Proteomic analysis reveals potential therapeutic targets for childhood asthma through Mendelian randomization.

BACKGROUND: Asthma is the most common chronic disease among children and poses a significant threat to their health. This study aims to assess the relationship between various plasma proteins and childhood asthma, thereby identifying potential therapeutic targets. METHODS: Based on publicly available genome-wide association study summary statistics, we employed a two-sample Mendelian randomization (MR) approach to elucidate the causal relationship between plasma proteins and asthma. Mediation analysis was then conducted to evaluate the indirect influence of plasma proteins on childhood asthma mediated through risk factors. Comprehensive analysis was also conducted to explore the association between plasma proteins and various phenotypes using the UK Biobank dataset. RESULTS: MR analysis uncovered a causal relationship between 10 plasma proteins and childhood asthma. Elevated levels of seven proteins (TLR4, UBP25, CBR1, Rac GTPase-activating protein 1 [RGAP1], IL-21, MICB, and PDE4D) and decreased levels of three proteins (GSTO1, LIRB4 and PIGF) were associated with an increased risk of childhood asthma. Our findings further validated the connections between reported risk factors (body mass index, mood swings, hay fever or allergic rhinitis, and eczema or dermatitis) and childhood asthma. Mediation analysis revealed the influence of proteins on childhood asthma outcomes through risk factors. Furthermore, the MR analysis identified 73 plasma proteins that exhibited causal associations with at least one risk factor for childhood asthma. Among them, RGAP1 mediates a significant proportion (25.10%) of the risk of childhood asthma through eczema or dermatitis. Finally, a phenotype-wide association study based on these 10 proteins and 1403 diseases provided novel associations between these biomarkers and multiple phenotypes. CONCLUSION: Our study comprehensively investigated the causal relationship between plasma proteins and childhood asthma, providing novel insights into potential therapeutic targets.

Case report: One case of umbilical vein thrombosis in the second trimester with associated portal vein thrombosis after childbirth.

Background: Umbilical vein thrombosis is a rare pregnancy complication, that is difficult to detect prenatally but can lead to poor fetal outcomes. Case presentation: We described a 33-year-old primiparae who was identified as having umbilical vein thrombosis by ultrasound at 21 weeks gestation, and the neonate was found to have a portal vein thrombus after delivery. Following enoxaparin anticoagulant therapy, the thrombus disappeared within 4 weeks. No thrombus formation occured during the 10-month follow-up, and the baby was in excellent clinical condition. Conclusion: Owing to the poor fetal outcomes related to umbilical thrombosis, pay attention to abnormal clinical signs during prenatal ultrasound, fetal heart monitoring and counting fetal movements can help in the early identification of umbilical cord thrombosis.The findings highlight the importance of regular prenatal ultrasound evaluation, enabling early detection and monitoring of any anomalies or vascular abnormalities related to the fetal umbilical vein. Further research is warranted to explore the clinical implications and long-term outcomes associated with these findings.

Soluble Triggering Receptors Expressed on Myeloid Cells-1 as a Neonatal Ventilator-Associated Pneumonia Biomarker.

BACKGROUND: Neonatal ventilator-associated pneumonia (NVAP) is one of the main infections acquired in hospitals, and soluble triggering receptors expressed on myeloid cells-1 (sTREM-1) are a TREM-1 subtype that can be released into the blood or bodily fluids during an infection. METHODS: The patients included in the present study were divided into three groups: the NVAP group, the first control group, and the second control group (n = 20, each). Children requiring respiratory treatment were assigned to the NVAP group, newborns who received mechanical ventilation and had neonatal respiratory distress syndrome were assigned to the first control group, and newborns with normal X-ray and electrocardiogram results but no non-pulmonary infection was assigned to the second control group. The blood and bronchoalveolar lavage fluid (BALF) sTREM-1 levels in all newborns were analyzed. RESULTS: The acute-phase blood and BALF sTREM-1 levels were significantly higher in the NVAP group than in the first control group, and the blood sTREM-1 expression level was lower in the second control group than in the NVAP group. CONCLUSION: The present results suggest that sTREM-1 might be a useful biomarker for NVAP prediction in the Department of Pediatrics.

Neferine Protects against Hypoxic-Ischemic Brain Damage in Neonatal Rats by Suppressing NLRP3-Mediated Inflammasome Activation.

