Oxcarbazepine Therapy Research Articles

Liver injury and polyserositis as rare side effects of oxcarbazepine

We report the case of apatient with trigeminal neuralgia who developed cholestatic liver injury with systemic inflammation and polyserositis after starting oxcarbazepine therapy. No other causes could be identified. After discontinuation of the drug, there was acomplete remission. This case shows that the more modern oxcarbazepine can also cause idiosyncratic liver damage and underlines the importance of high vigilance concerning drug reactions in clinical practice.

Oxcarbazepine and Hyponatremia.

Background and Objectives: Hyponatremia is one of the most common adverse effects in patients treated with oxcarbazepine (OXC). Different risk factors for OXC-induced hyponatremia have been described as age, female gender, dosage, and combination with other drugs During our clinical practice, we noticed that a longer duration of treatment with OXC could be associated with a higher risk of hyponatremia, therefore, in this study, we aimed to evaluate factors that may increase the risk of OXC-induced hyponatremia. Materials and Methods: Data were retrospectively collected from our clinical database at the Department of Neurology of the Hospital of Lithuanian University of Health Sciences Kaunas Clinics. The sample was divided into three groups: OXC consumers (n = 31), other anti-seizure medications (ASMs) consumers (n = 43), and controls absent ASMs (n = 31). All groups were matched by age and gender. Hyponatremia was defined as <136 mmol/L. Results: The frequency of hyponatremia was significantly higher among OXC patients (61.3%) compared to other ASM patients (5.4%) and controls (3.2%). The mean serum sodium concentration in the OXC group was 133.1 ± 5.1 mmol/L. The frequency of severe hyponatremia among OXC-treated patients was 19.4%; this subgroup was older than patients with moderate hyponatremia and normonatremia and had a longer OXC treatment duration compared to a subgroup of normonatremia. The average duration of OXC therapy was 8.7 ± 5.5 years with a range from 1 to 21 years. Serum sodium concentration and duration of treatment with OXC demonstrated a significant negative correlation (r = −0,427, p = 0.017). Each year of therapy with OXC increased the risk of hyponatremia 1.3 times (OR = 1.326, 95% Cl 1.027–1.712, p = 0.031). Other factors (gender, age, polypharmacy, OXC dosage, and serum concentration) did not show a significant association with the development of hyponatremia. Conclusions: Longer duration of treatment with OXC is an important factor in the development and severity of hyponatremia.

Epileptiform activity index for assessing oxcarbazepin therapy of newly-diagnosed focal epilepsy in adolescents and adults

Introduction. Oxcarbazepine (OXC) is approved for initial and adjunctive therapy of focal epilepsy (FE), being also a drug of choice in case of pediatric FE. Despite that OXC has been used in the Russian Federation (RF) since 2007, studies assessing its efficacy and tolerability are scarce. Aim. To evaluate efficacy and tolerability of OXC therapy in patients with newly-diagnosed epilepsy. Patients and methods . There were enrolled 103 patients (56 (54.4%) into the study: males and 47 (45.6%) females with FE, aged 44.32±19.71 years. Depending on the OXC daily dose, all patients were divided into 3 subgroups: 1200 mg/day (n=16; 15.5%). Video-electroencephalographic (video-EEG) monitoring was performed at each visit (at baseline, 1, 3, 6 and 12 months after then onset of therapy). Treatment efficacy was assessed by using the criteria of retention on treatment, seizure absence, seizure rate decrease by >50%, seizure rate decrease by <50% (insufficient efficacy). Adverse effects (AEs) were assessed in accordance to the Side Effects of Anti-Epileptic Drugs (SIDAED) treatment scale and emerging pharmacodynamics aggravation (increased seizure rate compared to baseline/emergence of new seizure type). Results . It was found that retention on OXC monotherapy during the 12-month follow-up period was achieved in 69.0% (n=71) patients, among which 15.5% (n=16) received less than OXC at dose of 1200 mg/day, 44.7% (n=46) - 1200 mg/ day, and 8.8% (n=9) - more than 1200 mg/day, respectively. Total rate of intolerable AEs during the follow-up period was 13.6% (n=14). Comparing initial vs. 12-month timepoint EAI magnitude after the onset of OXC therapy revealed that it was significantly decreased by 6.9-fold (p<0.05). Conclusions. OXC is an effective drug for the initial treatment of FE in adolescents and adults highlighted with favorable tolerability profile. 12-month follow-up monitoring demonstrated that EAI was reduced almost by 7-fold allowing to consider it as an objective quantitative marker for assessing treatment efficacy.

