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Background: Despite technical and scientific improvements in neonatal medicine, there is still no efficient treatment for or prevention of neonatal necrotizing enterocolitis (NEC)., Objective: The aim of this study was to determine the protective effect of surfactant on intestinal cells in hypoxia-induced experimental NEC in rats., Methods: The study was performed on Sprague Dawley rat pups divided into three groups. Group 1 served as nonhypoxic controls (n = 15). Group 2 rats (untreated; n = 15) were subjected to hypoxia and reoxygenation (H/O). Group 3 rats (surfactant treated; n = 15) were treated with surfactant (Curosurf; 400 mg/kg enterally) for 5 days and then subjected to H/O. All animals were killed on day 5, and histological and biochemical examinations were performed on intestinal samples., Results: There were no histopathological changes in the control group. The histological findings in untreated rats were similar to those seen in neonatal NEC, with destruction of villi and crypts and extension to the muscularis layer. The mean histological grade of group 1 was 0.2 (range 0-1), and in group 2, it was 2.1 (range 1-3). There was no statistical difference between the histological grades of groups 2 and 3 (p > 0.05). However, there was a difference between the groups that did and did not receive surfactant with regard to superoxide dismutase (SOD), glutathione peroxidase (GSH) and malondialdehyde (MDA)., Conclusion: Although surfactant did not have a protective effect on histological changes in hypoxic neonatal rat intestine, it improves biochemical markers such as SOD and GSH and reduces MDA levels., (Copyright © 2012 S. Karger AG, Basel.)

Objective: To evaluate the efficacy of inhaled salbutamol, a beta-2 adrenergic agonist, for the treatment of transient tachypnea of the newborn (TTN) and to determine whether inhaled salbutamol is safe in newborn infants., Study Design: Inhaled salbutamol or normal saline solution was administered to 54 infants with gestational ages ranging from 34 to 39 weeks and TTN. The response to salbutamol therapy was evaluated by determining respiratory rate, clinical score of TTN, level of respiratory support, and fraction of inspired oxygen before and at 30 minutes and 1 and 4 hours after salbutamol nebulization., Results: Among the 54 infants with TTN, 32 received salbutamol and 22 received normal saline solution. After one dose, the salbutamol group showed significant improvements in respiratory rate, clinical score of TTN, fraction of inspired oxygen, and level of respiratory support (P < .05). After treatment, the mean pH, partial pressure of arterial oxygen, and partial pressure of arterial carbon dioxide values were better in the salbutamol group when compared with the placebo group (P < .05). Duration of hospitalization in the neonatal intensive care unit was also shorter for the salbutamol group (P < .05)., Conclusion: Inhaled salbutamol treatment was effective with respect to both clinical and laboratory findings of TTN and without adverse events., (Copyright © 2011 Mosby, Inc. All rights reserved.)

Bronchopulmonary dysplasia (BPD) survivors from the surfactant era were evaluated by echocardiography in a few studies and no significant differences were found between BPD and non-BPD children. In this study, we evaluated these children with myocardial performance index (MPI), which was obtained by tissue Doppler echocardiography (TDE) in addition to the conventional methods. Fifteen children with BPD who did not have any cardiopulmonary symptoms at the time of the study were examined. All children were studied with M-mode, two-dimensional and DE. Pulmonary artery systolic pressures (PAPs) were estimated from tricuspid regurgitant velocity, and MPI for both ventricles were obtained by TDE. Results were compared with those of term-born, age- and sex-matched control children. While the variables obtained by M-mode and DE did not differ between the groups, the right and left ventricular MPI were found to be significantly higher in the BPD group compared with the control group (mean right ventricular MPI 0.48 +/- 0.04 vs. 0.41 +/- 0.05; mean left ventricular MPI 0.47 +/- 0.05 vs. 0.39 +/- 0.06). In addition, mean PAPs values of the patients were found to be significantly higher than those of the controls (30.4 +/- 6.9 mmHg vs. 23.3 +/- 5.3 mmHg), and there was a positive correlation between PAPs and right ventricular MPI values in the BPD group (r = 0.5). While routine echocardiographic examinations revealed no difference between the groups, MPI measurements by TDE technique yielded significantly higher values in the BPD group. To this extent, our study is the first to show that survivors of BPD may, in fact, have a subclinical ventricular dysfunction.

