|Values are valid only on day of printing.|
Gabapentin is an antiepileptic drug that is effective in treating seizures, neuropathies, and a variety of neurological and psychological maladies. Although designed as a gamma amino butyric acid (GABA) analogue, gabapentin does not bind to GABA receptors, nor does it affect the neuronal uptake or degradation of GABA. In fact, the precise mechanism by which it exerts its analgesic and anticonvulsant effects is unknown.
After oral administration and absorption, gabapentin circulates essentially unbound to serum proteins. In addition, gabapentin does not undergo hepatic metabolism unlike most other antiepileptic drugs and is eliminated almost entirely by renal excretion with a clearance that approximates the glomerular filtration rate. The elimination half-life is 5 to 7 hours in patients with normal renal function.
Since gabapentin does not bind to serum proteins, it does not exhibit pharmacokinetic variability and interactions with other highly protein-bound medications (ie, phenytoin). In addition, the lack of hepatic metabolism eliminates the interactions with other hepatically cleared medications which can induce/inhibit hepatic drug metabolizing enzyme systems (cytochrome P450s). Therefore, gabapentin serum concentrations are not changed following the addition or discontinuation of other common anticonvulsants (ie, phenobarbital, phenytoin, carbamazepine, or valproic acid), nor are their serum concentration altered upon the addition or discontinuation of gabapentin.
In general, adverse effects with gabapentin are infrequent and usually resolve with continued treatment. The most common side effects include somnolence, dizziness, ataxia, and fatigue. Experience to date indicated that gabapentin is safe and relatively nontoxic.
Toxic Range: > or =25.0 mcg/mL
Therapeutic ranges are based on specimens drawn at trough (ie, immediately before the next dose).
Most individuals display optimal response to gabapentin with serum levels of 2 to 20 mcg/mL. Some individuals may respond well outside of this range, or may display toxicity within the therapeutic range; thus, interpretation should include clinical evaluation. Some patients require high doses to achieve response, resulting in concentrations as high as 80 mcg/mL. Dosage reduction should be based on signs of toxicity, not the serum concentration.
This test cannot be performed on whole blood. Serum must be separated from cells within 2 hours of draw. Specimens that are obtained from gel tubes are not acceptable.
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3. Johannessen SI, Tomson T: Pharmacokinetic variability of newer antiepileptic drugs: when is monitoring needed? Clin Pharmacokinetics 2006;45(11):1061-1075