Lamotrigine is rapidly absorbed, reaching peak concentrations in 1 to 3 hours. It is well absorbed and has an oral bioavailability of 98%. The protein binding of lamotrigine is only 55%. It is metabolized by glucuronide conjugation and less than 1% is excreted renally.33-35

Effect of liver disease

One report describes the metabolism of lamotrigine in seven subjects with Gilbert’s syndrome, a benign deficiency in the enzyme bilirubin uridine diphosphate glucuronyl transferase. Although clearance was reduced and half-life was prolonged, these effects were considered clinically insignificant.36

Because lamotrigine is extensively metabolized, loss of hepatocyte function may decrease clearance. Phase I metabolism is generally affected more by loss of hepatocyte function than is phase II, however. Protein binding of lamotrigine would not be expected to be significantly altered by liver disease.

Effect of GI disease

The effect of GI disease on the pharmacokinetics of lamotrigine 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: 
Monday, March 1, 2004