Hypoxic-ischemic encephalopathy (HIE) is recognized as the main cause of neonatal death, and efficient treatment strategies remain limited. Given the prevalence of HIE and the associated fatality, further studies on its pathogenesis are warranted. Oxidative stress and neuroinflammatory injury are two important factors leading to brain tissue injury and nerve cell loss in HIE. Neferine, an alkaloid extracted from lotus seed embryo, exerts considerable effects against several diseases such as cancers and myocardial injury. In this study, we demonstrated the neuroprotective effect of neferine on HIE and hypothesized that it involves the inhibition of neuronal pyroptosis, thereby ameliorating neurological inflammation and oxidative stress. We demonstrated that the mRNA levels of proteins associated with pyroptosis including caspase-1, the caspase adaptor ASC, gasdermin D, interleukin- (IL-) 18, IL-1ß, and some inflammatory factors were significantly increased in neonatal HIBD model rats compared to those in the control group. The increase in these factors was significantly suppressed by treatment with neferine. We stimulated PC12 cells with CoCl2 to induce neuronal HIBD in vitro and investigated the relationship between neferine and pyroptosis by altering the expression of the NLRP3 inflammasome. The overexpression of NLRP3 partially reversed the neuroprotective effect of neferine on HIBD, whereas NLRP3 knockdown further inhibited caspase-1 activation and IL-1ß and IL18 expression. In addition, simultaneous alteration of NLRP3 expression induced changes in intracellular oxidative stress levels after HIBD. These findings indicate that neferine ameliorates neuroinflammation and oxidative stress injury by inhibiting pyroptosis after HIBD. Our study provides valuable information for future studies on neferine with respect to neuroinflammation and pyroptosis.

LXA4 protects against hypoxic-ischemic damage in neonatal rats by reducing the inflammatory response via the IκB/NF-κB pathway.

Hypoxia and the resultant decreases in cerebral blood flow in the perinatal period can lead to neonatal hypoxic-ischemic (HI) brain injury, which can, in turn, cause severe disability or even death. However, the efficacy of current treatment strategies remains limited. Several studies have demonstrated that lipoxin A4 (LXA4), as one of the earliest types of endogenous lipid mediators, can inhibit the accumulation of neutrophils, arrest inflammation, and promote the resolution of inflammation. However, research on LXA4 in the nervous system has rarely been carried out. In the present study, we sought to investigate the protective effect of LXA4 on HI brain damage in neonatal rats, as well as the underlying mechanisms. Through experiments conducted using an HI animal model, we found that the LXA4 intervention promoted the recovery of neuronal function and tissue structure following brain injury while maintaining the integrity of the blood-brain barrier in addition to reducing cerebral edema, infarct volume, and inflammatory responses. Our results suggest that LXA4 interfered with neuronal oxygen-glucose deprivation insults, reduced the expression of inflammatory factors, inhibited apoptosis, and promoted neuronal survival in vitro. Finally, the LXA4 intervention attenuated HI-induced activation of inhibitor kappa B (IκB) and degradation of nuclear factor-κB (NF-κB). In conclusion, our data suggest that LXA4 exerts a neuroprotective effect against neonatal HI brain damage through the IκB/NF-κB pathway. Our findings will help inform future studies regarding the effects of LXA4 on neuroinflammation, blood-brain barrier integrity, and neuronal apoptosis.

Concentrations of Polybrominated Diphenyl Ethers in Maternal Blood, Placental Size, and Risk for Fetal Growth Restriction: A Nested Case-control Study.

OBJECTIVE: To explore the effects of prenatal exposure to polybrominated diphenyl ethers (PBDEs) on placental size and birth outcomes. METHODS: Based on the perspective Wenzhou Birth Cohort, this nested case-control study included 101 fetal growth restriction (FGR) and 101 healthy newborns. Maternal serum samples were collected during the third trimester and measured for PBDEs by gas chromatography tandem mass spectrometry. The basic information of mother-newborn pairs was collected from questionnaires, whereas the placental size and birth outcomes of newborns were obtained from hospital records. RESULTS: A total of 19 brominated diphenyle ether (BDE) congeners were detected in maternal serum samples. Higher concentrations of BDE-207, -208, -209, and ∑ 19PBDEs were detected in FGR cases than in controls. Increased BDE-207, -208, -209, and ∑ 19PBDEs levels in maternal serum were related to decreased placental length, breadth, surface area, birth weight, birth length, gestational age, and Quetelet index of newborns. After adjusting for confounders, BDE-207 and ∑ 19PBDE concentrations in maternal serum were significantly associated with an increased risk of FGR. CONCLUSION: A negative association was found between PBDE levels in maternal serum and placental size and birth outcomes. Prenatal PBDE exposure may be associated with elevated risk of the incidence of FGR birth.