A Case Series of Patients With Central Hypothyroidism From Oxcarbazepine Therapy

Many medications can impact thyroid function. Antiseizure medications have been shown to disrupt thyroid function in adults, but information is limited about how antiseizure medications may affect thyroid function in children. Oxcarbazepine is an analog of carbamazepine designed to minimize effects from the hepatic P450 metabolic enzymes. We have found that in the pediatric population, serum free thyroxine is reduced and thyroid-stimulating hormone concentrations are unchanged in patients taking oxcarbazepine with the mechanism thus being central hypothyroidism.

Central hypothyroidism secondary to oxcarbazepine therapy in children-a clinical case report

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Population pharmacokinetics of oxcarbazepine active metabolite in Chinese paediatric epilepsy patients and its application in individualised dosage regimens.

Oxcarbazepine (OXC) is an antiepileptic drug metabolised to active 10-monohydroxy derivative (MHD) following oral administration. There are no MHD population pharmacokinetic (PPK) models that describe the influence of genetic factors on MHD pharmacokinetics (PK). We developed a PPK model of MHD to investigate gene polymorphism of enzymes associated with MHD PK in Chinese paediatric epilepsy patients and evaluated its utility for dose individualisation. Data were prospectively collected from 141 paediatric epilepsy patients (aged ≤ 14years) who received OXC therapy at the First Affiliated Hospital of Fujian Medical University. The trough concentrations at steady state were determined by enzyme-multiplied immunoassay. Patients were genotyped for four single nucleotide polymorphisms (UGT2B7 802T>C, UGT1A9 I399C>T, ABCB1 3435C>T, and ABCB2 1249G>A). Patient gender, age, body weight (BW), hepatorenal function, and co-administrations were recorded. The PPK model was developed using nonlinear mixed-effects modelling software. The clinical performance of the final model was evaluated by including additional paediatric patients (n = 20) in the validation group. Oral clearance of MHD was significantly influenced by BW. The MHD PK was unrelated to the other covariates, such as the four single nucleotide polymorphisms and co-administration with new-generation antiepileptic drugs. The final BW-dependent exponent model showed the best fit with our data and predicted the trough concentrations in the validation group more accurately than the basic model. A new dosing strategy combining the dosage guideline and Bayesian method is proposed to individualise OXC regimens. A PPK model was established to estimate individual MHD clearance in paediatric patients taking OXC to develop individualised OXC dosing regimens for Chinese paediatric epilepsy patients.

Efficacy and safety of Carbamazepine in treatment of vestibular complications

Objective To evaluate the efficacy and safety of Carbamazepin(CBZ)compared with Oxcarbazepine(OXC)therapy for vestibular paroxysmia. Methods Eighty-two patients with vestibular paroxysmia were admitted during June 2013 and June 2017 in this study.According to the agents administered, all patients were divided into the CBZ group(n=31), CBZ+ Betahistine(BMT)group(n=26)and OXC+ BMT group(n=25). The clinical efficacy, frequency, vertigo and adverse reactions of three groups were compared after 3 months follow-up. Results In CBZ group, 14 cases were cured, 13 were improved, and the effective rate was 87.1%.In CBZ+ BMT group, 18 cases were cured, 7 were recovered, and the effective rate was 96.2%.In OXC+ BMT group, 15 cases were cured, 8 cases were recovered, and the effective rate was 92.0%.There was no significantly difference in effective rate among the three groups(χ2=0.783, P=0.129). Meanwhile, the CBZ+ BMT group had the lowest frequency of vestibular paroxysmia and vertigo degree, while the CBZ group was the highest; the difference in the frequency and vertigo degree between groups was statistically significant(P<0.05). Furthermore, the incidences of side-effects were 51.6%(n=16), 30.8%(n=8)and 16.0%(n=4)in the CBZ group, CBZ+ BMT group and OXC+ BMT group, respectively. Conclusions The effect of Carbamazepine and Oxcarbazepine for vestibular paroxysmia is similar, and is safely and significantly improved when combined with Betahistine. Key words: Carbamazepine; Betahistine; Vestibular diseases

Severe recurrent hypothermia in an elderly patient with refractory mania associated with atypical antipsychotic, valproic acid and oxcarbazepine therapy

Hypothermia is a rare but serious condition that has been associated with various psychiatric medications. We present a 76-year-old woman with refractory mania who developed multiple episodes of severe hypothermia...

