Owing to the irreversible mode of action of the drug, the serum half-life bears practically no relationship to the duration of pharmacological effect, which will depend on resynthesis of new GABA transaminase.45 Hence, the antiepileptic effect of vigabatrin long outlasts its presence in serum.

The irreversible action of vigabatrin, and the following dissociation between serum concentration and clinical effects, complicates the interpretation of concentration-effect relationships and limits the potential value of monitoring vigabatrin. The fact that vigabatrin is a racemate and that only the s-enantiomer is active adds further to the complexity, in particular since the kinetics of the enantiomers differ. Consequently, Arteaga et al46 found no correlation between vigabatrin plasma levels and seizure control in a study of 16 children with refractory epilepsy treated with vigabatrin as add-on, and nor did platelet GABA transaminase inhibition correlate with effect.

It has been suggested that monitoring plasma GABA levels may be a better alternative. In a cross-sectional study, patients with complex partial seizures who responded to vigabatrin had significantly higher plasma GABA levels than non-responders.47 The results indicate that plasma GABA levels might reflect central nervous system GABA concentrations and could serve as an intermediate physiological marker of effect. However, according to a recent prospective study from the same group, plasma GABA does not seem to be a reliable marker of clinical response to viagatrin.48 Although responders showed a significant increase in plasma GABA concentrations, a similar increase was found also among a subgroup of non-respon-ders.

TDM of vigabatrin has been advocated for checking compliance.7

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