Clinical analysis of a case of neonatal exfoliative esophagitis in an 18-day-old neonate.

BACKGROUND: This study aims to provide guidance for clinical work through analysis of the clinical characteristics, endoscopic and pathological manifestations, diagnosis, and treatment of an 18-day-old neonate with exfoliative esophagitis. CASE PRESENTATION: The patient presented with vomiting but the parents did not pay too much attention. The pathological report revealed numerous fibrinous exudative necrotic, and inflammatory cells, as well as a small amount of squamous epithelium. Furthermore, milk allergy factors were considered. Conservative treatments, such as fasting, acid suppression, mucosal protection, parenteral nutrition, and the replacement of anti-allergic milk powder were given. Thereafter, endoscopic examination revealed that the patient returned to normal, and was discharged after 21 days. CONCLUSIONS: Exfoliative esophagitis has multiple causes; and has characteristic clinical and endoscopic manifestations. Endoscopic examination after 18 days presentation and conservative therapy revealed that the esophagus had returned to a normal appearance and the patient was discharged. Following discharge, the parents were advised to feed the patient ALFERE powder. Attention should be given to the timely detection of complications and corresponding treatment.

Treatment With Liraglutide Exerts Neuroprotection After Hypoxic-Ischemic Brain Injury in Neonatal Rats via the PI3K/AKT/GSK3ß Pathway.

Neonatal hypoxic-ischemic (HI) brain injury is a detrimental disease, which results in high mortality and long-term neurological deficits. Nevertheless, the treatment options for this disease are limited. Thus, the aim of the present study was to assess the role of liraglutide in neonatal HI brain injury in rats and investigate the associated mechanisms. The results showed that treatment with liraglutide significantly reduced infarct volume and ameliorated cerebral edema, decreased inflammatory response, promoted the recovery of tissue structure, and improved prognosis following HI brain injury. Moreover, treatment with liraglutide inhibited apoptosis and promoted neuronal survival both in the rat model and following oxygen-glucose deprivation (OGD) insult. LY294002, an inhibitor of phosphoinositide 3-kinase (PI3K), partially reversed these therapeutic effects, suggesting that the PI3K/protein kinase B (Akt) pathway was involved. In conclusion, our data revealed that treatment with liraglutide exerts neuroprotection after neonatal HI brain injury via the PI3K/Akt/glycogen synthase kinase-3ß (GSK3ß) pathway and may be a promising therapy for this disease.

Identification and antimicrobial resistance of pathogens in neonatal septicemia in China-A meta-analysis.

OBJECTIVES: The purpose of this study was to analyze the distribution and antimicrobial resistance of common bacterial pathogens causing neonatal septicemia based on a systematic review of published studies in China. METHODS: Articles on neonatal sepsis published in the Chinese literature from 2009 to 2014 were identified according to the inclusion and exclusion criteria. Data were extracted and analyzed using Comprehensive Meta-Analysis software. RESULTS: A total of 71 studies were included, in which a total of 8080 bacterial species were isolated from culture-positive blood samples. The pooled distribution rates of common bacterial pathogens were as follows: Staphylococcus 67.1% (95% confidence interval (CI) 63.3-70.6%), Enterococcus 4.1% (95% CI 3.5-4.8%), Streptococcus 2.3% (95% CI 1.6-3.2%), Escherichia coli 7.4% (95% CI 6.4-8.7%), Klebsiella 6.5% (95% CI 5.2-8.2%), Enterobacterium 2.3% (95% CI 1.9-2.8%), Acinetobacter 1.6% (95% CI 1.3-2.0%), Pseudomonas 1.7% (95% CI 1.3-2.2%). Among the Staphylococcus aureus strains isolated, more than 60% were methicillin-resistant (MRSA). In addition, over 50% of the Gram-negative isolates, including Escherichia and Klebsiella, were resistant to the commonly used third-generation cephalosporins. Most of the Gram-positive and Gram-negative bacteria isolated were sensitive to aminoglycosides, especially amikacin. CONCLUSIONS: It is concluded that Staphylococcus, especially coagulase-negative Staphylococcus, continues to be the principal organism responsible for neonatal septicemia in China; Enterobacteriaceae are common among the Gram-negative isolates. Significant numbers of MRSA and multidrug-resistant Gram-negative bacteria are being isolated as pathogens responsible for neonatal septicemia in China.

