More than 96% of an oral dose of oxcarbazepine is absorbed. Oxcarbazepine is rapidly converted to a monohydroxy derivative (MHD), the active component, by cytosol arylketone reductase. The MHD is further metabolized by glucuronide conjugation. There is no evidence of autoinduction, but the metabolism of oxcarbazepine to an inactive metabolite may be induced. About 60% of oxcarbazepine and 40% of MHD are bound to plasma proteins.42-43

Effect of liver disease

Oxcarbazepine is only about 60% protein-bound and is rapidly converted to its active metabolite MHD by non-liver enzymes. Therefore, it is unlikely that liver disease will alter the pharmacokinetics of the parent drug. MHD does undergo metabolism to an inactive metabolite by glucuronide conjugation. Phase II metabolism is less likely to be affected by liver disease than phase I pathways (e.g., CYP). Therefore, it is unlikely that liver disease will affect the pharmacokinetics of oxcarbazepine or its active metabolite MHD. Patients with liver impairment are unlikely to require dosage adjustments.

Effect of GI disease

The effect of GI disease on oxcarbazepine is unknown.

Adapted from: Garnett WR. Gastrointestinal and hepatic disease. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;63-74.
With permission from Elsevier ( 

Reviewed By: 
Steven C. Schachter, MD
Monday, March 1, 2004