Akin Iscan

The Effects of Carbamazepine, Valproic Acid and Phenobarbital on the Oxidative and Antioxidative Balance in Epileptic Children

Background: Oxidative stress has been related in a wide variety of ways with nervous tissue. We studied the effect of antiepileptic monotherapy on serum level of total antioxidant capacity, lipid hydroperoxide, total peroxide, oxidative stress index, and individual serum antioxidants such as albumin, bilirubin and uric acid. Patients and Methods: We studied 122 subjects including healthy controls, untreated epileptic patients and epileptic patients treated with valproic acid, carbamazepine or phenobarbital. Serum total antioxidant capacity was measured as an index of antioxidants, and total peroxide was measured as index of oxidative stress. The serum concentrations of uric acid, albumin, bilirubin and lipid hydroperoxide were monitored simultaneously. Results: We found that serum total antioxidant capacity levels were significantly decreased in the untreated group compared with the controls. Serum total peroxide levels were markedly increased in the untreated and carbamazepine-treated groups compared to in the controls; and lipid hydroperoxide and oxidative stress index levels were significantly higher in the phenobarbital-treated group than in the controls. Uric acid concentrations were significantly lower in the valproic-acid-treated group than in the untreated group, and total bilirubin concentrations were higher in the untreated group than in the controls. Conclusion: Epileptic children exposed to oxidative stress and conventional antiepileptic drugs change the oxidative/antioxidative balance. The serum oxidant and antioxidant status of epileptic children with valproic acid monotherapy are better regulated compared with children with carbamazepine and phenobarbital monotherapy.

Elevated serum S-100B levels in children with temporal lobe epilepsy

PURPOSE An elevated level of S-100B in serum is generally considered to be a biochemical marker of nervous tissue damage. According to our knowledge, no studies have evaluated the serum S-100B protein concentration in children with temporal lobe epilepsy. The objective of this study was to measure the serum levels of S-100B protein in pediatric cases with temporal epilepsy. METHODS This case-controlled cross-sectional study was performed at the Department of Pediatric Neurology, Harran University School of Medicine, Sanliurfa, in Turkey. Serum S-100B protein levels were studied in 19 (12 females, 7 males) children with temporal lobe epilepsy and in 25 (15 females, 10 males) healthy control subjects. Serum samples were collected within 30min after a complex partial seizure, and serum S-100B protein levels were measured with an electrochemiluminescence immunoassay for the quantification of protein (ECLIA kit, Roche(®) Diagnostics, Germany). RESULTS The mean serum concentration of S-100B protein was 0.12±0.02μg/L in the temporal lobe epilepsy group and 0.07±0.01μg/L in the control group. The patients showed significantly elevated S-100B protein levels compared with healthy controls (P<0.001). CONCLUSION Our data suggest that increased S-100B protein levels in the serum might reflect neuronal damage in the brains of children with temporal lobe epilepsy. These results do confirm the previous findings of elevated S-100B protein levels in adult patients with temporal lobe epilepsy.

Oxidative and antioxidative capacity in children with cerebral palsy

The superiority of oxidative stress and/or the inadequacy of antioxidant capacity have an important role in disease. Decreased antioxidant availability has been observed in the pathogenesis of many different diseases affecting the brain, such as mitochondrial disorders, cerebral ischaemia and epilepsy. Oxidative and antioxidative status in children with cerebral palsy aged 1-12 years was investigated in this study and compared with healthy controls. Sixty-nine patients with cerebral palsy and 42 controls were enrolled in the study. Lipid peroxidation in the cerebral palsy group was significantly higher than that in the controls (7.54+/-3.64 micromol H(2)O(2)/L and 5.84+/-1.25 micromol H(2)O(2)/L, respectively) (P=0.02). Serum total antioxidant capacity levels were also markedly lower in the CP group than in the control group (1.42+/-0.22 mmol Trolox equiv./L and 1.64+/-0.17 mmol Trolox equiv./L, respectively) (P=0.003). Uric acid and albumin concentrations were lower in the study group than in the control group. Based on these results, we concluded that oxidants were increased and antioxidants were decreased in the cerebral palsy group, and, as a result, the oxidative/antioxidative balance shifted to the oxidative side in children with cerebral palsy.