Postnatal hyperoxia or DEHP exposure leads to growth restriction and delayed lung development in newborn rats.

BACKGROUND: Di-(2-ethylhexyl) phthalate (DEHP) is commonly used as a plasticizer in many medical devices. We previously showed that maternal DEHP exposure led to restricted growth and delayed lung maturation in newborn rats. As oxygen toxicity continues to be a major risk factor for bronchopulmonary dysplasia, the aim of this study was to examine the effect of hyperoxia, DEHP or DEHP combined with hyperoxia on the growth and lung maturation of newborn rats. METHODS: Newborn rats received DEHP injection, hyperoxia exposure or DEHP injection combined with hyperoxia exposure for one week or two weeks. A control group received an equal volume of vehicle and was maintained in room air. RESULTS: Hyperoxia and hyperoxia + DEHP exposure for one week led to growth failure in newborn rats. Pups in the hyperoxia group showed catch-up growth after being maintained in room air for an additional 7 days but this was not the case with the latter group, which continued to receive DEHP. Hyperoxia and DEHP both delayed lung development, as evidenced by decreased radial alveolar count. Quantitative RT-PCR showed that hyperoxia decreased the transcripts of VEGF, VEGFR-2 and eNOS on days 7 and 14, and DEHP exposure alone also led to decreased expression of VEGF gene in 14-day-old rat pups. CONCLUSION: Postnatal hyperoxia and/or DEHP exposure lead to growth restriction and delayed lung alveolar development. The VEGF gene expression was altered and may be involved as one of the possible molecular mechanisms.

Exposure levels of environmental endocrine disruptors in mother-newborn pairs in China and their placental transfer characteristics.

There is a growing concern about the potential health effects of exposure to various environmental chemicals during pregnancy and infancy. The placenta is expected to be an effective barrier protecting the developing embryo against some endocrine disruptors (EDs) circulating in maternal blood. The current study was designed to assess in utero exposure levels of non-persistent organic pollutants (non-POPs) and persistent organic pollutants (POPs) in Chinese newborns and potential role of placenta barrier against fetal exposure to these commonly-used environmental endocrine disruptors. A total of 230 newborn-mother pairs were enrolled during 2010-2011, 201 pairs of which were recruited from Shanghai, and the other 29 pairs came from Wenzhou. Maternal blood, cord blood, and meconium specimens were collected in the subject population from Shanghai and analyzed for non-POPs, including mono-2-ethylhexyl phthalate (MEHP), octylphenol (OP) and 4-nonylphenol (4-NP). A total of 19 polybrominated diphenyl ethers (PBDEs) congeners, which belong to POPs, were detected in maternal and cord blood specimens from the other 29 pairs. Fetal-maternal ratios (F-M ratios) and regression coefficients were presented to assess potential function of placenta on barricading the mother/fetal transfer of these EDs. Concentrations of the detected non-POPs in cord blood samples were approximately 20% lower than those in maternal blood, and regression coefficients of which were all over 0.80. In contrast, PBDEs levels in cord blood samples were significantly higher than those in maternal blood. MEHP levels in meconium were much higher than those in cord blood samples, and highly correlated. Therefore, observations demonstrated that the placental barrier slightly decreased the fetal exposure to most non-POPs, while PBDEs seemed to be totally transferred across the placenta and finally reached the fetus. For in utero exposure assessment of Di-2-ethylhexyl phthalate (DEHP), MEHP level in meconium may be a useful biomarker.

[Investigation and analysis of nosocomial infection in neonates].