Humerus fractures in neonates are rare, but can occur during cesarean section and bilateral humerus fracture has not been reported yet. This case represents a newborn delivered by cesarean section for breech presentation which resulted in bilateral humerus fracture.

Genetic polymorphisms in the gene that codes for endothelial nitric oxide synthase (eNOS) have been associated with less nitric oxide availability and with various cardiovascular diseases in humans. The objective of this study was to analyze the genotype distributions and allele frequencies for the Glu298Asp (G894T) and T(-786)C polymorphisms of the eNOS gene among neonates with respiratory distress in comparison to healthy control subjects. Fifty premature neonates with respiratory distress and 55 neonates without any respiratory problem were included in the study. Genomic DNA from all the neonates was analyzed by polymerase chain reaction. A polymerase chain reaction-restriction fragment length polymorphism analysis of eNOS gene polymorphisms was performed, and the results were compared. There were no significant differences between the groups regarding either genotype distributions or the allele frequencies for the Glu298Asp and T(-786)C polymorphisms. These results suggest that eNOS Glu298Asp and T(-786)C polymorphisms are not associated with development of respiratory distress.

The aim of this study was to investigate the differences in mean platelet volume (MPV) between neonates with and without neonatal respiratory distress syndrome (RDS). Eighty-three premature infants who were admitted to the neonatal intensive care unit were included in the study. Forty-four of these infants were diagnosed as having RDS and the other 39 infants were non-RDS patients. Infants born to mothers with pre-eclampsia, or a drug history that had negative effects on platelet count, perinatal hypoxia, sepsis and necrotizing enterocolitis were excluded. Blood collection was done on the first and third days of life. There were no demographic, gestational or platelet count differences between groups, but MPV was higher in RDS patients and this difference was statistically significant (P= 0.011). High platelet volumes in RDS patients is probably related to young platelet production and may be a result of increased platelet consumption in pulmonary damage due to RDS.

Cystatin C (CysC) is a low-molecular-mass protein (13,343 dalton, 120 amino acids) belonging to the cystatin superfamily of reversible inhibitors of cysteine proteases. CysC appears to be eliminated from the circulation almost exclusively by glomerular filtration, which makes it a promising endogenous marker of renal function. CysC has been demonstrated to reflect glomerular filtration rate better than other low-molecular-weight proteins, including creatinine (Cr). We established reference values for serum CysC and compared them with Cr in 108 preterm infants by particle-enhanced nephelometric immunoassay. On the first day, serum CysC values ranged from 1.25 to 2.84 mg/L, significantly decreasing after 3 days of life. Cr levels determined simultaneously on the first day ranged from 0.05 to 1.12 mg/dl and were also significantly different from day 3 levels. Both CysC and Cr levels were independent of gender, birth weight, hemoglobin levels, and hydration state. Cr correlated negatively with gestational age (r = -0.25, p = 0.009), but not CysC. A significant correlation was found between CysC and Cr on day 1 (r = 0.21, p = 0.031), but no correlation was found according to day 3 blood samples (r = 0.19, p = 0.053). CysC is regarded as an alternative for assessing renal function in preterm neonates, but its advantages over Cr are not yet proven.

In this study, risk factors of developmental dysplasia of the hip (DDH) were evaluated. History, clinical examination and risk factors for DDH of the babies were recorded. The hips were evaluated with ultrasonography. Infantile hip ultrasonography is one of the best methods for screening of DDH. Ultrasonography is easy, repeatable and provides visualization of the cartilage part of the hip joint. Graf's method of infantile hip ultrasonography was used to evaluate the hip in this study. Both hips of 371 babies and 32 unilateral hips of 32 babies were included in the study. In 403 babies, 14 (3.4%) had DDH. There were 5 type IIB, 7 type IIC, 1 type D, and 1 type IV hips. Physiological immaturity was present in 81 hips (19% of babies). According to risk factor analysis, the only risk factor in unilateral analysis was presence of oligohydramnios (odd ratio-OR: 11.8, confidence interval-CI: 2.7-52.7). In correlation analysis, there was a correlation between female gender and swaddling. There was overall increase in DDH in female babies who were swaddled compared to those who were not. The results of this study showed that the most important risk factor was oligohydramnios for DDH. Swaddling and female gender increased the risk of the disease, but further studies in larger series are necessary for the confirmation of these results.