Oxidative Status and DNA Damage in Chidren With Marasmic Malnutrition

Malnutrition as a lack of several substances containing antioxidants such as vitamins and micronutrients, while showing a predisposition for lipid peroxidation and DNA damage, is also characterized by a slowing down of the metabolic processes, which may then have protective properties against DNA damage due to a reduction in endogenous free radical production. This study aimed to examine the oxidative status and DNA damage in cases of marasmus. The study comprised 28 infants aged 6–24 months with marasmus only and 28 age‐matched healthy infants. DNA damage was examined by the alkali single cell electrophoresis method (Comet assay) on mononuclear leukocytes. The total oxidant status (TOS) and total antioxidant status (TAS) were measured by colormetric auto‐analyzer and the oxidative stress index (OSI) was calculated. The TOS, TAS, and OSI levels of the patient group were found to be significantly lower compared to the control group (P < 0.01, P < 0.01, P < 0.01, respectively). No statistically significant difference was found between the two groups in terms of mononuclear leukocyte DNA damage (P > 0.05). The findings of this study showed that in marasmus cases, the oxidative and antioxidative processes, which have a counteractive effect, decreased together. The other results of the study indicate that there is no increase in DNA damage in marasmus cases. J. Clin. Lab. Anal. 26:161‐166, 2012.

Epidemiological findings and clinical and magnetic resonance presentations in subacute sclerosing panencephalitis.

Subacute sclerosing panencephalitis (SSPE) is a rare, progressive, inflammatory neurodegenerative disease. This study investigated the relationships of clinical stage with epidemiological and magnetic resonance imaging (MRI) findings in SSPE by retrospective review of 76 cases (57 male) diagnosed by typical periodic electroencephalographic features, clinical symptoms and elevated measles antibody titre in cerebrospinal fluid. Clinical stage at diagnosis was I or II in 48 patients, III in 25 and IV in three. Prominent findings at presentation were atonic/myoclonic seizures (57.9%) and mental deterioration with behaviour alteration (30.3%). Frequent MRI findings (13 – 32 patients) were subcortical, periventricular and cortical involvement and brain atrophy; the corpus callosum, basal ganglia, cerebellum and brainstem were less frequently involved. Five patients had pseudotumour cerebri. Cranial MRI at initial diagnosis was normal in 21 patients (19 stage I/II, two stage III/IV). Abnormal MRI findings were significantly more frequent in the later stages, thus a normal initial cranial MRI does not exclude SSPE, which should, therefore, be kept in mind in childhood demyelinating diseases even when the presentation is unusual.

Interictal serum S-100B protein levels in intractable epilepsy: a case-control study.

Epilepsy is the most common neurologic disorder of childhood. In approximately 6-14% of all patients with epilepsy, complete seizure control is difficult to achieve with current antiepileptic treatments. Several current studies have shown in both animals and people that the lengthening of epileptic seizures and frequent recurrence increases the likelihood of neuronal damage. S-100B protein is the most analyzed brain derived peripheral biochemical marker in brain damage. This study aimed to evaluate interictal serum S-100B protein levels in children diagnosed with intractable epilepsy. A group of 32 patients with intractable epilepsy and 25 healthy controls were recruited. Serum S-100B protein levels were measured using a commercially available electrochemiluminescence immunoassay (ECLIA kit, as supplied and according to the manufacturers standards. The serum S-100B protein levels of the patient group in the study were found to be 0.094±0.011 μm/L, and 0.083±0.014 μm/L in the age-matched control group. The difference between the groups was determined to be statistically significant (P=0.004). In conclusions, it can be said that as the serum S-100B protein levels of the patients with focal epilepsy were high compared to those of the control group, this can be reliable peripheral biomarker for neuronal damage in patients with focal intractable epilepsy.

PD-1 gene polymorphism in children with subacute sclerosing panencephalitis.

