Serdal Güngör

Proinflammatory Cytokines and Leptin Are Increased in Serum of Prepubertal Obese Children

It has not yet been shown in prepubertal children how cytokines, leptin, and body mass, as well as parameters of obesity are interrelated. The aim of this study was to explore the relation between circulating levels of some cytokines with leptin and body mass index. A case control study was carried out in obese children of both sexes. An obese group was carried out with 63 school prepubertal children and a control group comprised the same number of nonobese children paired by age and by sex. Mean serum leptin concentration was significantly higher in the obese children at 19.9 ± 7.4 ng/mL, than the control group (7.9 ± 5.1 ng/mL). Serum IL-1β, IL-6, and TNF-α levels were also significantly higher in the obese group than controls (33.0 ± 8.9, 45.2 ± 11.8, and 9.2 ± 2.3 pg/mL, versus 3.6 ± 1.0, 13.1 ± 3.9, and 3.9 ± 1.0 pg/mL, resp). In controversy, serum IL-2 level was diminished in the obese group as 0.4 ± 0.1 versus 0.9 ± 0.1 U/L. Obesity may be a low-grade systemic inflammatory disease. Obese prepubertal children have elevated serum levels of IL-1β, IL-6, and TNF-α which are known as markers of inflammation.

A Chryseobacterium meningosepticum Outbreak in a Neonatal Ward

OBJECTIVE To report epidemiologic, bacteriologic, and clinical features of a Chryseobacterium meningosepticum outbreak. DESIGN Outbreak investigation. SETTING A neonatal intensive care unit (NICU) of a referral teaching hospital. METHODS During 2 weeks in September 2001, four neonates in the NICU developed sepsis and underwent laboratory investigation. Multiple samples were obtained for cultures from endotracheal tubes, mechanical ventilators and humidifier boxes, infant incubators, parenteral and antiseptic solutions, feeding bottles, sinks, faucets, doors, and healthcare workers. RESULTS C. meningosepticum was isolated from the blood cultures of four patients. The first isolate was identified 5 days after the death of the index case. Although all isolates were ciprofloxacin susceptible in vitro, the remaining three patients did not respond to ciprofloxacin therapy given for 6 or 7 days. Therapy was switched to vancomycin and rifainpin and all three patients survived, with one having a complication (hydrocephalus). Environmental surveillance revealed C. meningosepticum in the stock lipid solution as the source of the epidemic. The outbreak was controlled after discontinuation of intravenous lipid solution, restriction of further neonatal admissions, and thorough disinfection of the unit and its equipment. CONCLUSION Early identification of an epidemic and its source is important in avoiding morbidity and mortality. A contaminated lipid stock bottle was the source of this outbreak associated with multiple cases and one death.

Cerebral malaria owing to Plasmodium vivax: case report.

Abstract Cerebral malaria is a diffuse encephalopathy associated with seizures and status epilepticus which can occur in up to one-third of children with severe malaria, particularly that caused by Plasmodium falciparum. We report a unique case of P. vivax infection complicated by status epilepticus. A 4-year-old boy was admitted to the emergency outpatient clinic with intractable seizures for the previous hour. During resuscitation, two episodes of left-focal tonic convulsions occurred and he received phenytoin. Because of a history of P. vivax infection in the family 3 months previously, a blood slide for malaria was undertaken. Thin blood smears demonstrated P. vivax. He was treated with chloroquine and primaquine. An initial EEG was normal but after 3 months of follow-up a second EEG showed generalised epileptic activity. Rarely, cerebral malaria is a presenting complication or occurs during the course of P. vivax infection. In endemic areas such as Turkey, the possibility of cerebral malaria should be considered.

The Role of Ghrelin in Weight Gain and Growth in Epileptic Children Using Valproate

Ghrelin is a major hormone, regulating the energy balance of the body. Weight gain is a significant side effect of valproic acid, which has not been clearly identified pathogenetically. The aim of this study was to investigate the effect of valproic acid on ghrelin and its potential effects on weight gain and growth. Each patient and control group consisted of 35 children aged 3 to 15 years. Fasting serum glucose, insulin, C-peptide, leptin, ghrelin, insulin-like growth factor-1, and insulin-like growth factor binding protein-3 levels were measured in patients treated with valproic acid before and at month 6 of treatment. A significant increase in body weight, body mass index, height, and height standard deviation scores was observed in all patients after 6 months of treatment. Significant increases in growth velocity and weight gain were observed in the patient group compared with controls at 6 months of therapy. A significant increase in serum ghrelin levels (P < .01) was detected at the same time in the study group. A negative correlation of ghrelin with insulin-like growth factor-1 and insulin-like growth factor binding protein-3 was detected. Serum ghrelin levels were significantly increased (P < .05), and insulin-like growth factor-1 and insulin-like growth factor binding protein-3 levels were significantly decreased ( P < .01 and P < .05, respectively) in the prepubertal group at 6 months of treatment, but no significant change was observed in the pubertal group. Consequently, ghrelin levels significantly increase in the prepubertal children treated with valproic acid. The weight gain in using valproic acid may be associated with the increase in ghrelin level in the early treatment period.