Enteral and parenteral glutamine supplementation in preterm infants has been shown to have some beneficial effects on neonatal morbidity and mortality, although the results are controversial. In this study, we aimed to determine if long-term glutamine-supplemented enteral nutrition affects growth parameters in very-low-birth-weight (VLBW) preterm infants. Preterm infants with a birth weight of < or = 1500 g were assigned to receive enteral glutamine supplementation (300 mg/kg/day) or placebo between 8-120 days (4 months) of life. At the end of each month, growth parameters [weight, length, head circumference, left upper mid-arm circumference (MAC) and left mid-thigh circumference (MTC)] were determined and enteral glutamine dose was adjusted according to the current weight. In VLBW infants (n = 69), the glutamine-supplemented group (n = 36) had significantly higher mean weight, length, head circumference, MAC and MTC than the control group (n=33) at the end of the fourth month. These findings suggest that long-term enteral glutamine supplementation may lead to significant improvements in growth in all body measures in VLBW infants, possibly in a time-dependent pattern.

In this study we aimed to evaluate the relationship between serum granulocyte colony stimulating factor (G-CSF) levels and absolute neutrophil counts (ANC) in infants of preeclamptic mothers. The study group consisted of 31 infants of preeclamptic mothers while the control group consisted of 24 gestational age-adjusted infants of normotensive mothers. G-CSF levels were determined by enzyme-linked immunosorbent assay (ELISA). The mean G-CSF level was 981.8 +/- 1682.5 (25.7-5924) pg/ml in the study group and 770.8 +/- 1779 (18-8526) pg/ml in control group (p > 0.05). There was no correlation between G-CSF levels and absolute or total neutrophil counts on the 1st, 2nd and 7th days in infants of preeclamptic mothers. There were positive correlations between G-CSF levels and ANC on the 1st and 7th days of life in infants of normotensive mothers. Neutropenia developed in 42.3% of the study group and in 21.7% of the control group on the 1st day of life (p > 0.05). On the 2nd day, neutropenia was observed in 61.5% of the study group and 26.1% of the control group (p = 0.013). Serum G-CSF levels were not low in neutropenic babies of preeclamptic mothers. In contrast, higher G-CSF levels in neutropenic infants suggest impaired G-CSF response in infants of preeclamptic mothers.

The objective in this study was to evaluate the angiotensin converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism in premature infants with and without respiratory distress within the first 24 hours of life. Totally, 87 premature babies who were followed up in the neonatal unit were included in the study. Of these babies, 41 had respiratory distress, and constituted the patient group. The remaining 46 babies who did not have respiratory distress constituted the control group. Blood samples were obtained from the babies within the first few days of life prior to administration of any blood product. The ACE gene insertion (I) and deletion (D) polymorphism was investigated using polymerase chain reaction method. The I/I polymorphism was frequent in the patient group and the D/D polymorphism was frequent in the control group (p < 0.05). There was no relationship between the ACE gene polymorphism and hospital stay, ventilation or oxygen consumption duration of the patients. In addition, taking into consideration the gestational age, no association was found between ACE gene polymorphism and birth weights of the babies. The I/I genotype was considered a risk factor for pulmonary disorders in neonates as the I/I variant was more frequent in the neonates with respiratory distress than in healthy newborns. The ACE I/I genotype is associated with an increased risk of respiratory disorders among premature infants and the D/D genotype is a protective factor for respiratory disorders, but these infants with ACE D/D genotype might be at risk for the development of cardiovascular disorders later in life.

Twin pregnancies are becoming common as a result of increased assisted reproduction. Studies have shown that the smaller twin of a pair is at greater risk of morbidity and mortality. Our aim was to determine if there is a relation between birth-weight discordancy and neonatal morbidity and mortality and to test the occurrence of respiratory distress syndrome (RDS) in discordant twins. For 5 years all twins admitted to our intensive care unit were included in the study. Discordance was calculated as the difference between twins' weights divided by the heavier weight. Diagnosis of RDS was made by typical clinical and radiographic methods. Multiple logistic regression was performed with gender, weight order and birth order as the independent variables and RDS as the dependent variable. Two hundred and sixty-six twin pairs with a mean gestation of 33 weeks and a mean birth-weight of 1890 g were evaluated. Multiple logistic regression revealed that being the heavier twin was a more important risk factor for RDS (odds ratio 4.5; 95% confidence interval 2.2-9.2) than being the male or second-born twin. Based on neonatal outcomes a birth-weight discordance equal or greater than 20% in twin pairs was accepted as the discordance criterion. Discordant and concordant groups were statistically different in neonatal mortality, necrotizing enterocolitis, polycytemia and hypoglycemia. Our data demonstrated that being the heavier twin is a risk factor for RDS and a birth-weight difference of 20% or more in twin pairs should be accepted as discordance.

