Vigabatrin, Lamotrigine, Topiramate and Serum Carnitine Levels

Zelnik, Nathanel; Isler, N.; Goez, Helly; Shiffer, Mirta; David, Miriam; Shahar, Eli

doi:10.1016/j.pediatrneurol.2008.03.005

Cited by 14 publications

(7 citation statements)

References 18 publications

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“…These results were in agreement with Zelnik et al [23]; who had studied serum carnitine in epileptic children treated with VPA, vigabatrin, lamotrigine, and topiramate. These drugs were given as monotherapy or polytherapy and had found that, newgeneration AEDs probably do not cause carnitine deficiency.…”

Section: Discussionsupporting

confidence: 92%

Plasma carnitine levels in children with idiopathic epilepsy treated with old and new antiepileptic drugs

El-Aziz

El-Serogy

2015

J Pediatr Neurol

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Prolonged antiepileptic drugs (AEDs) treatment can result in secondary carnitine deficiency. Clinical studies indicate a decrease in free and total carnitine levels in children treated with old-generation AEDs (especially valproate). A number of studies on the effect of valproic acid and/or other AEDs on carnitine concentrations yielded contradictory results. The effect of new AEDs as oxcarbazepine and lamotrigine on carnitine metabolism has not been reported previously. The aim of this study was to evaluate the plasma carnitine level in children with idiopathic epilepsy treated with old AEDs (valproic acid and carbamazepine) and new AEDs (lamotrigine and oxcarbazepine). Fifty children with newly diagnosed idiopathic epilepsy were selected from those attending the pediatric neurology out-patient clinic at Tanta University Hosptial. Thirty-four males and 16 females were enrolled in the study with the mean age was (6.8 ? 3.1 yr). Patients were grouped according to their antiepileptic treatment into: group 1, 20 patients received valproic acid as monotherapy with no prior AEDs use. Group 2, 10 patients received valproic acid as polytherapy after 3 mo treatment with carbamazepine. Group 3, 10 patients received lamotrigine as monotherapy, and group 4, 10 patients received oxcarbazepine as monotherapy. Twenty healthy children served as control group with mean age was (8.5 ? 2.3 yr). Estimation of the plasma carnitine levels were done for all the studied groups. Group 1 and group 2 epileptic children, treated with valproic acid monotherapy and polytherapy respectively had significantly lower plasma carnitine levels than that of the control group (P < 0.05). There was significant correlation between the age and the plasma carnitine in group 1 and group 2 epileptic children, the younger the age the greater the reduction in the plasma carnitine levels. Patients treated with valproic acid polytherapy had significantly lower plasma carnitine levels than those of the patients treated with valproic acid monotherapy (P < 0.05). There was no significant difference in the plasma carnitine levels between the controls and children with epilepsy treated with oxcarbazepine and lamotrigine (P > 0.05). In conclusion, carnitine deficiency is not uncommon among children with epilepsy and is mainly linked to valproate therapy. In contrast, new-generation AEDs probably do not cause carnitine deficiency. These findings suggest a need to monitor serum carnitine levels in children treated with valproic acid therapy.

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Section: Discussionsupporting

confidence: 92%

Plasma carnitine levels in children with idiopathic epilepsy treated with old and new antiepileptic drugs

El-Aziz

El-Serogy

2015

J Pediatr Neurol

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“…with the metabolism of vitamin D increase the risk of osteopenia and osteoporosis [8,9]. PHT and PB decreases the absorption of vitamin B12 and folic acid [10]. Valproic acid (VPA), vigabatrin (VGB), lamotrigine (LMT) and TPM, have shown a decrease in serum total and free carnitine [11,12].…”

