Levetiracetam, Serum or Plasma

Levetiracetam (LTA), a piracetam analogue, is an antiepileptic drug (AED) structurally unrelated to other AEDs. The exact mechanism by which LTA acts has not been determined at this time; however, binding sites for the drug have been identified in synaptic plasma membranes of CNS neurons. Secondary alteration in GABA-related enzymes may result from binding to neurons in specific regions of the CNS.¹ While approximately one-fourth of LTA is converted by enzymatic hydrolysis to a carboxylic acid metabolite, the drug has no effect on UDP glucuronyltransferase, epoxide hydrolase, or enzymes in the CYP system,^1,2 resulting in minimal interactions with other AEDs in a polypharmacy regimen. LTA has minimal protein binding (<10%), an elimination half-life of six to eight hours in healthy adults, six hours in children, and 10-11 hours in the elderly. In healthy adults, approximately 95% of LTA and metabolites are excreted in the urine. Renal impairment can, therefore, decrease clearance from 35% to 60%.^3,4

A single 1000 mg dose or 1000 mg twice daily doses produced peak levels of 31 μg/mL and 43 μg/mL, respectively.³ Neuropsychiatric adverse events of aggression, anger, and irritability, as well as adverse reactions of leukopenia, neutropenia, pancytopenia, and thrombocytopenia have been reported.⁵