Özmert M.A. Özdemir

Electrophysiological assessment of the brain function in term SGA infants.

Small for gestational age (SGA) infants are defined as babies having a birth weight below the 10th percentile for gestational age. A great number of studies have shown that children with SGA have an increased risk of impaired neurodevelopment. Electroencephalography (EEG) is an excellent method for measuring brain maturation in newborns. In this study, the effect of SGA on the maturation of cerebrocortical electrographic activity was investigated by the EEG and also analyzed with power spectral analysis. Serial EEGs were performed in 40 term SGAs, and 20 term appropriate for gestational age (AGA) infants in 1st week, 1st and 3rd month. Power spectral analysis was performed quantitatively in five channels (Fp1-C3, C3-O1, Fp2-C4, C4-O2, and Cz-C4 channels). Amplitude levels of the SGA group were significantly lower than the AGA group in all records. Delta frequency was the major frequency component in the groups. Delta frequency activities in the midline vertex region were decreased in the AGA group with increasing postconceptual age while the activities of the SGA group were increased. Contrarily, beta frequency activities in the midline vertex region were increased in the AGA group with increasing postconceptual age while these activities of the SGA group were decreased. Theta frequency activities in the fronto-central regions were lower in the SGA group. In terms of the vertex, k-complex, and sleep spindle, there was no difference between the two groups. We conclude that cerebrocortical electrophysiological maturation has been delayed in term SGA infants during the first three months of postnatal life.

Are C-reactive protein and homocysteine cardiovascular risk factors in obese children and adolescents?

Background: Several prospective epidemiological studies have demonstrated that high‐sensitivity C‐reactive protein (hsCRP) and plasma homocysteine (hcy) are predictors of future coronary events among healthy men and women. The aim of the present study was therefore to investigate a possible relationship between hsCRP, hcy levels and body mass index (BMI), relative weight (RW), serum leptin levels, and cardiovascular risk factors in obese children and adolescents.

Protective effects of clarithromycin in rats with hypoxia/reoxygenation-induced intestinal injury.

BACKGROUND This study was designed to determine the role of oxidative stress, nitric oxide (NO), and glutathione-related antioxidant enzymes in rat pups with hypoxia/reoxygenation (H/R)-induced bowel injury and to evaluate the potential benefits of prophylactic clarithromycin. METHODS One-day-old Wistar albino rat pups (N = 21) were randomly divided into 3 groups: group I (control), group II (exposed to H/R), and group III (clarithromycin + H/R). Clarithromycin was administered (40 mg/kg) subcutaneously to group III for 3 days. On the fourth day, all rats except controls were exposed to H/R and were killed at 6 hours after H/R. Histopathologic injury scores (HIS), malonyldialdehyde, glutathione (GSH), glutathione-peroxidase (GSH-Px) activities, and NO levels were measured on intestinal samples. RESULTS Whereas there was no difference for malonyldialdehyde levels among groups, HIS and NO levels were higher in group II than groups I and III (P < .05). However, GSH and GSH-Px activities were lower in group II than groups I and III (P < .05). Clarithromycin significantly increased GSH and GSH-Px activities and reduced HIS and NO levels in group III. CONCLUSION This study showed that oxidative stress and NO contributed to the pathogenesis of H/R-induced bowel injury and that clarithromycin had a protective effect on bowel injury owing to anti-inflammatory and antioxidant effects.

The protective effect of docosahexaenoic acid on the bilirubin neurotoxicity

Usually, all newborns demonstrate high serum unconjugated bilirubin (UCB) level. UCB may induce adverse effects in the central nervous system. We aimed to evaluate the cytotoxic effects of UCB and the protective effects of docosahexaenoic acid (DHA) on astrocyte cell cultures. The viability of astrocyte cells decreased after UCB treatment in a dose-dependent manner. Pre-incubation of DHA prevents the cells from UCB-mediated neurotoxicity. Our results shown that UCB leads to inhibition of antioxidant enzymes superoxide dismutase (SOD), catalase and GPx activity and induction of apoptosis. But only 4-h pretreatment of DHA can suppress of UCB-mediated inhibition of antioxidant enzymes SOD, catalase and GPx activity and induction of apoptosis in astrocytes. Our results strongly indicated that DHA has a protective effect on UCB-mediated neurotoxicity through inhibition apoptosis and antioxidant enzymes activity of SOD, CAT and GPx in rat primer astrocyte cell line

Protective effects of Ginkgo biloba extract in rats with hypoxia/reoxygenation-induced intestinal injury.

