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Öğe Serum insulin, leptin, and neuropeptide Y levels in epileptic children treated with valproate(B C DECKER INC, 2005) Aydin, K; Serdaroglu, A; Okuyaz, C; Bideci, A; Gucuyener, KWeight gain is a common side effect of valproate treatment. The potential mechanisms of valproate-associated weight gain are not yet clear. Decreased blood glucose level, impairment of P-oxidation of fatty acids, and increased insulin levels are some of the possible mechanisms. The aim of the present study is to evaluate the role of insulin, leptin, and neuropeptide Y in valproate-related weight gain in epileptic children. In 20 epileptic children treated with valproate before treatment and after a follow-up period of 3 and 6 months, body mass index and fasting insulin glucose ratio were calculated and serum glucose, insulin, cortisol, leptin, and neuropeptide Y levels were measured. At the end of 3 months, the mean body mass index values and the mean serum insulin, fasting insulin glucose ratio, and neuropeptide Y levels increased, whereas the serum glucose levels decreased. After 6 months of treatment, the mean serum cortisol and leptin levels were high, in addition to the body mass index, neuropeptide Y, and fasting insulin glucose ratio. These results suggest that weight gain during valproate treatment might be related to low glucose and high insulin, cortisol, leptin, and neuropeptide Y levels.Öğe Treatment of electrical status epilepticus during slow-wave sleep with high-dose corticosteroid(ELSEVIER SCIENCE INC, 2005) Okuyaz, C; Aydin, KA; Gucuyener, K; Serdaroglu, AA 4-year-old female patient with epilepsy with continuous spike-and-waves during slow-wave sleep not classified as Landau-Klefner syndrome, refractory to antiepileptic drugs including valproate, benzodiazepines, and lamotrigine, was treated successfully with high-dose intravenous methylprednisolone therapy. Valproate, clobazam, and lamotrigine were continued at the same dose during and after high-dose intravenous corticosteroid therapy. During corticosteroid therapy, awake and sleep electroencephalogram was recorded every day. On day 7, a dramatic clinical and electroencephalographic response was observed. After high-dose intravenous methylprednisolone, prednisolone was administered orally (2 mg/kg daily) for 2 months, then gradually withdrawn. After the withdrawal of corticosteroid therapy, the patient maintained the clinical improvement in behavior, and no continuous spike-and-wave electrical status epilepticus during slow-wave sleep occurred on routine monthly sleep electroencephalogram performed for the last 6 months. In the present case, an add-on high-dose intravenous corticosteroid seems to be effective in the treatment of patients with electrical status epilepticus during slow-wave sleep syndrome, especially when antiepileptic drugs fail. (C) 2005 by Elsevier Inc. All rights reserved.