The role of cytokines and growth factors in the pathophysiology of neonatal necrotizing enterocolitis (NEC) is not defined clearly yet. The aim of this study was to determine the effects of recombinant human granulocyte colony stimulating factor (G-CSF) on intestinal cells in hypoxia-induced experimental NEC in rats. The study was experimented on Sprague Dawley rat pups. Group 1 (untreated, n = 7) rats were subjected to hypoxia-reoxygenation (H/O) and then were returned to standard conditions. Group 2 (G-CSF treated, n = 7) rats were subjected to H/O, and then were treated with G-CSF (100 microg/kg enterally) for 5 days. Group 3 was served as nonhypoxic controls. All animals were killed on day five, and histological examination was performed on intestinal samples. There were no histopathological changes in the control group. The histological findings in untreated rats were similar to those seen in neonatal NEC, with destruction of villi and crypts with extension to the muscularis layer. Intestinal damage was mild in group 2 and these histological changes were better than group 1, and worse than group 3. The mean of histologic grade of group 1 was 2.4 (range 2-3), and in the group 2, it was 1.2 (range 0-2). A difference was found when two groups were compared with each other (P < 0.05). In an experimental model of NEC, G-CSF could have a protective effect on intestinal damage.

Pleurodesis with fibrin glue has been used to treat bronchopleural fistulas and persistent air leaks in adults and neonates. We report successful use of fibrin glue in an extremely premature infant to seal a pneumothorax that had persisted for more than one week despite high-frequency ventilation.

Objective: To compare perinatal outcomes in spontaneous twins compared with those conceived by intracytoplasmic sperm injection (ICSI)., Design: Retrospective case-control study., Patients: Cases consisted of 274 intracytoplasmic sperm injection twins, controls were 348 naturally conceived twins delivered between 1999 and 2003 in a tertiary hospital., Main Outcome Measures: Birth weight, gestational age at birth, cesarean delivery rate, perinatal mortality and morbidity, congenital anomalies, gestational diabetes and pregnancy induced hypertension., Results: Preterm deliveries (76.6% vs. 64.1% <37 weeks and 19.7% vs. 13.2% <32 weeks) and low birth weight (73% vs. 60.3% <2500 g and 19.7% vs. 12.6% <1500 g) were significantly higher in the ICSI group compared with controls. Gestational diabetes mellitus (8% vs. 2.9%) and cesarean deliveries (95.2% vs. 77.6%) were more common in cases compared with the control group. There was a significantly higher rate of perinatal morbidity (16.4% vs. 7.8%) and mortality (8% vs. 2.6%) in ICSI twins. The incidence of congenital malformations diagnosed at birth was higher in cases (4.4%) compared with controls (0.9%) but the difference was not significant when adjusted for maternal age., Conclusion: Perinatal outcomes of twins after ICSI treatment are less optimal than naturally conceived twins.

L-arginine is the precursor of nitric oxide which plays an important role on pulmonary circulation and pulmonary vascular tone. Our aim was to compare the levels of L-arginine between infants with respiratory distress syndrome and infants without respiratory distress syndrome and to determine the relationship between plasma L-arginine concentrations and severity of disease. Thirty premature infants who were admitted to our neonatal intensive care unit were included the study. Seventeen of these infants with respiratory distress syndrome were study group and the other 13 infants without respiratory distress syndrome served as controls. Blood collection was made before any treatment or intervention given to infants and tandem mass spectrometry was used for laboratory testing. In the respiratory distress syndrome group mean L-arginine level was 33.0 (+/- 11.5) mM/l, and in controls it was 79.0 (+/- 23) mM/l. This difference was statistically significant (P < 0.05). There was a reverse relationship between L-arginine levels and oxygenation index (r = 0.732, P = 0.001). If level of L-arginine is low or insufficient in respiratory distress syndrome patients' nitric oxide level would decrease in pulmonary circulation and results increased pulmonary resistance and severity of respiratory distress syndrome. We concluded that L-arginine levels are low in patients with rspiratory distress syndrome and for further investigations, supplementation of respiratory distress syndrome patients with L-arginine may decrease disease severity., ((c) 2005 Wiley-Liss, Inc.)

