Cerebral blood flow and serum neuron-specific enolase in early-onset neonatal sepsis.

BACKGROUND AND OBJECTIVES: Sepsis leads to systemic inflammatory response with cerebral blood flow (CBF) alteration and blood-brain barrier disruption that contribute to sepsis-associated encephalopathy (SAE). We aimed to evaluate cord blood neuron-specific enolase (cNSE) and CBF in early-onset neonatal sepsis (EONS) as predictors of SAE and to define short-term neurodevelopmental outcomes among survivors. METHODS: cNSE was measured in 200 neonates with antenatal risk factors for EONS, stratified into two groups: sepsis (n = 96) and no-sepsis (n = 104). Trans-cranial Doppler of peak systolic velocities (PSV), end diastolic velocities (EDV) and resistive indices (RI) of anterior (ACA) and middle (MCA) cerebral arteries recorded on day 1 postnatal. Griffiths mental developmental scale (GMDS) was assessed at 6 months. RESULTS: Increased cNSE, PSV, EDV, and decreased RI of both ACA and MCA were found in sepsis group compared to no-sepsis group (p < 0.001 for all). Patients with SAE (n = 34) had higher NSE, PSV, and EDV as well as lower RI of ACA and MCA compared to those without (p < 0.01 for all). SAE neonates had lower GMDS than those without. ACA RI of ≤0.61 was the best predictor of SAE. CONCLUSION: High CBF and cNSE could be useful markers for prediction of SAE. SAE impairs neurodevelopmental scales at 6 months.

Enteral granulocyte-colony stimulating factor and erythropoietin early in life improves feeding tolerance in preterm infants: a randomized controlled trial.

OBJECTIVE: To evaluate the efficacy and safety of enteral recombinant human granulocyte colony-stimulating factor (rhG-CSF) and recombinant human erythropoietin (rhEPO) in preventing feeding intolerance. STUDY DESIGN: An interventional randomized control trial was conducted in 90 preterm infants born at ≤33 weeks gestational age. The neonates were assigned to 4 groups; 20 received rhG-CSF, 20 received rhEPO, 20 received both, and 30 received distilled water (placebo control). The test solution was given at the beginning of enteral feeding and was discontinued when enteral intake reached 100 mL/kg/day or after a maximum of 7 days, whichever came first. Feeding tolerance and adverse effects of treatment were assessed. Serum granulocyte colony-stimulating factor and erythropoietin levels were measured on days 0 and 7 of treatment. RESULTS: All neonates tolerated the treatment without side effects. Neonates who received rhG-CSF and/or rhEPO had better feeding tolerance, as reflected by earlier achievement of 75 mL/kg/day, 100 mL/kg/day, and full enteral feeding of 150 mL/kg/day with earlier weight gain and a shorter hospital stay (P < .05). The risk of necrotizing enterocolitis was reduced from 10% to 0% in all treatment groups (P < .05). There was a shorter duration of withholding of feeding secondary to feeding intolerance among neonates receiving both rhG-CSF and rhEPO compared with those receiving placebo (P < .05). Serum levels of granulocyte colony-stimulating factor and erythropoietin at 0 and 7 days did not differ across the treatment groups. CONCLUSIONS: Enteral administration of rhG-CSF and/or rhEPO improves feeding outcome and decreases the risk of necrotizing enterocolitis in preterm neonates. The mechanism may involve the prevention of villous atrophy.

Trauma profile in Egyptian adolescents with first-episode schizophrenia: relation to psychopathology and plasma brain-derived neurotrophic factor.

We aimed to investigate the relation of trauma profile to schizophrenia psychopathology in a sample of Egyptian drug-naïve adolescent patients with first-episode schizophrenia. In addition, a hypothesized mediating effect of brain-derived neurotrophic factor (BDNF) in this relation was formally tested. We assessed 74 eligible outpatients using the Positive and Negative Syndrome Scale (PANSS) for measuring psychopathology. Trauma histories were recorded with the help of the Cumulative Trauma Measure. Serum BDNF levels were estimated by enzyme-linked immunosorbent assay. Total cumulative trauma, personal identity trauma, and survival trauma were found to be the significant predictors for schizophrenia psychopathology. BDNF fully mediated the associations between total cumulative trauma and overall schizophrenia psychopathology. BDNF also mediated the associations between some types of trauma and both PANSS-positive and PANSS-negative symptom factors. We concluded that total cumulative trauma and certain trauma types are linked with schizophrenia psychopathology. BDNF appears to mediate these links.