Because low tumor necrosis factor-alpha (TNF-alpha) production has been reported in malnourished children, in contrast with high production of TNF-alpha in experimental protein-energy malnutrition, we reevaluated the production of TNF-alpha in whole blood cultures from children with primary malnutrition free from infection, and in healthy sex- and age-matched controls. Mononuclear cells in blood diluted 1:5 in endotoxin-free medium released TNF-alpha for 24 h. Spontaneously released TNF-alpha levels (mean ± SEM), as measured by enzyme immunoassay in the supernatants of unstimulated 24-h cultures, were 10,941 ± 2,591 pg/ml in children with malnutrition (N = 11) and 533 ± 267 pg/ml in controls (N = 18) (P < 0.0001). TNF-alpha production was increased by stimulation with lipopolysaccharide (LPS), with maximal production of 67,341 ± 16,580 pg/ml TNF-alpha in malnourished children and 25,198 ± 2,493 pg/ml in controls (P = 0.002). In control subjects, LPS dose-dependently induced TNF-alpha production, with maximal responses obtained at 2000 ng/ml. In contrast, malnourished patients produced significantly more TNF-alpha with 0.02-200 ng/ml LPS, responded maximally at a 10-fold lower LPS concentration (200 ng/ml), and presented high-dose inhibition at 2000 ng/ml. TNF-alpha production a) was significantly influenced by LPS concentration in control subjects, but not in malnourished children, who responded strongly to very low LPS concentrations, and b) presented a significant, negative correlation (r = -0.703, P = 0.023) between spontaneous release and the LPS concentration that elicited maximal responses in malnourished patients. These findings indicate that malnourished children are not deficient in TNF-alpha production, and suggest that their cells are primed for increased TNF-alpha production

Background Prediction of outcome based on certain prognostic factors is still challenging in paediatric traumatic brain injuries (TBI). Purpose of our study is to evaluate prognostic factors and outcome in children with TBI admitted in PICU. Methods The sample was 252 children with TBI who were admitted to PICU of Hippokratio General Hospital of Thessaloniki from 1999 to 2012. The statistical analysis was performed with the statistical package SPSS 17 and the application of statistical tests x 2-test, anova, Mann Whitney test, t-test and Pearson Correlation. Age, sex, Glasgow Coma Scale (GCS), Paediatric Risk Index of Mortality (PRISM score), days of mechanical ventilation, hypotension and need of inotropic support as well as late hyperglycemia were correlated to outcome. Results Age groups, sex and mechanism of injury showed no correlation to outcome. Patients who died had statistically significant higher mean PRISM score (25,7 ± 8,4),compared with patients with good outcome (7,5 ± 4,7). The application of Pearson Correlation showed that the increased rating of PRISM score, as well as the low grading GCS were positively correlated to death, late hyperglycemia, haemodynamic instability, use of inotrops, poor outcome and disabilities (p < 0,001). Conclusion A high PRISM score, a low GCS, hypotension and hyperglycemia after the first 48 h, are directly associated with poor outcome and death. Knowledge of these prognostic factors may help neurocritical care specialists to improve outcome in paediatric TBI.