Neuroblastoma is the most common malignant tumor of the newborn, comprising 20% of all malignancies encountered during the neonatal period. We herein report a newborn who was born after 29 weeks' gestation and died unexpectedly at the 12th hour of life with no response to vigorous cardiopulmonary resuscitation. Autopsy findings revealed a right pararenal mass; microscopic examination showed neuroblastoma. Although the pancreas was grossly normal, its microscopic sections revealed a reduced number of islets of Langerhans and dispersion of the islet cells throughout the exocrine cells of the pancreas, and immunocytochemistry for the pancreatic hormones confirmed the dispersion of the islet cells. Final pathologic interpretation thus concluded the presence of nesidioblastosis. Furthermore, microscopic examination of the kidney showed glomerulocystic disease. Although the association of congenital neuroblastoma and nesidioblastosis has recently been defined as a new complex, neurocristopathy, the triad of congenital neuroblastoma, nesidioblastosis and glomerulocystic disease of the newborn has not been reported previously. To our knowledge, our case is the first reported newborn presenting with this triad. In conclusion, the association of nesidioblastosis and/or renal glomerulocystic disease should be kept in mind when encountering a case of congenital neuroblastoma. However, whether the presence of glomerulocystic disease in association with those other neurocristopathic pathologies is a coincidental finding or shares a common pathophysiological mechanism remains to be determined.

Objectives: Multisystem pseudohypoaldosteronism (PHA) is a rare autosomal recessive aldosterone unresponsiveness syndrome that results from mutations in the genes encoding epithelial sodium channel (ENaC) subunits alpha, beta and gamma. In this study we examined three PHA patients to identify mutations responsible for PHA with different clinical presentations., Patients: All three patients presented uniformly with symptoms of severe salt-loss during the first week of life and were hospitalized for up to a year. Beyond infancy, one of the patients showed mild renal salt loss and had no lower respiratory tract infections until 8 years of age, while the other patients continue with a severe course., Results: We sequenced the complete coding regions and intron-exon junctions of the genes encoding alpha, beta and gamma subunits of ENaC for all patients. The results revealed that the mild case represents a novel compound heterozygote including a missense (Gly327Cys) mutation in the alphaENaC gene. Sequences of relatives over three generations confirmed that the missense mutation co-segregates with PHA. This mutation was not found in 60 control subjects. The other patients with severe PHA had two homozygous mutations, a novel deletion mutation in exon 8 of the alphaENaC gene and a splice site mutation in intron 12 of the betaENaC gene. Most of the PHA-causing mutations appear in the alphaENaC gene located on chromosome 12 rather than in the beta and gammaENaC genes located tandemly on chromosome 16. However, the frequency of sequence variants in patients and control subjects showed no difference between genes., Conclusions: Severe PHA cases are associated with mutations leading to absence of normal-length alpha, beta or gammaENaC, while a mild case has been found to be associated with a missense mutation in alphaENaC. The predominance of PHA-causing mutations in the alphaENaC gene may be related to the function of this subunit.

In this study we investigated the presence of placental apoptosis in pregnancies with intrauterine meconium passage. Placental tissue samples at term were obtained from 15 normal and 15 pregnancies with intrauterine meconium passage. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling method was applied to confirm apoptosis in all placental samples. The mean apoptotic ratio was significantly higher in placentas of pregnancies with intrauterine meconium passage when compared with normal ones (0.37 +/- 0.06% and 0.29 +/- 0.07%, respectively; p < 0.01). The mean apoptotic ratios in trophoblastic and stromal cells were significantly higher in placentas of pregnancies with intrauterine meconium passage than normal placentas (0.47 +/- 0.10% and 0.36 +/- 0.11% [ p < 0.05] and 0.29 +/- 0.07% and 0.22 +/- 0.07% [ p < 0.05], respectively). Increased placental apoptosis in pregnancies with intrauterine meconium passage could be a causative factor in the pathophysiology of the disorder or a direct effect of meconium on placental cells.

