Oxcarbazepine dosage

Lab test abnormalities Serum sodium levels less than 125 mmol/L have been observed in patients treated with oxcarbazepine. Experience from clinical trials indicates that serum sodium levels return toward normal when the oxcarbazepine dosage is reduced or discontinued or when the patient was treated conservatively (eg, fluid restriction). 

Oxcarbazepine Trileptal Tablet 150, 300,600 mg Suspension 300 mg/5 mL 300-1,200 mj day in two divided doses. Dosage should be slowly adjusted up and down according to response and adverse effects (e.g, 150-300 mg twice daily and increase by 300-600 mg/day at weekly intervals). Dose can be increased rapidly for inpatients. 

Oxcarbazepine is typically started at a dosage of 150 mg twice a day and titrated by 300 mg/day at weekly intervals. Therapeutic dosages are in the range of 450 mg twice a day to 1,200 mg twice a day. The conversion from carbamazepine to oxcarbazepine is approximately 1 to 1.5. Oxcarbazepine has a higher risk of hyponatremia than does carbamazepine. Serum sodium should be monitored in patients at risk for hyponatremia, such as the elderly or patients who are also taking diuretics. Stevens-Johnson syndrome and toxic epidermal necrolysis may occur between 3 and 10 times more frequently in oxcarbazepine-treated patients than in the general population. Median time from starting treatment to the development of these serious reactions is 19 days. 

A 31-year-old man developed ocnlogjric crises after starting to take oxcarbazepine, and the freqnency of these episodes correlated with the dosage of the dmg (11). Similar episodes had occnrred in the past after exposure to carbamazepine. The implantation of a vagus nerve stimulator led to the disappearance of the oculogyric crises. 

All anticonvulsants (except gabapentin), atypical antipsychotics, benzodiazepines, and calcium channel blockers require liver metabolism, and dosage adjustments may be needed (e.g., 25-50% reduction of normal doses) Carbamazepine or oxcarbazepine Alternative lamotrigine Acute mania or mixed episode first choice lithium... 

The interaction between warfarin and earbamazepine is moderately well documented, established and clinically important. The incidence is uncertain, but monitor the anticoagulant response if earbamazepine is added to established treatment with warfarin and anticipate the need to double the dosage. Oxcarbazepine appears to be a relatively non-interaeting alternative. 

Carbamazepine serum levels can be raised by dextropropoxyphene. Toxicity may develop unless suitable dosage reductions are made. Oxcarbazepine appears not to interact with dextropro-pox3q hene. 

The interaction between carbamazepine and dextropropoxyphene is very well established and clinically important. If concurrent use is necessary reduce the dosage of carbamazepine appropriately to prevent the development of toxicity. In many cases it may be simpler to use a non-interacting analgesic, although the occasional single dose of dextropropoxyphene probably does not matter. No special precautions seem necessary with oxcarbazepine. 

Information seems to be limited to the reports cited. If concurrent use is undertaken, serum carbamazepine levels should be monitored closely and suitable dosage reductions made as necessary to avoid possible toxicity. No special precautions seem necessary with oxcarbazepine. 

Serum ciclosiporin levels are markedly reduced by car-bamazepine, phenobarbital, or phenyiioin. The dosage of ciclosporin may need to be increased two- to fourfold to maintain adequate immunosuppression. Oxcarbazepine may cause a smaii decrease in ciclosporin leveis. Vaiproate appears not to affect ciclosporin levels but two case reports suggest that it may damage renal grafts and cause hepatotoxicity in patients taking ciclosporin. 

None of these interactions is extensively documented but all appear to be established and of clinical importance. Serum ciclosporin levels should be well monitored if carbamazepine, phenobarbital or phenytoin are added and the ciclosporin dosage increased appropriately. Primidone is metabolised to phenobarbital by the liver, and therefore would be expected to reduce ciclosporin levels. Information about oxcarbazepine is very limited but small reductions in its dose, together with an increase in ciclosporin dose, may be adequate to control any interaction. However, more study is required before oxcarbazepine can be recommended as a suitable alternative. The effects of the interaction may persist for a week or more after the anticonvulsant is withdrawn. Sodium valproate seems not to alter ciclosporin levels, but the case reports of nephritis and hepatotoxicity suggest some caution is warranted. 

Drug formulations Extended-release oxcarbazepine should cause fewer adverse effects because of the less marked peak serum oxcarbazepine concentration before metabolism to its active monohydroxy derivate. In an open study, 27 patients with difiicult-to-treat localization-related epilepsies who had been taking immediate-release oxcarbazepine were abruptly switched to extended-release oxcarbazepine in identical dosages and the concentrations of oxcarbazepine and its active metabolite were measured before and after the switch [229. The new formulation was associated with significantly fewer adverse effects and better quality of life, and this was explained by lower peak oxcarbazepine concentrations. 

Steinhoff BJ, WendUng AS. Short-term impact of the switch from immediate-release to extended-release oxcarbazepine in epilepsy patients on high dosages. Epilepsy Res 2009 87(2-3) 256-9. 

Drug dosage regimens The efficacy and tolerability of an oral oxcarbazepine loading dose of 30 mg/kg was assessed in 40 adolescent and adult patients. The most common adverse effect was dizziness, followed by nausea/ vomiting, nystagmus, ataxia, and diplopia. Most of these adverse effects occurred shortly after administration, and did not correlate with plasma levels of the medication [113 ]. 

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