Malnutrition and Obesity in Children With ADHD

Objective: Low threshold of dissatisfaction and frustration in child and adolescent patients with ADHD lead to changes in dietary pattern with contribution to the development of obesity and other nutritional disorders. Methods: A total of 362 patients with the diagnosis of ADHD and 390 children without any chronic disease were included to the study. We evaluated the anthropometric measurements for all cases. Results: The overweight/obese cases according to weight for height (WFH) and body mass index scores were more likely in ADHD cases than control group. Malnourished cases according to WFH were more common in ADHD cases. Patients with weight standard deviation scores between <−2 and >2 were significantly higher in ADHD cases than the control group patients. Conclusion: Frequency of malnutrition and overweight/obese patients was found higher in ADHD cases compared with control group, and this situation suggested that ADHD is a risk factor for the development of eating disorders.

Frequency of celiac disease in attention-deficit/hyperactivity disorder.

Objective: Although it is well known that celiac disease (CD) is associated with neurologic disorders, association with psychiatric problems is not well defined. In this report, we aimed to detect CD prevalence in patients with attention-deficit hyperactivity disorder (ADHD). Methods: A total of 362 patients between the ages 5 and 15 years with the diagnosis of ADHD according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) diagnostic criteria and 390 sex- and age-matched healthy children were included in the present study. Serum levels of tissue transglutaminase (tTg) immunoglobulin (Ig) A and IgG were studied in both groups. Serum IgA levels were also studied in patients with positive tTG IgG for the exclusion of selective IgA deficiency. Endoscopic duodenal biopsy was provided in seropositive patients, whose parents approved the procedure. Biopsy samples were evaluated according to Marsh-Oberhuber classification. Results: tTg IgA was positive in 4 patients with ADHD (1.1%). Endoscopic duodenal biopsy was suggestive of CD in one of them (0.27%). tTg IgA was positive in 3 of control group patients (0.8%). Duodenal biopsy of the only patient from control group, who underwent upper gastrointestinal endoscopy, revealed normal intestinal mucosa. Conclusions: The seropositivity rates for CD were found similar in ADHD and control groups. Thus, neither routine screening for CD nor empirical recommendation of gluten-free diet seems necessary in children with ADHD.

Neuroimaging Findings in Hyperargininemia

In hyperarginenemia, there is a defect in argininase enzyme, which is a catalyzer of urea cycle. Though the pathogenesis of neuronal damage in hyperargininemia is not clear, high serum and cerebrospinal fluid arginine levels can be directly related with neuronal damage. In this study, our aim was to assess brain magnetic resonance images and magnetic resonance spectroscopy (MRS) patterns of two siblings with hyperarginenemia. We acquired single voxel MRS from the white matter to show the myelination pattern and to figure out any abnormal peak of metabolite stored due to enzymatic defect. We observed mild cerebral and cerebellar atrophy and infarct at bilateral posterior putamen and insular cortex localization on conventional images and elevated choline/creatine ratios and abnormal peak at 3.8 ppm, most likely representing arginine deposition. To the best of our knowledge, this is the first article revealing the brain MRS pattern of hyperargininemia. We reported the clinical and imaging findings of patients and discuss the correlation.

Doppler Studies in Normal Kidneys of Preterm and Term Neonates Changes in Relation to Gestational Age and Birth Weight

The purpose of this study was to establish normative data for the flow velocity waveform indices of the renal arteries in the neonatal population and to evaluate the differentiation between birth weight and gestational age of neonates.

Plasma Leptin, Adiponectin, Neuropeptide Y Levels in Drug Naive Children With ADHD

Objective: ADHD is one of the most common childhood psychiatric disorders. Research indicates that there is some link between obesity/overweight and ADHD, though the mechanism of this association remains uncertain. It is the aim of the present study to explore the association between ADHD, obesity, and plasma leptin, neuropeptide Y (NPY), and adiponectin levels. Method: Thirty-six patients diagnosed with ADHD were included in the study. The control group consisted of 40 healthy children and adolescents who had similar age and gender features with the patient group. Plasma leptin, adiponectin, NPY levels were measured, and body mass index (BMI), weight for height, and standard deviation scores (SDS) of height, weight, and BMI were calculated. Results: No significant difference was found between patients and healthy children in terms of BMI and BMI percentile. Participants were classified into three groups according to their weight to height values. There was no significant difference between the two groups, but 10% of the control group and 30.6% of the ADHD group were classified as overweight, which was 3 times higher than the control group. The adiponectin plasma level was significantly lower and leptin/adiponectin (L/A) ratio was significantly higher in the ADHD group. There was no significant difference between serum NPY levels. In the ADHD group, the mean leptin plasma level was high, but was not statistically significant. Conclusion: We think that a low adiponectin level and high L/A ratio may be the underlying mechanism of the obesity in ADHD patients.

Multiple sulfatase deficiency: A case series of four children

Multiple sulfatase deficiency is biochemically characterized by the accumulation of sulfated lipids and acid mucopolysaccharides. The gene sulfatase-modifying factor 1 (SUMF1), recently identified, encodes the enzyme responsible for post-translational modification of a cysteine residue, which is essential for the activity of sulfatases. We describe clinical findings and mutation analysis of four patients. The patients presented with hypotonia, developmental delay, coarse face, ichthyosis, and hepatosplenomegaly. The diagnosis was made through clinical findings, enzymatic assays, and mutation analysis. We were detected to be homozygous for a novel missense mutation c. 739G > C causing a p.G247R amino acid substitution in the SUMF1 protein.