Abstract
Of 242 patients who were given antiepileptic drugs (AEDs), 40 exhibited a high level of serum γ-glutamyl transpeptidase (γ-GPT). The significance of the high level was examined. “Antipyrine test” was also performed on 9 healthy controls and 39 patients with AEDs administration, and the antipyrine half-life (APt1/2), a reliable index for hepatic microsomal enzyme activity (MEA), was calculated for each subiect.
A high level of serum γ-GTP occurred more frequently in phenytoin (PHT) administered group than in PHT non-administered group. Furthermore, the maximam level was significantly higher in the former than in the latter. In 17 out of the 40 cases, the serum γ-GTP level was decreased to a normal level without reducing AED doses or stopping the AED administration, or changing to different AEDs. On the other hand, in almost all cases with AED administration, APt1/2 was shortened (i. e., induction of the microsomal enzyme). Furthermore, there was no correlation between serum γ-GTP level and APt1/2 in the cases with AED administration, indicating that the serum γ-GTP level was not a proper index for MEA. It was also shown that phenobarbital, PHT and carbamazepine, each being used alone within the therapeutic dose, could cause almost the maximal degree of hepatic micresomal enzyme induction.
Thus it is suggested that the elevation of serum γ-GTP level due to AED does not necessarily indicate hepatocellular damages. If this is accepted, it follows that even if patients with AED administration have a high level of serum γ-GTP, it is not necessary to reduce the AED doses, or discontinue them, or change to different AEDs.
