Antiepileptic drugs: combination therapy and interactions by Jerzy Majkowski,NetLibrary, Inc.

By Jerzy Majkowski,NetLibrary, Inc.

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2003), raises the possibility that certain AED interactions could be explained by competitive inhibition of these drug transporters. In such instances, polymorphisms could determine the degree to which such interactions occur. Pharmacodynamics There is, at present, scant human evidence that genotype contributes to AED responsiveness, despite considerable evidence that receptor and channel subtypes determine drug pharmacodynamics. Genes that determine the type of epilepsy can influence drug pharmacodynamics by two specific mechanisms.

The use of such markers for drug resistance could be useful for determining early referral for surgery, the spectrum of drug responsiveness or even the use of concomitant blockers of such transporters. , 2003), raises the possibility that certain AED interactions could be explained by competitive inhibition of these drug transporters. In such instances, polymorphisms could determine the degree to which such interactions occur. Pharmacodynamics There is, at present, scant human evidence that genotype contributes to AED responsiveness, despite considerable evidence that receptor and channel subtypes determine drug pharmacodynamics.

2 Problems with combination AED therapy Increased adverse effects Pharmacokinetic interactions New active metabolites Choice of combination Method of initiation/discontinuation Additive adverse effects Add-on trials for licensing of all the new AEDs have demonstrated a statistically significant improvement in the percentage of patients achieving a 50% or greater reduction in seizures compared to placebo. Although this seems to provide clear evidence of better control with use of combined agents, virtually all trials reveal more adverse effects in the arm with an add-on drug than in the placebo arm.

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