Abstract

Abstract

Antiepileptic drugs (AEDs) are routinely prescribed for the management of a variety of neurologic and psychiatric conditions, including epilepsy and epilepsy syndromes. Physiologic changes due to aging, pregnancy, nutritional status, drug interactions, and diseases (ie, those involving liver and kidney function) can affect pharmacokinetics of AEDs. This review discusses foundational pharmacokinetic characteristics of AEDs currently available in the United States, including clobazam but excluding the other benzodiazepines. Commonalities of pharmacokinetic properties of AEDs are discussed in detail. Important differences among AEDs and clinically relevant pharmacokinetic interactions in absorption, distribution, metabolism, and/or elimination associated with AEDs are highlighted. In general, newer AEDs have more predictable kinetics and lower risks for drug interactions. This is because many are minimally or not bound to serum proteins, are primarily renally cleared or metabolized by non–cytochrome P450 isoenzymes, and/or have lower potential to induce/inhibit various hepatic enzyme systems. A clear understanding of the pharmacokinetic properties of individual AEDs is essential in creating a safe and effective treatment plan for a patient.

Abstract

Abstract

The goal of pharmacogenetic research is to assist clinicians in predicting patient response to medications when genetic variations are identified. The pharmacogenetic variation of antiepileptic drug response and side effects has yielded findings that have been included in drug labeling and guidelines. The goal of this review is to provide a brief overview of the pharmacogenetic research on antiepileptic drugs. It will focus on findings that have been included in drug labeling, guidelines, and candidate pharmacogenetic variation. Overall, several genes have been included in guidelines by national and international organizations; however, much work is needed to implement and evaluate their use in clinical settings.

Abstract

Treatment of depression often requires long-term management with medication. Practitioners should be aware of potentially significant drug interactions with the use of antidepressants in order to effectively prevent or manage adverse events while optimizing patient response to treatment. Most antidepressants are metabolized by the liver, primarily via the CYP450 system. Pharmacokinetic profiles of the most recently approved antidepressants are reviewed in addition to evidence supporting potentially significant interactions. In addition, pharmacokinetic interactions between multiple antidepressants and other drug classes, including opiates, antineoplastics, antiepileptics, and antipsychotics, are discussed. This article provides recommendations for the monitoring and management of drug interactions. In addition, limitations of the evidence are reviewed.

Abstract

Abstract

The study of pharmacogenomics is rapidly growing, particularly in the field of mental health. Understanding pharmacogenomic principles can be a challenge for many clinicians. Most mental health genomic data concentrates on variability (response, side effects) with antidepressants and atypical antipsychotics. Current pharmacogenomic practice and research primarily focuses on two areas: pharmacodynamics and pharmacokinetics. Based on the current literature, genetic polymorphisms of pharmacodynamics and pharmacokinetics parameters likely influence medication efficacy, therefore affecting the therapeutic benefit. Additionally, certain pharmacodynamic and pharmacokinetic polymorphisms have been linked to an elevated risk of side effects and adverse events with these medications. In this review, specific pharmacodynamic and pharmacokinetic polymorphisms related to antidepressants and atypical antipsychotics will be discussed, as well as the potential clinical effect these genomic abnormalities have within psychiatric care.

Abstract