Changes in the concentration of serum alpha 1-acid glycoprotein in epileptic patients.

Factors leading to elevation of the serum level of alpha 1-acid glycoprotein (AAG), the principal binding protein of cationic drugs in the systemic circulation, were investigated in 142 epileptic patients receiving long-term therapy with carbamazepine (CBZ), phenytoin (DPH), phenobarbital (PB), or valproate (VPA). The mean serum activity of gamma-glutamyl transpeptidase (gamma-GTP), an indicator of enzyme induction, in the groups of patients receiving enzyme inducers such as CBZ, DPH, and/or PB was at least some 5-fold higher than in patients receiving VPA alone, which is well known to be a non-inducer. There was no significant difference in the mean serum level of AAG between the former and the latter groups, i.e. there was no correlation between AAG and gamma-GTP levels in serum, and it is unlikely that the enzyme inducing properties of CBZ, DPH and PB are associated with an increased level of AAG. The mean serum level of AAG in the patients with poorly controlled seizures was significantly higher than in those with well controlled seizures (0.81 vs. 0.56 milligram). The serum AAG level in individual patients changed in parallel with the frequency of seizures. The present results strongly suggest that elevation of serum AAG level in epileptic patients may not be associated with the enzyme-inducing activities of anticonvulsants, but with the epileptic seizures per se.