Three-Year Retention Rates of Levetiracetam, Topiramate, and Oxcarbazepine: A Retrospective Hospital-Based Study.

We evaluated and compared the 3-year retention rates of levetiracetam (LEV), topiramate (TPM), and oxcarbazepine (OXC) in patients with epilepsy in routine clinical practice. We retrospectively reviewed medical records of patients with epilepsy who were newly prescribed LEV, TPM, or OXC from 2006 to 2010. The retention rates were estimated by the Kaplan-Meier analysis, and independent risk factors for drug discontinuation were analyzed by the Cox regression method. A total of 588 patients were included: LEV (n = 345), TPM (n = 190), and OXC (n = 53). Among them, 82% had focal epilepsy, whereas 14.8% had generalized epilepsy. The 3-year retention rates for LEV, TPM, and OXC, were 81.2%, 78.3%, and 54.7%, respectively. Levetiracetam and TPM had equivalent retention rates, whereas patients remained on OXC for a significantly shorter amount of time (P < 0.001). A lower retention rate for OXC was also evident in the subgroup analysis of focal epilepsy (P < 0.001). In generalized epilepsy, LEV and TPM revealed comparable retention rates (P = 0.255). The seizure-freedom rate did not differ among groups, whereas the rate of adverse effects leading to drug withdrawal of OXC (87.5%) was higher than that of LEV (34.4%, P < 0.001) and TPM (52.5%, P = 0.012). The current study suggested that LEV and TPM had comparable retention profiles in the long-term treatment for both focal and generalized epilepsy. Meanwhile, OXC therapy seemed to be relatively less useful because of its poor tolerability.

Effects of UGT1A9 genetic polymorphisms on monohydroxylated derivative of oxcarbazepine concentrations and oxcarbazepine monotherapeutic efficacy in Chinese patients with epilepsy.

The human UDP-glucuronosyltransferase which is genetically polymorphic catalyzes glucuronidations of various drugs. The interactions among UGT1A4, UGT1A6, UGT1A9, and UGT2B15 genetic polymorphisms, monohydroxylated derivative (MHD) of oxcarbazepine (OXC) plasma concentrations, and OXC monotherapeutic efficacy were explored in 124 Chinese patients with epilepsy receiving OXC monotherapy. MHD is the major active metabolite of OXC, and its plasma concentration was measured using high-performance liquid chromatography when patients reached their maintenance dose of OXC. Genomic DNA was extracted from whole blood and SNP genotyping performed using PCR followed by dideoxy chain termination sequencing. We followed the patients for at least 1year to evaluate the OXC monotherapy efficacy. Patients were divided into two groups according to their therapeutic outcome: group 1, seizure free; group 2, not seizure free. The data were analyzed using T test, one-way analysis of variance (ANOVA), Kruskal-Wallis test, chi-square test, Fisher's exact test, correlation analysis, and multivariate regression analysis. T test analysis showed that MHD plasma concentrations were significantly different between the two groups (p=0.002). One-way ANOVA followed by Bonferroni post hoc testing of four candidate SNPs revealed that carriers of the UGT1A9 variant allele I399 C>T (TT 13.28±7.44mg/L, TC 16.41±6.53mg/L) had significantly lower MHD plasma concentrations and poorer seizure control than noncarriers (CC 22.24±8.49mg/L, p<0.05). In our study, we have demonstrated the effects of UGT1A9 genetic polymorphisms on MHD plasma concentrations and OXC therapeutic efficacy. Through MHD monitoring, we can predict OXC therapeutic efficacy, which may be useful for the personalization of OXC therapy in epileptic patients.

Potential effects of valproate and oxcarbazepine on growth velocity and bone metabolism in epileptic children- a medical center experience.

