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Oxcarbazepine Metabolite : 36637
Test CodeOXCRB or 36637
Alias/See Also
Hydroxycarbazepine,10-Hydroxycarbazepine,Trileptal
CPT Codes
80183
Transport Container
Preferred Specimen
1 mL serum collected in a red-top tube (no gel)
Minimum Volume
0.25 mL
Alternative
Plasma collected in EDTA (lavender-top) tube
1 mL serum collected in a red-top tube (no gel)
Minimum Volume
0.25 mL
Alternative
Plasma collected in EDTA (lavender-top) tube
Transport Temperature
Refrigerated.
Specimen Stability
Room temperature: 72 hours; Refrigerated: 14 days; Frozen: 60 days
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
Gel barrier/ Serum Separator Tube (SST®)
Methodology
Liquid Chromatography/Tandem Mass Spectrometry (LC/MS/MS)
Setup Schedule
Monday - Saturday
Report Available
3 days
Reference Range
10-Hydroxycarbazepine 8.0-35.0 mcg/mL
Clinical Significance
Oxcarbazepine (trileptal) is an anti-convulsant used for treating generalized tonic-clonic and partial seizures. It can be administered alone or as an adjunct to other anti-convulsants.
Clinically significant effects of oxcarbazepine are observed when plasma levels of its active metabolite, 10-OH-carbazepine, are between 15 and 35 ug/mL. Toxic symptoms may occur when plasma levels exceed 35 ug/mL. Therapeutic monitoring of oxcarbazepine and its active metabolite are important for achieving proper serum/plasma concentration to inhibit epileptic seizures and avoid adverse effects. Precise mechanism of the action by which oxcarbazepine and its active metabolite exert their antiseizure effect is unknown. However, in vitro electro-physiological studies indicate that produce blockade of voltage-sensitive sodium channels, resulting in stabilization of hyperexcited neural membranes, inhibition of repetitive neuronal firing, and diminution of propagation of synaptic impulses. These are important in prevention of seizure spread in the brain. In addition, increased potassium conduction and calcium channel activities may contribute to antiseizure treatment effects. After oral administration, oxcarbazepine is readily absorbed in the body, followed by rapid and almost complete metabolization to 10-OH-carbazepine, active metabolite. The half-life of oxcarbazepine is only 1 to 2.5 hours, while that of 10-OH-carbazepine is 11 to 15 hours. The protein binding of oxcarbazepine is about 67%, whereas that of the metabolite is about 38%. The clearance of oxcarbazepine and its active metabolite from the body is mainly through ketone reduction and O-site conjugation with glucuronic acid rather than oxidative processes via cytochrome P450 system. More than 95% of the treatment dosage is excreted by the kidneys. Fecal excretion only accounts for less than 4%.
Clinically significant effects of oxcarbazepine are observed when plasma levels of its active metabolite, 10-OH-carbazepine, are between 15 and 35 ug/mL. Toxic symptoms may occur when plasma levels exceed 35 ug/mL. Therapeutic monitoring of oxcarbazepine and its active metabolite are important for achieving proper serum/plasma concentration to inhibit epileptic seizures and avoid adverse effects. Precise mechanism of the action by which oxcarbazepine and its active metabolite exert their antiseizure effect is unknown. However, in vitro electro-physiological studies indicate that produce blockade of voltage-sensitive sodium channels, resulting in stabilization of hyperexcited neural membranes, inhibition of repetitive neuronal firing, and diminution of propagation of synaptic impulses. These are important in prevention of seizure spread in the brain. In addition, increased potassium conduction and calcium channel activities may contribute to antiseizure treatment effects. After oral administration, oxcarbazepine is readily absorbed in the body, followed by rapid and almost complete metabolization to 10-OH-carbazepine, active metabolite. The half-life of oxcarbazepine is only 1 to 2.5 hours, while that of 10-OH-carbazepine is 11 to 15 hours. The protein binding of oxcarbazepine is about 67%, whereas that of the metabolite is about 38%. The clearance of oxcarbazepine and its active metabolite from the body is mainly through ketone reduction and O-site conjugation with glucuronic acid rather than oxidative processes via cytochrome P450 system. More than 95% of the treatment dosage is excreted by the kidneys. Fecal excretion only accounts for less than 4%.
Performing Laboratory
med fusion
