Samy I
Antiepileptic drugs and bone metabolism
title Antiepileptic drugs and bone metabolism
title_full Antiepileptic drugs and bone metabolism
title_fullStr Antiepileptic drugs and bone metabolism
title_full_unstemmed Antiepileptic drugs and bone metabolism
title_short Antiepileptic drugs and bone metabolism
title_sort antiepileptic drugs and bone metabolism
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1586194/
https://www.ncbi.nlm.nih.gov/pubmed/16956398
http://dx.doi.org/10.1186/1743-7075-3-36
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