Antiepileptic Drugs Interaction

Population-based studies of drug utilization demonstrate that 19-24 % of patients with epilepsy use polytherapy with AEDs. In recent studies of children and adults with refractory epilepsy, 64 % used polytherapy with two or more AEDs, and 35 % of the adults suffered from CNS-related co morbid conditions, resulting in a considerable risk of interactions. Most drug interactions in the past were discovered due to unexpected change in the clinical status of a patient after addition or withdrawal of a drug from existing medication. Interactions between antiepileptic drugs, or between antiepileptic drugs and other drugs, can be pharmacokinetic or pharmacodynamic in nature. Pharmacokinetic interactions involve changes in absorption, distribution or elimination, whereas pharmacodynamic interactions involve synergism and antagonism at the site of action. Most clinically important interactions of antiepileptic drugs result from induction or inhibition of drug metabolism. By far the most important pharmacokinetic interactions are those involving cytochrome P450 isoenzymes and glucuronyl transferase (GT) enzymes in hepatic metabolism. Among old generation AEDs, carbamazepine, phenytoin, phenobarbital, and primidone induce the activity of several enzymes involved in drug metabolism, leading to decreased plasma concentration and reduced pharmacological effect of drugs, which are substrates of the same enzymes (lamotrigine, and topiramate). Practically for preventing antiepetic drugs interaction it is prefer prescribe drugs with different mechanism and their metabolite sites, like the new AEDs such as gabapentin, levetiracetam, tiagabine and vigabatrin do not induce the metabolism of other AEDs.

Keywords:

Antiepileptic drugs , interactions