BackgroundChildren with longstanding use of antiepileptic drugs (AEDs) are susceptible to developing low bone mineral density and an increased fracture risk. However, the literature regarding the effects of AEDs on growth in epileptic children is limited. The aim of this study was to investigate the potential effects of valproate (VPA) and/or oxcarbazepine (OXC) therapy on growth velocity and bone metabolism.MethodsSeventy-three ambulatory children (40 boys and 33 girls) with epilepsy, aged between 1 and 18 years (mean age 9.8 ± 4.1 years), were evaluated for growth velocity before and for 1 year after VPA and/or OXC treatment. The bone resorption marker serum tartrate-resistant acid phosphatase 5b (TRAcP5b) and the bone formation marker serum bone-specific alkaline phosphatase (BAP) were measured post-AEDs therapy for 1 year.ResultsThe difference in growth velocity (ΔHt) and body weight change (ΔWt) between pre- and post-AEDs treatment were -1.0 ± 2.8 cm/year (P < 0.05) and 0.1 ± 3.9 kg/year (P = 0.84), respectively. The study population had serum TRAcP5b-SDS of -1.6 ± 1.2 and BAP-SDS of 1.7 ± 3.7 compared with sex- and age-matched healthy children. Significant correlation between serum TRAcP 5b and BAP activities was noted (r = 0.60, p < 0.001). There was a positive correlation between growth velocity and serum TRAcP 5b activity after AED treatment (r = 0.42, p < 0.01). No correlation was found between ΔHt, ΔWt, serum TRAcP 5b, BAP activity and types of AEDs.ConclusionGrowth velocity was significantly decreased in epileptic children after 1 year of VPA and/or OXC treatment. The effect of VPA and/or OXC therapy on dysregulation of bone metabolism might play a crucial role in physical growth.Electronic supplementary materialThe online version of this article (doi:10.1186/s12887-016-0597-7) contains supplementary material, which is available to authorized users.

Weight gain in children on oxcarbazepine monotherapy

BackgroundStudies of the effect of oxcarbazepine (OXC) on body growth of children with epilepsy are rare and their results are controversial. To the contrary, many studies have shown significant weight gain following valproate (VPA) treatment. PurposeTo prospectively evaluate the effect of OXC monotherapy on growth patterns of children with epilepsy and compare it with the effect of VPA monotherapy. MethodFifty-nine otherwise healthy children, aged 3.7–15.9 years, with primary generalized, partial or partial with secondary generalization seizure disorder, were included in the study. Twenty six children were placed on OXC and thirty three on VPA monotherapy. Body weight (BW), height and body mass index (BMI) as well as their standard deviation scores (SDS), were evaluated prior to as well as 8 months post initiation of OXC or VPA therapy. ResultsEight months post OXC-treatment, BW, SDS-BW, BMI and SDS-BMI increased significantly. The increase was similar to that observed in the VPA group. An additional 15.4% of children in the OXC group and 21.2% in the VPA group became overweight or obese. The effect of both OXC and VPA therapy on linear growth did not reach statistical significance. ConclusionSimilarly to VPA, OXC monotherapy resulted in a significant weight gain in children with epilepsy. Careful monitoring for excess weight gain along with counseling on adapting a healthy lifestyle should be offered to children on OXC therapy.

SCN1A, ABCC2 and UGT2B7 gene polymorphisms in association with individualized oxcarbazepine therapy.

Associations between the effects of SCN1A, SCN2A, ABCC2 and UGT2B7 genetic polymorphisms and oxcarbazepine (OXC) maintenance doses in Han Chinese epileptic patients were investigated. Genetic polymorphisms were detected in 184 epileptic patients receiving OXC monotherapy by high-resolution melting curve and TaqMan method. Carriers of the SCN1A IVS5-91G>A, UGT2B7 c.802T>C and ABCC2 c.1249G>A variant alleles required significantly higher OXC maintenance doses than noncarriers (p < 0.05). Corresponding relative ln (concentration-dose ratios) values for SCN1A IVS5-91 variants differed by the genotypic order GG > GA > AA. SCN1A, UGT2B7 and ABCC2 genetic polymorphisms are associated with OXC maintenance doses and may be useful for the personalization of OXC therapy in epileptic patients. Further studies are needed. Original submitted 6 June 2014; Revision submitted 5 September 2014.

Acute dyskinesia: A rare adverse effect of oxcarbazepine in epilepsy with neurobehavioral symptoms

We are reporting an 11-year-old female child of febrile partial seizure since age of 3 months and transient neurobehavioral changes of psychic, gelastic semiology since childhood. She had no history of continued febrile seizure, but had 3 admissions for 3 episodes of status epilepticus in last 3 years. She experienced acute generalized dyskinesia (torticollis, oromandibular dystonia, spasmodic dysphonia, right lower limb eversion plantarflexed type feet dystonia) soon after oxcarbazepine (OXC) therapy from last episode of status epilepsy on 15 April 2013 with similar semiology. We failed to explain the considered infectious, non-convulsive state and hyponatremic extra pyramidal syndrome. We used the Naranjo adverse drug reaction probability scale and stopped OXC. After state intravenous diazepam 2 nd day, she was starting to improve and over a period of 4 days she was asymptomatic. We shifted on clonazepam, sodium valproate for further. She was asymptomatic until 1 month follow-up.