Section: Open Access Journal Of Neurology and Neurosurgerymentioning

confidence: 99%

Malnutrition, an Important Comorbidity in Patients with Lennox Gastaut Syndrome

Segovia¹

2017

OAJNN

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Background: Lennox Gastaut Syndrome (LGS) is an epileptic encephalopathy that occurs in the pediatric age is associated with cognitive impairment. It is also considered as refractory epilepsy due to its frequent resistance to antiepileptic drugs, which implies the use of multiple antiepileptic drugs for long periods of treatment, the adverse effects of which could affect the patient's nutrition.Objective: To determine malnutrition in patients with Lennox Gastaut Syndrome and its clinical repercussion.Methods: A retrospective cohort study was performed in patients aged 5 to 19 years with diagnosis of Lennox Gastaut Syndrome, in control of at least 5 years.Anthropometric measurements were recorded and nutritional status was determined. Demographic and clinical characteristics were recorded: type of crisis, age of diagnosis, electro encephalographic characteristics, neuro imaging, number of drugs and comorbidities.Results: Thirty-five patients were studied, the mean age was 6 years (CI 95%: 2-10), 55% were men. Nutritional status was classified as normal (20%), mild malnutrition (11.4%) moderate malnutrition (48.5%), severe malnutrition (17%), and 3.1% of the patients were overweight or obese. Alterations in the electro encephalogram were significantly more frequent in patients with malnutrition (p=0.02). Patients with malnutrition required more drugs (2.8; CI 95%: 2-4) and however, the number of epileptic events was significantly higher. Conclusion:Malnutrition is a common phenomenon in pediatric patients with Lennox-Gastaut Syndrome, and in accordance to gravity has a greater impact on crisis management by promoting refractoriness and thereby the quality of life.

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“…L-Carnitine (levocarnitine) supplementation has been recommended to reverse the adverse metabolic effects of VPA in cases of VPA-induced hepatotoxicity, VPA overdose, and primary carnitine-transporter defects [211,212]. Hyperammonemia and serum and muscle carnitine deficiency are well described in patients chronically taking VPA [213][214][215]. Several studies and case reports demonstrate that carnitine supplementation reverses clinical symptoms, hypocarnitinemia, hyperammonemia, and VPA half-life prolongation in patients with toxicity due to chronic administration [216][217][218].…”

Section: L-carnitinementioning

confidence: 99%

Drugs and pharmaceuticals: management of intoxication and antidotes

Smith

2010

Experientia Supplementum

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The treatment of patients poisoned with drugs and pharmaceuticals can be quite challenging. Diverse exposure circumstances, varied clinical presentations, unique patientspecific factors, and inconsistent diagnostic and therapeutic infrastructure support, coupled with relatively few definitive antidotes, may complicate evaluation and management. The historical approach to poisoned patients (patient arousal, toxin elimination, and toxin identification) has given way to rigorous attention to the fundamental aspects of basic life supportairway management, oxygenation and ventilation, circulatory competence, thermoregulation, and substrate availability. Selected patients may benefit from methods to alter toxin pharmacokinetics to minimize systemic, target organ, or tissue compartment exposure (either by decreasing absorption or increasing elimination). These may include syrup of ipecac, orogastric lavage, activated single-or multi-dose charcoal, whole bowel irrigation, endoscopy and surgery, urinary alkalinization, saline diuresis, or extracorporeal methods (hemodialysis, charcoal hemoperfusion, continuous venovenous hemofiltration, and exchange transfusion). Pharmaceutical adjuncts and antidotes may be useful in toxicant-induced hyperthermias. In the context of analgesic, anti-inflammatory, anticholinergic, anticonvulsant, antihyperglycemic, antimicrobial, antineoplastic, cardiovascular, opioid, or sedative-hypnotic agents overdose, N-acetylcysteine, physostigmine, L-carnitine, dextrose, octreotide, pyridoxine, dexrazoxane, leucovorin, glucarpidase, atropine, calcium, digoxin-specific antibody fragments, glucagon, high-dose insulin euglycemia therapy, lipid emulsion, magnesium, sodium bicarbonate, naloxone, and flumazenil are specifically reviewed. In summary, patients generally benefit from aggressive support of vital functions, careful history and physical examination, specific laboratory analyses, a thoughtful consideration of the risks and benefits of decontamination and enhanced elimination, and the use of specific antidotes where warranted. Data supporting antidotes effectiveness vary considerably. Clinicians are encouraged to utilize consultation with regional poison centers or those with toxicology training to assist with diagnosis, management, and administration of antidotes, particularly in unfamiliar cases.

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Vigabatrin, Lamotrigine, Topiramate and Serum Carnitine Levels

Cited by 14 publications

References 18 publications

Plasma carnitine levels in children with idiopathic epilepsy treated with old and new antiepileptic drugs

Plasma carnitine levels in children with idiopathic epilepsy treated with old and new antiepileptic drugs

Malnutrition, an Important Comorbidity in Patients with Lennox Gastaut Syndrome

Drugs and pharmaceuticals: management of intoxication and antidotes

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