Subacute sclerosing panencephalitis (SSPE) is a progressive inflammatory and degenerative disorder of the central nervous system. Several factors influence the risk of chronic brain infection with the mutant measles virus. However, to date, no pathogenic mechanism that may predispose to SSPE has been determined. Studies have indicated that specific polymorphisms in certain host genes are probably involved in impairing the ability of host immune cells to eradicate the measles virus in SSPE patients. Programmed cell death protein 1 (PD-1), a member of the CD28 family, is a negative regulator of the immune system. The purpose of our study was to investigate whether PD-1 gene polymorphisms affect susceptibility to the development of SSPE in Turkish children. In total, 109 subjects (54 SSPE patients and 55 healthy controls) were genotyped for the PD-1.9 C/T (rs2227982) single-nucleotide polymorphism (SNP). The distributions of T alleles in the PD-1.9 polymorphism in SSPE patients and healthy controls were 2.8 and 10.9%, respectively. There was a statistically significant difference between the groups; the 95% confidence interval (CI) was 0.06 to 0.85 and the odds ratio (OR) was 0.23 (χ(2) test). Thus, we identified an association between SSPE and the PD-1 rs2227982 gene polymorphism; the frequency of T alleles was higher in controls than in SSPE patients.

Association of interleukin 18, interleukin 2, and tumor necrosis factor polymorphisms with subacute sclerosing panencephalitis.

Subacute sclerosing panencephalitis (SSPE) is a progressive inflammatory and degenerative disorder of the central nervous system. The measles virus (MV) and host and environmental factors are involved in the development of SSPE, but the precise mechanism by which the MV causes SSPE is still unknown. Studies have indicated that in SSPE patients, specific polymorphisms of certain genes are most likely involved in impairing the hosts ability to eradicate the MV. The purpose of our study was to elucidate the role of polymorphisms in the genes encoding interleukin (IL)-2, IL-18, and tumor necrosis factor alpha (TNF-α) in the development of SSPE. Using the polymerase chain reaction with sequence-specific primers, the single-nucleotide polymorphisms (SNPs) of the promoter regions of IL-2 (-330), TNF-α (-308), and IL-18 (-137 and -607) were studied in 54 patients with SSPE and 72 healthy controls. The frequency of SSPE patients with the AA genotype of IL-18 at position -607 was significantly higher than the frequency of those with the CC genotype (p<0.001, odds ratio [OR]: 5.76), and a significantly higher proportion of patients had the C allele at -137 compared with the controls (p=0.002, OR: 2.72). In a haplotype analysis of two SNPs in the IL-18 gene, the frequency of the CA haplotype was significantly higher in SSPE patients (p<0.001, OR: 3.99) than in the controls. The IL-2 (-330) and TNF-α (-308) polymorphisms revealed no significant differences. In conclusion, these data suggest that the IL-18 gene polymorphisms at position -607 and -137 might be genetic risk factors for the SSPE disease.

Rapidly improving, severe, acute myocarditis after a scorpion bite: an extremely rare complication and successful management

Scorpion bites are common in various countries worldwide. In Turkey, scorpion bite cases occasionally are reported in rural areas. Such bites infrequently have serious clinical sequelae, including acute pulmonary edema, cardiogenic shock, and even death. In this case, a scorpion bite led to myocardial injury and consequent pulmonary edema and third degree mitral insufficiency. With aggressive medical management, the patient recovered within a few days. We present this case because of its unusual presentation, unexpected complications, and prompt resolution. Scorpion bites are frequent in certain areas of the world where temperatures are warm and a rural lifestyle predominates [1,2]. Most scorpion bites are harmless; however, some patients present with neurotoxic or cardiotoxic manifestations [3]. In Turkey, scorpion bites occasionally are reported in rural areas. Below, we present the case of a scorpion bite with an extremely unusual presentation and complications. A 12-year-old boy was bitten by a scorpion on the first hallux of his foot. Initially, he was admitted to another Fig. 1 Pretreatment (left, on admission) and posttreatm 0735-6757/

Pseudotumor Cerebri Secondary to Subacute Sclerosing Panencephalitis

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