左乙拉西坦和奥卡西平治疗伴中央颞区棘波儿童良性癫痫的对比研究

目的：为明确左乙拉西坦(Levetiracetam, LEV)单药治疗首发伴中央颞区儿童良性癫痫(benign child-hood epilepsy with centro-temporal spikes, BECT)患儿的疗效及对认知的影响，采用奥卡西平(Oxcar- bazepine, OXC)作为对照进行开放性、平行性研究。方法：在来我院门诊就诊符合BECT诊断标准的患儿中选取104例，随机分为2组。OXC组51例，LEV组53例。以实验前3个月的每月平均发作次数为基线发作水平，每2~4周电话或门诊回访，记录临床发作次数。服药前、服药后3个月、6个月、12个月进行认知功能评定(4~6岁采用韦氏学龄前及小学智力量表，6~16岁采用韦氏儿童智力量表)。结果：1) 疗效比较：3次回访二组有效率、各组组内不同回访时间有效率比较无差异。2) 认知功能比较：基线时及12个月治疗后两组儿童比较无统计学差异。两组患儿用药后自身对照比较均显示多项分测验得分有增高趋势，OXC组治疗前后得分改变无统计学意义，LEV组的词汇及数字广度分测验得分的提高幅度与治疗前相比有统计学意义。结论：首选LEV治疗儿童BECT疗效与OXC相似，对BECT患儿的认知无不良影响。Objective: To clarify the therapeutic effect and the cognitive improvement of Levetiracetam (LEV) monotherapy on the first BECT (benign childhood epilepsy with centro-temporal spikes, BECT) compared with Oxcarbazepine (OXC) in an open and parallel study. Methods: 104 patients who were admitted in our hospital and conformed to the BECT diagnostic criteria were divided into two groups randomly: OXC therapy group (51 cases) and LEV therapy group (53 cases). The monthly average seizure times of the 3 months before the beginning of the study were taken as the baseline seizure level, while the seizures times were recorded after telephone follow-up or clinical return visits per 2 - 4 weeks. Evaluations on cognitive functions were conducted before the treatment and 3 months, 6 months and 12 months after the treatment (Wechslet preschool and primary scale of intelligence were applied to the patients at the age of 4 - 6, and Wechsler intelligence scale for children were applied to those at the age of 6 - 16). Results: 1) Comparison of curative effects: The curative effect difference between the LEV group and OXC group and the difference during the different period of each group were both not significant. 2) Comparison of cognitive function: There is no statistical difference between the two groups before and after treatment. Both the two groups showed an increasing trend of intelligence test scores after treatment. There was no statistical significance between scores before and after OXC treatment, while the scores difference of words and digit span before and after the treatment of LEV had statistical significance. Conclusions: The curative effect of LEV on the first BECT patients is similar to OXC without adverse influence on cognition.

Frequency of and risk factors for oxcarbazepine-induced severe and symptomatic hyponatremia

PurposeHyponatremia is one of the most common adverse effects in patients treated with oxcarbazepine (OXC). Most patients with OXC-induced hyponatremia are asymptomatic, so the presence of severe or symptomatic hyponatremia, which requires electrolyte correction or discontinuation of OXC therapy, has more important clinically implications. However, data for OXC-induced severe and symptomatic hyponatremia are limited. MethodsWe reviewed medical records of all patients with epilepsy who were treated with OXC at the Seoul National University Hospital. We analyzed serum sodium level results and attempted to identify correlations between various factors and the frequency of severe and symptomatic OXC-induced hyponatremia. ResultsData from a total 1009 patient were examined. The frequency of severe and symptomatic hyponatremia was 11.1% and 6.8%, respectively. Multivariate analysis revealed that age (P=0.014, OR 1.014), antiepileptic drug (AED) polytherapy (P=0.040, OR 1.540), and the concomitant use of diuretics (P<0.001, OR 5.597) were independent risk factors for OXC-induced severe hyponatremia. Age (P=0.001, OR 1.034) and the concomitant use of diuretics (P=0.035, OR 2.222) were independent risk factors for OXC-induced symptomatic hyponatremia. The frequency of OXC-induced symptomatic hyponatremia that was judged to be clinically significant was 2.8% among the total OXC-treated epilepsy patients. ConclusionOur study recommended that serum sodium be monitored regularly in patients taking OXC, especially in old age, AED polytherapy or concomitant use of diuretics, to assist in the early recognition of hyponatremia and to increase the awareness of symptoms that might be attributable to this.

