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Studies about the effects of inhaled nitric oxide (iNO) on bleeding time and platelet aggregation in newborns are limited in number and have inconclusive results. Thromboelastogram (TEG) shows the combined effects of coagulation factors and platelet functions. In this preliminary study, we aimed to evaluate the effects of iNO on coagulation using TEG in newborns with persistent pulmonary hypertension (PPH). TEG assays were performed in 10 term infants receiving iNO treatment for PPH and 32 healthy term infants. Samples of the iNO group were collected before and during iNO. Clot reaction time (R), clot kinetics (K), maximum amplitude (MA), and alpha angle were obtained from the TEG tracing. TEG-R values were statistically higher during iNO treatment (7.75 ± 3.34) when compared to the values before iNO (4.83 ± 1.38) and the healthy controls (3.75 ± 0.98). The alpha angle was lower in iNO treated infants at both periods (before iNO, 55.33 ± 8.58; during iNO, 42.90 ± 18.34) compared to the control group (64.95 ± 6.88). MA values before iNO treatment were the lowest (44.43 ± 14.09) and improved with the iNO treatment (48.40 ± 9.49) despite still being lower compared to the controls (53.67 ± 5.56). Conclusion: Both PPH and iNO may negatively effect in vitro coagulation tests. Therefore, newborns with PPH requiring iNO treatment should be closely monitored for coagulation problems.

Intrauterine transfusion is the standard of care in the management of severe Rh isoimmunization. Desferrioxamine has been used for the treatment of iron overload secondary to hemolysis and intrauterine transfusions in Rh isoimmunization cases. Here, we report a preterm infant born at 34 weeks of gestational age who had formerly received intrauterine transfusions for Rhesus hemolytic disease and presented with severe hyperferritinemia and elevated liver enzymes in the first week of life. Desferrioxamine treatment was started due to a ferritin level of 28,800 ng/ml and continued for 13 weeks. Although the treatment was successful, we observed resistant leukopenia which resolved after the cessation of treatment. In conclusion, iron overload secondary to intrauterine transfusions can be treated successfully with desferrioxamine; however, neonatologists must be aware of the possible side effects of this drug which has been used in only a limited number of newborns.

This paper was designed to investigate whether phototherapy is an oxidative stress in newborn infants undergoing phototherapy. A day-light continuous phototherapy was given to jaundiced 20 term and 16 preterm newborns for 72 hours. We measured serum vitamin E and the activities of red blood cell anti-oxidation enzymes (superoxide dismutase, catalase and glutathione peroxidase) before and after 72 h of phototherapy. Serum vitamin E levels were not different before and after 72 h of phototherapy in both preterm and term infants. In several studies, antioxidant enzyme activities have been shown to increase in response to oxidative stresses. In this study, however, the antioxidant enzyme activities in the hemolysate were similar before and at the end of the phototherapy in both preterm and full term. In conclusion, the results of our in vivo study do not confirm the thesis that phototherapy is an oxidative stress in newborn infants. Therefore, phototherapy would preferably seem to be safe and efficient method of treatment for all neonates presenting with hyperbilirubinemia.

Diabetes mellitus (DM) alters carbohydrate and lipid metabolism to a great extent. This study was planned to determine whether infants of insulin dependent and gestational diabetic mothers have abnormal lipid metabolism. Three groups of newborns were included in the study; group I consisted of 7 infants of diabetic mothers (IDM) with insulin dependent DM (Type 1 DM), group Il of 18 infants of gestational diabetic mothers and group III of 20 control neonates whose mothers had no history of DM. Total cholesterol (TC), triglyceride (TG) and high density lipoprotein-cholesterol (HDL-C) values in groups I and II were no different compared to those in group III (p>0.05). However, low density lipoprotein-cholesterol (LDL-C) and LDL-C/HDL-C ratio were similar between groups I and II (p>0.05) but significantly higher in both infants of type I diabetic mothers and gestational diabetic mothers compared to control infants (p

Intraventricular hemorrhage remains associated with high mortality and morbidity. Its most serious complication is posthemorrhagic hydrocephalus caused by multiple small blood clots obstructing the arachnoid villi. We treated three newborn infants (one term, two preterm) with posthemorrhagic hydrocephalus using recombinant tissue plasminogen activator, a thrombolytic agent, injected into the ventricles with a spinal needle. Sufficient fibrinolysis was achieved in these preterm patients. They all survived, and shunt surgery was only required in one. No adverse reactions or side effects have occurred. Intraventricular fibrinolysis with tissue plasminogen activator seems to be safe and effective for the treatment of intraventricular hemorrhage. However, controlled studies are needed for assessing treatment efficiency.

Background and Aims: Apoptosis, that occurs after hypoxia/reoxygenation (H/R), has an important role in the pathogenesis of necrotizing enterocolitis (NEC) which is a major cause of morbidity and mortality in premature infants. Telomerase activity, showing the regenaration capacity, may also be important in the recovery process. We aimed to see the effects of insulin-like growth factor-1 (IGF) and erithropoetin (EPO) on apoptosis and telomerase activity in a H/R model.

Platelet-activating factor levels were measured in nine preterm infants with Klebsiella pneumonia septicaemia, eight healthy preterm infants of similar gestational age and ten healthy full-term infants of the same postnatal age at sampling. The platelet-activating factor levels of the healthy preterm and term groups did not differ significantly, but were elevated compared to the other two groups in the septic preterm infants (P0.01). Platelet-activating factor levels increase upon stimulation by Gram negative bacteraemia and are a important mediator of neonatal sepsis.

Objective: The aim of present study was to investigate whether hypoxia-reoxygenation (H/R)-induced necrotizing enterocolitis (NEC) was due to increased apoptosis of the intestinal mucosa in the young mice and whether pre-treatment of the animals with recombinant human Insulin-like growth factor-I (IGF-I), known anti-apoptotic factor, could protect the intestinal cells from H/R-induced apoptosis or intestinal injury. Study design: Young mice were divided into three groups; Group 1 mice (H/R) were hypoxia-reoxygenation; Group 2 mice (H/R + IGF-I) were treated with recombinant human IGF-I by intraperitoneal injection (1 μg/g BW; once daily) for 7 days; Group 3 mice were served as control. Hypoxia was induced by placing young mice in Plexiglas chamber, consisting 10% oxygen for 60 min. After hypoxia, the young mice were reoxygenated for 10 min with 100% oxygen. Intestinal generation of substances reactive to thiobarbituric acid (TBARS) and active caspase-3 were measured in H/R-induced intestinal injury. Results: Increased numbers of apoptotic cells (apoptotic index) across the villi in young mice subjected to H/R were observed with the TUNEL reaction whereas few apoptotic cells existed in the control animals. In addition, H/R-induced intestinal damage in H/R + IGF-I group was greatly attenuated, with necrosis limited partially to the mucosa. Tissue active caspase-3 levels in H/R group were found to be significantly higher when compared with that of H/R + IGF-I group of mice and control. However, TBARS concentrations in the intestine were similar in H/R groups when compared to the intestine of control animals. Conclusion: The present study suggests that both necrosis and apoptosis via mechanisms occurring oxygen-derived free radicals and activation of caspase-3 play a role in the pathogenesis of H/R-induced NEC. We also show that IGF-I protect intestinal mucosa from necrosis and apoptosis from intestinal H/R injury.