Although genetic factors are assumed to have a role in the etiology of respiratory distress syndrome (RDS), specific genes underlying this susceptibility are incompletely known. The most promising candidates are the genes coding for the lung-specific protein components of the surfactant. In congenital absence of surfactant protein A in mice, lung mechanics or surfactant homeostasis is normal. However, there is an increased susceptibility to infections. The major surfactant protein A alleles, 6A(2) and 1A(0), are the general high-risk RDS alleles, while the allele 6A(3) carries a decreased risk of RDS. The allele 6A(6) is also over-represented in infants with bronchopulmonary dysplasia. To date, no human infants who lack surfactant protein A have been identified, and the human respiratory phenotype associated with the 1A(0) allele has been demonstrated to be variable, therefore, surfactant protein A polymorphisms are not currently useful for estimation of individual risk of having an affected infant. Surfactant protein B (SP-B) plays an essential role in the structure of tubular myelin. Mutations resulting in an absence of surfactant protein B have been identified. They cause a recessively inherited, progressive respiratory disease. More than 27 loss of function mutations have been identified in the surfactant protein B gene that result in lethal neonatal respiratory failure. Of the several known common variants of the surfactant protein B gene, the most common mutation is 121ins22 that accounts for 60-70% of the mutant cases. Although the frequency of the 121ins2 mutation is rare, the consistent phenotype is exhibited by infants with a homozygous genotype. The clinical presentation in infants homozygous for the 121ins2 mutation is full-term infants who develop respiratory distress within the first 12-24 hours of life. Surfactant replacement therapy fails to reverse this outcome, and without lung transplantation, they expire within the first 1-6 months of life. Surfactant protein B gene mutations may also result in milder phenotypes. These mutations resulting in reduced synthesis of SP-B appear to be family-specific and result in respiratory distress, but sometimes with more gradually progressive or chronic respiratory failure. Surfactant protein C plays a role in the stabilization of surfactant and may also have a role in the intracellular processing of the surfactant complex. Surfactant protein B is important in the intracellular processing and production of surfactant protein C. Although surfactant protein C-deficient mice are viable and survive to adulthood without obvious pulmonary abnormalities, their lung have reduced viscoelasticty. Human respiratory disease in the neonatal period caused by loss-of-function mutations in the surfactant protein C gene has not been identified. However, an autosomal dominant inherited mutation at the surfactant protein C gene causes chronic interstitial lung disease. Surfactant protein D is a member of the collectin family like surfactant protein A, therefore it opsonizes pathogens and enhances their phagocytosis by alveolar macrophages and neutrophils. Unlike surfactant protein A, it does not contribute to lowering surface tension. Surfactant protein D-deficient mice have no respiratory abnormalities at birth, but it causes development of emphysema and predisposition to specific infections. No human infant or child with respiratory distress and mutation in the surfactant protein D gene has been identified.

Measurement of ionized magnesium (IMg) provides an accurate assessment of the free form of Mg, which is the physiologically active form and is most reflective of the biologically active and not easily measurable intracellular Mg fraction. Plasma levels of IMg were measured by ion-selective electrode method in premature newborns with respiratory distress syndrome (RDS), and relationships and correlations between IMg levels and various demographic, prognostic and laboratory characteristics were investigated by comparing the premature newborns with (study group; n = 19) and without RDS (control group; n = 20) in the present study. The values of the postnatal arterial pH and base excess and plasma IMg levels were significantly different between the study and control groups, and the number of newborns with any morbidity was significantly higher in the study group. Within the study group there were significant negative correlations between the plasma IMg levels and the values of the umbilical cord arterial pH (r = -0.621, p = 0.005) and base excess (r = -0.746, p = 0.001), and the value of the postnatal arterial base excess (r = -0.585, p = 0.008). The newborns who died later had higher plasma IMg levels than those who survived (0.89 +/- 0.45 vs. 0.63 +/- 0.24 mmol/l, p = 0.026). These findings suggest that increase of plasma IMg may be due to extracellular movement of Mg, which is a principally intracellular ion, as a result of acidosis, hypoxia and probable cellular injury during the early course of RDS. The exact pathophysiological mechanism responsible for IMg increase, and whether determination of plasma IMg level, including umbilical cord blood IMg measurement, can be used as an early or predictive indicator of RDS in the diagnosis remain to be determined in further large-scale studies., (Copyright 2004 S. Karger AG, Basel)

