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Endocrine and metabolic effects of antiepileptic drugs
Abstract
The antiepileptic drugs (AED) have been widely used for a great deal of people--in the treatment of epilepsy and other diseases--throughout the world. Continuous and prolonged use of AED may be associated with adverse effects in different systems, including a variety of endocrine and metabolic abnormalities. In this review, the relationship of AED with alterations in bone mineral metabolism, energy balance and body weight, gonadal function and thyroid metabolism was revised, as well as their clinical utility in the treatment of diabetic neuropathy.
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INTRODUCTION: New antiepileptic drugs are needed because many epileptic patients do not achieve complete control with current antiepileptic drugs. METHODS: We reviewed the historical origin of antiepileptic drugs, the different phases of the medical treatment related to monotherapy or polytheraphy, and the experimental models applied to develop new medications nowadays. RESULTS: Experimental models have been used for many years in order to detect some rational mechanisms of action. The results are interesting but limited. Some drugs fail the scrutiny and still they may be clinically effective. On the other hand, some drugs have good experimental profile but are extremely toxic in humans. CONCLUSION: Despite mild advance in the understanding of antiepileptic drug mechanism of action and experimental models of epilepsy, the development of antiepileptic drugs is mostly empirically oriented.
APPROXIMATELY 30 years ago, the association between use of anticonvulsant drugs (also called antiepileptic drugs) and the development of skeletal bone lesions was described.1 Accelerated catabolism of vitamin D was later demonstrated following phenobarbital treatment as a responsible mechanism for the low serum 25-hydroxyvitamin D concentrations in such patients.2 It is now recognized that reduced 25-hydroxyvitamin D levels may result from the up-regulation of the hepatic cytochrome P450 enzymes by anticonvulsant inducers, such as phenobarbital, phenytoin, and perhaps carbamazepine, or from the impairment of 25-hydroxylation of vitamin D.3
The potential of specific antiepileptic drugs (AEDs) to cause clinically significant changes in bodyweight is a key consideration in the management of epilepsy; changes in weight can pose health hazards, impair body image and self-esteem, and lead to noncompliance with therapy. This article reviews the data regarding the effects of conventional and newer AEDs on weight and discusses the clinical implications of these effects for the management of patients with epilepsy. The data demonstrate that AEDs can differ substantially in their effects on weight. Some, such as valproate and carbamazepine, increase weight; others, such as topiramate and felbamate, decrease it. Still others, such as lamotrigine, levetiracetam and phenytoin, are weight neutral.
Because most data regarding the effects of AEDs on weight are circumstantial, the incidence, magnitude and determinants of weight changes with AEDs remain poorly elucidated. Furthermore, little is known about the mechanisms of AED-induced changes in weight.
The importance of effects on weight in selecting an AED depends largely upon the individual patient’s needs and the risks and benefits of therapy for that patient. The most appropriate therapeutic choice is a weight-neutral medication unless circumstances dictate otherwise.