BACKGROUND The purpose of this study is to investigate the protective effects of Ginkgo biloba extract (EGb 761) in rat pups with hypoxia/reoxygenation (H/R)-induced bowel injury. METHODS One-day-old Wistar albino rat pups (n = 21) were randomly divided into 3 groups: group 1 (control, untreated and not exposed to H/R, n = 7), group 2 (untreated but exposed to H/R, n = 7), and group 3 (EGb 761 + H/R, n = 7). Ginkgo biloba extract was administered (100 mg/kg per day, subcutaneously) to group 3 for 3 days. On the fourth day, all animals except controls were exposed to H/R and were killed 6 hours after H/R. Histopathologic injury scores (HIS), malondialdehyde, glutathione (GSH), GSH-peroxidase (Px) activities, and nitric oxide (NO) levels were measured on intestinal samples. RESULTS Although the control group had normal HIS, group 2 had grade 3 HIS. In contrast, group 3 had minimal HIS, and these results were significantly better than those of group 2 (P < .001). Malondialdehyde and NO levels of group 3 were significantly lower than those of group 2 (P < .01). Glutathione and GSH-Px activities of group 1 were higher than those of groups 2 and 3 (P < .05). However, there were no significant differences for GSH and GSH-Px activities between groups 2 and 3. CONCLUSIONS This study showed that hypoxia and NO contributed to the pathogenesis of H/R-induced intestinal injury and that prophylactically administered EGb 761 had a protective effect on bowel injury.

Familial mutation in caffey disease with reduced penetrance: a case report

Caffey disease is a rare condition of early infancy, characterized by soft tissue swelling, bone lesions, and hyperirritability. Its typical radiological finding is periosteal new bone formation. It can be sporadic or inherited in an autosomal dominant manner. There is no specific treatment. In symptomatic cases, non-steroidal anti-inflammatory drugs such as ibuprofen, indomethacin, or naproxen can be used. This is a report of an infant who presented with restlessness, irritability, and swelling over his shins, diagnosed as Caffey disease. Although there was no family history, the genetic analysis revealed heterozygous missense mutation (c.3040C > T) in type-I-collagen-alpha-1-chain gene in the patient in addition to his mother, grandmother, aunt, and cousin. After indomethacin therapy, the complaints of the patient were completely resolved and his bone lesions were significantly improved. This case report is a familial form of Caffey disease from Turkey, with proven heterozygous mutation in the patient and the family members.

Ischemia-modified albumin in preterm infants born to mothers with pre-eclampsia

Pre‐eclampsia (PE) carries an increased risk for maternal and/or fetal mortality or serious morbidity. PE is associated with ischemia and increased oxidative stress in the placenta, which may lead to modification of plasma albumin to ischemia‐modified albumin (IMA). The aim of this study was to investigate IMA and hematological parameters in mothers and in premature infants in normal and in pre‐eclamptic pregnancies.

Caffeine prevents bilirubin-induced cytotoxicity in cultured newborn rat astrocytes

Abstract Objective: Unconjugated bilirubin (UCB) may cause neurotoxicity in preterm neonates due to immaturity of UGT1A1 leading to bilirubin accumulation in the brain. Caffeine used in the treatment of apnea of prematurity was reported to decrease mechanical ventilation requirement, the frequencies of bronchopulmonary dysplasia, patent ductus arteriosus, cerebral palsy and neurodevelopmental disorders in very low birth weight infants. However, the effect of caffeine on hyperbilirubinemia was not yet clarified. Methods: We used astrocyte cell cultures obtained from 2-day-old Wistar albino rats via modified Cole and de Vellis method. UCB concentration toxic to 50% of astrocytes, and caffeine concentration increasing cell viability 100% were used in experiments. While no medication was applied to the control group, UCB (50 μM) and caffeine (100 μM) were applied to the bilirubin and caffeine groups for 24 h. Prophylactic and therapeutic caffeine groups were treated with caffeine 4 h before and after UCB exposure. The effects of caffeine were investigated in rat astrocytes exposed to UCB in terms of cell viability, apoptosis, antioxidant defense, proinflammatory cytokines, and Toll-like receptor (TLR)s. Results: Compared to the control group, UCB increased apoptosis, malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, total nitrate/nitrite, and TLR4 levels, and decreased cell viability, catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD) activities, glutathione, and TLR9 levels (for all p < .001). Conversely, prophylactic and therapeutic caffeine improved the detrimental effects of UCB. Conclusions: Caffeine seems encouraging for the prevention and treatment of bilirubin neurotoxicity in rats by means of its antiapoptotic, antioxidant, anti-inflammatory, anti-nitrosative, and anti-TLR-4 properties.