Congenital contractural arachnodactyly (CCA, Beals syndrome) is an autosomal-dominant connective tissue disorder characterized by multiple flexion contractures, arachnodactyly, severe kyphoscoliosis, abnormal pinnae, and muscular hypoplasia. Although it is a connective tissue disorder affecting bone structure and formation, coexistence of bony fractures in CCA patients have not been reported before. In this article we report a newborn infant diagnosed with CCA who developed a femoral fracture possibly due to abnormal bone structure and birth injury in spite of cesarean delivery.

Unpredictable trancutaneous absorption of topically administered drugs and potential teratogenicity and toxicity of systemic drugs would make it mandatory to innovate more efficacious and less toxic drugs for the treatment of ichthyosis, which is not a fully curable disease in the neonatal period. In this article the clinical efficacy of 10% N-acetylcysteine emulsion in the topical treatment of congenital ichthyosis in a newborn was assessed, comparing simultaneously with 4% urea emulsion. After treating the skin of the left and right halves of the body with topical N-acetylcysteine and 4% urea, respectively, for nine days, the improvement was much more outstanding on the skin of the left half of the body when compared to the right half of the body. Topical N-acetylcysteine, to our knowledge, has not been used in a newborn with ichthyosis before, and this is the first report of a case of neonatal ichthyosis successfully treated with topical N-acetylcysteine. We conclude that 10% N-acetylcysteine emulsion, as an non-toxic and hypoallergic amino acid derivative, can be safely and efficaciously used in the topical treatment of neonatal ichthyosis, although the permanent cure may not always be possible.

The aim of this study is to determine whether circulating levels of sICAM-1 were changed in infants of preeclamptic mothers, and factors influencing these levels. Peripheral venous blood samples were obtained from preeclamptic and nonpreeclamptic pregnant women (control) and their babies in the first 2 hours post partum. The enzyme-linked immunoadsorbent assay (ELISA) technique was used to determine concentrations of sICAM-1. Compared with the control group, maternal and neonatal serum sICAM-1 levels were higher in the preeclamptic group. Neonatal levels were correlated with the maternal levels only, and there were no difference between premature and term babies and their mothers. In the control group, on the other hand, premature babies and their mothers had higher sICAM-1 levels than term babies and their mothers, with values close to those of premature group in the preeclamptic group. Neonatal sICAM-1 levels were correlated with gestational age, birth weight, and also with maternal levels. Linear regression analysis of these parameters, however, showed that only the gestational age was significant. The study suggests that perinatal sICAM-1 levels possibly are not independent from the maternal levels. High sICAM-1 levels in infants of preeclamptic mothers and premature babies might reflect the high maternal levels.

Preterm infants are more likely to have disabling cerebral palsy (CP) than term infants. It has been reported that early therapeutic approaches may be appropriate for infants at risk of neuromotor dysfunction, to minimize the degree of future handicaps. Two hundred and twenty-nine infants born at less than 34 weeks' gestation, with birth weight < or = 2,000 g, cared for in the neonatal intensive care unit of Hacettepe University Hospital between January 1997-June 1999 were included in this study. Of the 229 infants initially included, 39 (17%) were dropped from the study within the first 12 months' assessment, due to lack of participation from the families. Thirty of the remaining 190 infants were found to have perinatal hypoxia or abnormal neurosonography, and were taken as the group at risk of development of CP, thus receiving early intervention therapy; these are listed as "premature at risk". The study group consisted of 160 infants not considered at risk. These were randomly paired into two groups of 80 infants, one that was given early interventional therapy, and the control group that received no program. Eleven of the 30 infants at risk, 2 of the 80 infants from the intervention group, and 4 of the 80 from the control group were diagnosed as having CP within the first six months of life. There was no difference in the age of loss or acquisition of reflexes and general abilities between the intervention and control groups. There was no difference in the prevalence of CP between the intervention and control groups. In conclusion this study showed no effect of early intervention in premature babies without risk of CP other than prematurity.