OBJECTIVE: To investigate the incidence of nosocomial infections of newborn infants in neonates and to explore the risk factors and strategies of infection control. METHODS: There were 433 confirmed cases of nosocomial infection in the neonatal ward of the authors' hospital from January 2007 to December 2009. Their data of epidemiological and clinical characteristics, results of etiological examinations and antibiotic resistance were retrospectively analyzed. RESULTS: During the study, the number of hospitalizations were 6437. Nosocomial infection occurred in 433 patients 513 times. The overall nosocomial infection rate was 6.82%. The overall hospitalization days were 73 663 and nosocomial infection patient-day rates were 6.96‰. The VAP infection rate was 28.7‰. The CRBSI rate was 3.5‰. Gestational age (OR = 1.049), mechanical ventilation (OR = 1.810), umbilical vein catheter (OR = 1.106), hospitalization days (OR = 1.081), premature rupture of membrane (OR = 1.433) were the risk factors for the development of nosocomial infection. There were 197 (38.4%) cases of pneumonia, which was the most common nosocomial infection in Neonatal Ward. There were 129 cases of ventilator-associated pneumonia (VAP), which accounts for 65.5% of pneumonia and 24.4% of cases treated with ventilator. The next was sepsis, 124 cases (24.2%) and 64 cases of diarrheal disease (12.7%). One hundred and eighty two (54.4%) strains of isolates were Gram-negative bacteria, which accounted for the highest proportion. The predominant pathogens of Gram-negative bacteria were Klebsiella pneumoniae (19.6%), followed by Acinetobacter baumannii (8.1%), Pseudomonas aeruginosa (7.2%), Stenotrophomonas maltophilia (4.8%) and Escherichia coli (4.8%). The isolation rates of Klebsiella pneumoniae and Escherichia coli with positive extended-spectrum beta-lactamases (ESBLs) were 91.4% and 75%, respectively. Those two bacteria were universally resistant to cephalosporins. The rate of resistance to imipenem of Klebsiella pneumoniae, Acinetobacter baumannii and Pseudomonas aeruginosa were 1.5%, 11.1% and 41.7%. The isolation rates of methicillin-resistant Staphylococcus aureus and methicillin-resistant coagulase-negative Staphylococcus were 28.6% and 95.5%. CONCLUSION: It is important to identify the high risk factors for nosocomial infections in newborn infants. To shorten time for mechanical ventilation and hospitalization days, removal of the central venous catheter as early as possible would be conducive to reducing the morbidity of nosocomial infection. The main pathogens were Gram-negative bacteria. The multidrug resistance of Enterobacteriaceae and Non-fermenters is serious.

[Risk factors for ventilator-associated pneumonia in neonates and the changes of isolated pathogens].

OBJECTIVE: To study the risk factors for neonatal ventilator-associated pneumonia (VAP) and the changes of isolated pathogens in the last eight years. METHODS: The clinical data of 230 neonates who were admitted into the neonatal intensive care unit (NICU) and received mechanical ventilation for equal to or longer than 48 hrs in 2008 were retrospectively reviewed. The isolated pathogens were compared with those of eight years ago. RESULTS: The incidence of VAP (25.2%) in the year 2008 was lower than that of eight years ago (36.1%; P<0.05). The development of VAP was negatively correlated with the gestational age and the birth weight, but positively correlated with the duration of mechanical ventilation, intubation times, duration of hospitalization, presence of gastrointestinal bleeding and need for blood products transfusion. The main isolated pathogens were opportunistic antibiotics resistant bacteria, and the majority was gram negative bacilli (77%). The most frequently detected gram negative bacilli were Klebsiella (20%), Stenotrophomonas maltophilia (18%) and Acinetobacter (13%). Streptococcus mitis was the most frequently detected gram positive bacilli (14%). The distribution pattern of pathogens isolated in the same NICU eight years ago was somewhat different: Klebsiella (23%), Pseudomonas aeruginosa (17%), Acinetobacter (16%), Streptococcus mitis (11%), Fungi (1%) and Candida albicans (1%). CONCLUSIONS: The incidence of VAP is correlated with gestational age, birth weight, duration of mechanical ventilation and hospitalization, intubation times, presence of gastrointestinal bleeding and need for blood products transfusion. The main isolated pathogens are usually antibiotic resistant opportunistic bacteria. The detection rate of Stenotrophomonas maltophilia increased and that of Pseudomonas aeruginosa decreased when compared with eight years ago.

Perinatal exposure to di-(2-ethylhexyl) phthalate leads to restricted growth and delayed lung maturation in newborn rats.

