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This book reviews the use of antiepileptic drugs focusing on the interactions between these drugs and between antiepileptics and other drugs. These interactions can be beneficial or can cause harm. The aim of this book is to increase awareness of the possible impact of combination pharmacotherapies. Pharmacokinetic and pharmacodynamic interactions are discussed supported by clinical and experimental data. The book consists of five sections covering the general concepts and advantages of combination therapies, the principles of drug interactions, the mechanisms of interactions, drug interactions in specific populations or in patients with co-morbid health conditions, and concludes with a look at the future directions for this field of research. The book will be of interest to all who prescribe antiepileptics to epileptic and non-epileptic patients, including epileptologists, neurologists, neuro-pediatricians, psychiatrists and general practitioners.
Jerzy Majkowski, Center for Epilepsy Diagnosis and Treatment Foundation of Epileptology, Warsaw, Poland,
Philip N. Patsalos, Pharmocology and Therapeutics Unit, Department of Clinical and Experimental Epilepsy, Institute of Neurology, London; The National Society for Epilepsy, Chalfont St Peter, UK
Clinically important drug interactions occur essentially at two levels, at the pharmacokinetic level and at the pharmacodynamic level. This chapter describes the clinically significant interactions between antiepileptic drugs (AEDs) and non-AEDs. The interactions can be classified into three groups according to their risk of interaction with AEDs. Carbamazepine is a potent hepatic enzyme inducer and, as well as inducing its own metabolism via an action on CYP3A4, it also induces the metabolism of many other drugs that are CYP3A4 substrates. There are no clinical data to suggest ethosuximide induces or inhibits the metabolism of other non-AEDs. As a new AED, knowledge of the interaction profile of felbamate with non-AEDs is limited. Zonisamide undergoes extensive metabolism, via CYP3A4, and approximately 30% of zonisamide is excreted in urine as unchanged zonisamide. To date, there are no reports of zonisamide affecting the pharmacokinetics of non-AEDs.
This chapter emphasizes the spectrum and scale of antiepileptic drugs (AED) usage in medical disciplines other than epilepsy, and to increase awareness of unpredicted drug interactions when combination therapy with two/three drugs is used. There are many pharmacological reasons why AEDs have therapeutic effects in non-epileptic neurological and psychiatric conditions. The fact that over-the-counter drugs and nutritional supplements are increasingly being self-administered by patients creates the risk of drug interactions. In many countries folk medicine is frequently used for various reasons. Carbamazepine (CBZ) is one of the most commonly used AEDs in epilepsy and other neurological and psychiatric disorders. Many drug interactions can be demonstrated but only a few of them are so clinically significant that they require adjustment of drug dosages. Case reports of toxic effects due to drug interactions are presented in the chapter as a warning signal calling for attention when polytherapy has to be used.
This chapter discusses polytherapy with old and new antiepileptic drugs (AEDs), current clinical experience with drug combinations and future treatment strategies in pharmacoresistant epilepsies. The majority of patients with newly diagnosed epilepsy can apparently be controlled with a single AED. At present, selection of AED combinations is mainly based on personal experience and on a few clinically documented studies. The aim of rational polytherapy is to improve the effectiveness to toxicity ratio: effectiveness should be supra-additive or at least additive and toxicity should be lower than additive. Everyday clinical practice suggests that in some pharmacotherapy-resistant patients, combination of three AEDs has a better effect than two drugs. Drug interactions may produce increases in desired metabolites or decreases in the formation of undesired metabolites. Resistance to pharmacotherapy occurs in a significant number of patients with chronic epilepsy; its pathogenesis and mechanism(s) of development are not fully understood.