P389 Atypical prune-belly syndrome presented with isolated fetal ascite

Introduction Prune-Belly syndrome (PBS) is characterised by abdominal wall absence/hypoplasia, urinary system anomalies, and bilateral undescended testicle triad. The incidence is one in 30,000–50,000 live births, and 95% of the cases are male. Herein, we introduced a preterm infant with atypical PBS presented with fetal urinary ascite, abdominal wall defect, and bilateral undescended testicle. Case A male twin premature neonate was born 2800 gr (10–50p) at 34 weeks gestation by caesarean section due to preterm labour and fetal distress. His Apgar score is 6 and 8 at postnatal 1st and 5th minute. His parents were non-consanguineous. It was learned the presence of fetal ascite at 21st gestational age. On physical examination, abdominal distension due to fluid, bilateral undescended testicle were detected; abdominal muscles could not be palpated; eye examination and hearing test were normal. The abdominal ultrasonography (US) of the patient showed diffuse ascites, hypoplasia of the abdominal wall muscles, and bilateral testes in the inguinal canal. On his abdominal magnetic resonance imaging, ascites was detected. Transfontanel US, portal vein doppler US and voiding cystourethrography were normal. Echocardiography revealed patent ductus arteriosus, ventricular and atrial septal defect. Pericardial effusion was not observed. There were no anomalies of extremities and vertebra on his radiograms. The patient’s karyotype (male, 46, XY), routine biochemical evaluation, ferritin levels, viral serologies (TORCH, parvovirus B19) and metabolic scans were normal. While urea and creatinine levels were 19 mg/dl and 0.49 mg/dl in the serum, their levels were 23 mg/dl, and 0,55 mg/dl in the ascite fluid evacuated by paracentesis so, ascite fluid was considered urinary ascite in this case. The patient was discharged at 21 days of age. Conclusion Fetal urinary ascite may be seen even if there is no coexisting urinary anomaly in the cases with PBS.

P386 Acquired lung cysts in a premature infant with congenital cytomegalovirus infection

Introduction Cystic changes in the lung due to congenital/perinatal cytomegalovirus (CMV) infection have been reported in a few cases in the literature. In this case report, we presented a preterm infant with congenital CMV infection developed lung cysts during her clinical follow-up. Case A female neonate was delivered by caesarean section at 35 gestational week due to fetal distress. Her birthweight was 1870 g (10-50th percentile) and Apgar scores 7 and 9, first and fifth minutes, respectively. She was transferred to our intensive care unit because of the prematurity and ventriculomegaly. It was reported that fetal ultrasonography revealed bowel hyperechogenicity at the 18th week of gestation. The serologic examination was negative for CMV IgM. Fetal magnetic resonance imaging was normal and fetal karyotype was 46, XX. The lateral ventricles were observed to be dilated in the repeated ultrasonography performed at 34th week. On physical examination she was well-appearing, there was no abnormality except for hepatosplenomegaly (3 cm below costal margin) and bilateral chorioretinitis. She failed auditory-brainstem-response test. Cranial ultrasonography performed after birth revealed bilateral ventriculomegaly and germinal matrix haemorrhage. Complete blood count showed thrombocytopenia. CMV IgM was reactive and CMV PCR was positive (7.60E+4 cp/mL) in serologic examination. Chest radiography was normal. Intravenous ganciclovir therapy was initiated to the patient at the dose of 12 mg/kg/day due to symptomatic congenital CMV infection. At the postnatal 20th day, a cystic lesion was detected in the basal part of the left lung on the abdomen radiography performed for nutrition intolerance and abdominal distension. Thoracic computed tomography revealed pulmonary cavitary lesions, the largest of them was located in the left lower lobe posterior basal segment. No signs of respiratory distress were detected during this period, infection parameters and blood culture were negative. Cystic lesions in the lung regressed during her clinical follow-up. She was discharged with oral valganciclovir treatment when she was 55 days old. Conclusion It should be kept in mind that congenital CMV infection may cause lung cysts.