BACKGROUND: Pregnant women and infants have significant exposures to the most commonly used plasticizer di-(2-ethylhexyl) phthalate (DEHP). OBJECTIVES: This study was designed to evaluate the effects of DEHP exposure on growth and lung maturation in rats and determine if DEHP regulation of 11beta-hydroxysteroid dehydrogenase type 1 gene (Hsd11b1) expression in the lung tissue plays a role in its effects on lung maturation. METHOD: Pregnant Sprague-Dawley rats were treated from gestational day 12 to postnatal day (PND) 21 with DEHP orally at dosages of 0, 10, 100 or 750 mg/kg/day, respectively (n=8 for each group). Two rat pups (one male and one female) from each litter were sacrificed at PND 1 and 21. Body weight was measured and the lung was processed for histology and calculation of lung interstitial tissue proportion as well as real-time PCR determination of the expressions of Hsd11b1, surfactant associated protein-A1 gene (Sftpa1) and B gene (Sftpb). RESULTS: The perinatal DEHP exposure led to a dose dependent intrauterine and postnatal growth restriction (P<0.001). High dose DEHP (750 mg/kg/day) exposure led to decreased gas-exchange space as evidenced by increased lung interstitial tissue proportion (P<0.001), but did not cause significant changes in Hsd11b1, Sftpa1 or Sftpb gene expression in the rat lung at PND 1. The DEHP-induced change in lung histology remained significant at PND 21 with improvement despite continual exposure to DEHP. CONCLUSION: Perinatal DEHP exposure leads to growth restriction and delayed lung maturation in newborn rats.

[Role of Ommaya reservoir in the management of neonates with post-hemorrhagic hydrocephalus].

OBJECTIVE: Intra-ventricular hemorrhage (IVH) is one of the most serious complications of preterm infants. Significant numbers of the surviving infants with severe IVH go on to develop post-hemorrhagic hydrocephalus (PHH). The management of PHH remains a very challenging problem for both neonatologists and pediatric neurosurgeons. This study aimed to evaluate the efficacy and safety of the use of Ommaya reservoirs and serial cerebrospinal fluid (CSF) drainage in the management of a series of neonates with PHH. METHOD: Between January 1, 2003 and December 30, 2005, 15 consecutive newborn infants with IVH grades III to IV, complicated with progressive ventricular dilatation, underwent placement of an Ommaya reservoir. CSF was intermittently aspirated percutaneously from the reservoir. The amount and frequency of CSF aspiration were based on the clinical presentation and the follow-up results of serial cranial ultrasonograms or CT scans. The changes of CSF cell counts and chemistries were also followed. Patients whose progressive ventricular dilatation persisted despite serial CSF aspiration through Ommaya reservoir eventually had ventriculo-peritoneal shunts (V-P shunt) placed. All the patients were followed up in the outpatient clinic after discharge from the hospital and the neurodevelopmental outcomes were evaluated through 18-36 months of age. RESULT: A total of 15 infants were included in this series. Of them, 11 were preterm infants who were at gestational ages of 29 to 34 weeks and 4 infants were full-term. All of the 4 full term infants presented with progressive ventricular dilatation after suffering from the intra-cranial hemorrhage (3 infants were due to vitamin K deficiency and 1 was due to birth trauma). Thirteen infants had grade III IVH, and 2 had grade IV IVH based on initial cranial ultrasonographic and CT scans. The mean age when IVH was diagnosed was (9 +/- 1) days in preterm infants and (22 +/- 7) days in full-term infants; the mean age when Ommaya reservoir was placed was (18 +/- 11) days in preterm infants and (31 +/- 7) days in full-term infants. All the infants tolerated the surgical procedure well. The Ommaya reservoir was tapped for an average of (21.5 +/- 4.6) times per patient. The mean CSF volume per tap was (10.2 +/- 1.3) ml/kg. The values of CSF protein, glucose and cell counts slowly reached normal levels at approximately 3 - 5 weeks after the placement of the reservoir. The velocity of head circumference increase per week was less than 1 cm in 13 patients in 1 - 4 weeks after the placement of the reservoir and the size of ventricles decreased gradually. By 12 - 18 months, 12 infants had normal size ventricles, and 1 patient still had mild ventricular dilation at 36 months. Two infants developed progressive hydrocephalus after serial CSF aspiration through Ommaya reservoir. One infant had a V-P shunt placed at 2 months of age and another infant died at 3 months of age at home after parents refused further therapy. Complications consisted of reservoir leaking and CSF infection at 16th day of placement in one patient after repeated tapping. By the end of 18 - 36 months of follow-up, 11 of 14 infants were considered normal, two patients had mild impairment in neurodevelopmental outcome (both had spastic bilateral lower limbs paresis, and one of whom also had amblyopia) and the other had seizure disorder. CONCLUSION: The results from this series indicate that the placement of an Ommaya reservoir is relatively safe in newborn infants and is useful in the initial management of neonates with PHH and may be beneficial in improving their neurodevelopmental outcomes. A multicenter randomized trial may be needed to further validate the results of this report.