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Antiepileptic drugs and bone metabolism

Helen A Valsamis1 email, Surender K Arora2 email, Barbara Labban3 email and Samy I McFarlane2 email

Department of Neurology, SUNY Downstate Medical Center, and Kings County Hospital Center, Brooklyn, NY 11203, USA

Division of Endocrinology, Diabetes and Hypertension, SUNY Downstate Medical Center, and Kings County Hospital Center, Brooklyn, NY 11203, USA

Department of Medicine, Staten Island University Hospital, NY 10305, USA

author email corresponding author email

Nutrition & Metabolism 2006, 3:36doi:10.1186/1743-7075-3-36

Published: 6 September 2006

Abstract

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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