Oxcarbazepine-induced jerky see–saw nystagmus

A 43-year-old female presented to the emergency department because of dizziness, drowsiness and generalized urticaria that occurred the previous day. Patient’s history revealed protracted delivery with neonate asphyxia, following which she had been diagnosed with epilepsy at age 7 when she experienced her first generalized tonic–clonic seizure. Her MRI showed ulegyria and hypoxic–ischaemic changes characteristic for perinatal damage. Her last visit to an epilepsy clinic was 18 days before. At that time a change in her therapy was made with gradual initiation of oxcarbazepine (start dose of 300 mg QD in the evening for 5 days, than 300 mg BID for 5 days, than 300 mg in the morning and 600 mg in the evening for 5 days) and tapering of levetiracetame. Her therapy, at the time of her presentation to the emergency department, was (in total daily doses): oxcarbazepine 900 mg, sodium valproate 1,000 mg, levetiracetame 750 mg, clonazepam 4.5 mg, lamotrigine 100 mg. Neurologic examination revealed a jerky see–saw nystagmus (SSN) more pronounced on the right eye (Video 1). Brain CT scan was normal. Oxcarbazepine and lamotrigine were discontinued and carbamazepine was gradually introduced. The carbamazepine was chosen because this drug controlled her seizures very well in the past, however, pediatric neurologist chose to switch from carbamazepine to levetiracetame at one point. On follow-up, a week later, she did not have nystagmus and did not experience dizziness and drowsiness any more but still had residual urticaria on her face and neck. SSN is a torsional–vertical nystagmus in which one eye elevates and intorts, while the other depresses and extorts. Jerky SSN is reportedly caused by lesions in the chiasmal or parasellar area thus resulting from disruption of the visual pathway [1]. However, SSN was described in association with vascular and inflammatory lesions of the rostral midbrain, pons and cerebellum [1, 2]. Based on these reports, SSN can result from dysfunction of the medial longitudinal fasciculus (MLF) that coordinates input to the oculomotor and trochlear nuclei from the vestibular nuclei [2]. One of the most common side–effects of oxcarbazepine therapy is nystagmus and it is related to its mono-hydroxyderivative levels in serum [3]. The therapeutic effect of oxcarbazepine results from its effect of blocking neural ion channels. We hypothesize that the same effect caused SSN in our patient blocking neurons that are part of the MLF. As nystagmus is a well-described side–effect of antiepileptic therapy and given the fact that nystagmus in our patient commenced on initiation and disappeared on discontinuation of oxcarbazepine, we report on a yet undescribed case of jerky SSN caused by oxcarbazepine.

Possible induction of West syndrome by oxcarbazepine therapy in a patient with complex partial seizures

Oxcarbazepine has been reported to precipitate myoclonic, generalised tonic-clonic, absence, and complex partial seizures, and carbamazepine to precipitate absences, myoclonic seizures and spasms. Here, we report a one-year, six-month-old girl with complex partial seizures who developed infantile spasms, developmental regression, and hypsarrhythmia during the two weeks directly following initiation of oxcarbazepine (14 mg/kg/day). All of these resolved within a few days after discontinuation of this medication. Although we cannot rule out that the above association may have been coincidental, or that the improvement may have been due to concurrent therapy, this case raises the possibility that oxcarbazepine, like carbamazepine, may precipitate infantile spasms and West syndrome.

Serum insulin, cortisol, leptin, neuropeptide Y, galanin and ghrelin levels in epileptic children receiving oxcarbazepine

Purpose The aim of this study was to investigate whether oxcarbazepine (OXC) monotherapy causes weight gain in epileptic children. Methods A total of 22 children with epilepsy (age 3.0–16.4 years) were assigned to OXC therapy. Serum levels of glucose, insulin, cortisol, leptin, neuropeptide Y (NPY), galanin and ghrelin were assessed before OXC therapy (month 0) and after the 6th and 18th months. Results There was no statistically significant difference in weight–standard deviation score (SDS), Height–SDS, BMI–SDS, serum glucose, insulin, cortisol, leptin, NPY, galanin and ghrelin levels between initial values (month 0) and those in the 6th and 18th months after OXC therapy ( p > 0.05). Conclusions Our results indicate that OXC therapy causes neither weight change nor alterations in serum glucose, insulin, cortisol, leptin, NPY, galanin and ghrelin levels in children with epilepsy.

P14.7 May long tem oxcarbazepine therapy be leading to secondary hyperparathyroidism?

P14.7 May long tem oxcarbazepine therapy be leading to secondary hyperparathyroidism?