Interferon-gamma inducing factor [IL-18], interferon-gamma and cystatin C levels of children with meningitis

The objective of this study was to measure the levels of interleukin [IL]-18, interferon [IFN]- gamma and cystatin C in the cerebrospinal fluid [CSF] of children with meningitis. The study was carried out on 30 patients [12 males and 18 females] admitted to in-patient pediatric department in El Minya fever hospital and EL-Minya University hospital, for evaluation and treatment from meningitis during the period from January 2004 to December 2004. Within the entire group of the study the most common signs of meningitis were included. Thirteen children had septic meningitis [positive CSF culture] and 17 children had aseptic meningitis [negative CSF culture and lymphomonocytic pleocytosis in CSF analysis]. Twenty children of matched age and sex, having normal CSF during evaluation for meningitis, served as a control group. All CSF samples were obtained under aseptic conditions. CSF samples were cultured, analyzed for glucose, protein and WBCs. Another part from CSF samples assayed were immediately frozen at-70°C unit cystatin C, IFN-gamma and IL-18 in CSF were assaved by using a two -site enzyme linked immunosorbent assayed for cystatin C, IL-18 and IFN-gamma. The results showed that septic meningitis group had significantly higher CSF WBCs and protein levels than in aseptic meningitis and control groups [P<0.005]. IL-18 was significantly higher in septic group, it was detected in 95% of children with septic meningitis and only in the CSF of 48% of aseptic meningitis group. In control subjects, 10% had detectable levels of IL-18 in the CSF. IFN-gamma was significantly higher in aseptic group, it was detected in 96% of aseptic meningitis and 35% of children with septic meningitis, while 21% was detected in CSF of control subjects. cystatin C was detected in 44% of children with septic and aseptic meningitis, compared with control children [P<0.001], While cystatin C was significantly decreased in septic and aseptic groups. No significant correlation was found between IL-18,IFN-Y and cystatin C levels and total leukocyte count in the CSF of children with meningitis. Our data suggest that IL18, IFN-gamma and cystatin C are significantly changed in the CSF of children with meningitis. IL18 had greatest elevations while cystatin C was significantly decreased in those children with septic meningitis. IFN-gamma had greatest elevation seen in those children with aseptic meningitis. So, cystatin C and IL18 could be considered as sensitive and specific parameters for detection of septic meningitis, while IFN-gamma could be considered as sensitive and specific parameter for detection of aseptic meningitis

Cord blood activin A level as index of fetal hypoxia

Perinatal hypoxic-ischemic cerebral injury is a major determinant of neurologic morbidity and mortality in the neonatal period and later in childhood. Activin-A is a growth factor involved in cell growth and differentiation, neuronal survival, early embryonic development and erythropoiesis. Hypoxemia is a specific trigger for increasing activin-A in fetal lamb circulation. We evaluated the effects of asphyxia on cord blood activin-A levels. The study was carried out on 30 newborns who suffered from perinatal asphyxia and who selected from El-Minia university hospital from January 2005 through June 2005 in addition to 30 newborns of the same age and sex matched as a control group. Blood samples were obtained from the umbilical artery and vein for blood gas analysis, complete blood count with determination of nucleated red blood cells [nRBCs] and measurement of free activin-A. In this study, the arterial cord blood mean values of PH, PaO[2] and base deficit were lower and PaCO2 was higher in asphyxiated group than the control group. Newborns with clinical signs of perinatal asphyxia had higher activin-A levels, which were correlated with indices of hypoxia such as lower pH suggesting that hypoxia is a trigger to stimulate activin-A secretion. It was found that the mean value of activin-A was higher in arterial than in the venous cord blood in both asphyxiated and control groups suggesting that the fetus is the main source of activin-A. Nucleated RBCs were increased in asphyxiated group. The level of nRBCs per 100 WBCs correlated with asphyxia. The correlation found suggests that hypoxia is one of the common stimulus for increased erythropoiesis and activin-A release. intrauterine hypoxia is one of the common factors responsible for increasing activin-A levels in fetal circulation. The strong correlation between activin-A and clinical and biochemical signs of fetal and neonatal hypoxia lead us to suggest that activin-A is a possible indicator of intrauterine hypoxia

Evaluation of auditory brainstem evoked responses and neuron-specific enolase for detection of auditory neuropathy in neonatal hyperbilirubinemia

This study was designed to evaluate the correlation between neuron-specific enolase and neonatal hyperbilirubinemia in children diagnosed as having auditory neuropathy by auditory brainstem evoked responses. Thirty infants admitted in neonatology unit of AL-Minya university hospital in the period from July 2002 to January 2004 for treatment from hyperbilirubinemia and 20 neonates as a control group all infants and bilirubin levels above 20mg/dl and had a full work-up hyperbilirubinemia. All study group infants were treated with phototherapy. And 16 infants required blood exchange transfusion as well. Hyperbilirubinemic infants were placed into two groups according to serum bilirubin values group [A]: total bilirubin 20-25mg/dl, group [B]: total bilirubin >25mg/dl. The control group consisted of 20 healthy full-term neonates with bilirubin levels within physiologic ranges [<13mg/dl]. Serum samples for neuron specific enolase [NSE] determination were taken on the day of admission and stored at-20°C until the time of assayed by a commercial enzyme immunoassay [EIA] kit. All hyperbilirubinemic infants in the study were evaluated with auditory brain stem evoked responses [ABERs] and transient evoked otoacoustic emission [TEOAE] tests. ABERs were recorded using nihon kohden 4 channels equipment, while TEOAEs were obtained by using the quickscreen option of the ILO 92 OAE system. The results showed no significant differences between serum NSE value in hyperbilirubinemic groups [50.19 +/- 34.37] when compared with control infants [44.50 +/- 27.68 ng/ml] [p=0. 253]. A significant difference was detected between serum NSE values of group A [33.29 +/- 16.98 ng/ml] and group B [67.09 +/- 39.33 ng/ml] [p = 0.02]. NSE and total bilirubin levels of patients with absent ABRs but present TEOAEs [36.43 +/- 16.47 ng/ml and 25.06 +/- 4.25 mg/dl, reciprocal] were significantly higher than those of the patients with normal ABRs [70.83 +/- 43.82 ng/ml and 31.29 +/- 7.34 mg/dl, reciprocal], [p=0.001]. no correlation was found between serum NSE and bilirubin values [r-= 0.15, p= 0.33]. there was no relationship between NSE concentration and the duration of the hyperbilirubinemia [r = 0.29, p=0.23]. In this preliminary study, although we could not demonstrate any correlation between serum NSE and bilirubin levels but NSE levels were significantly higher in infants with auditory neuropathy which diagnosed by ABER. Thus, this finding indicated the importance of a close follow-up with dual screening of hearing by ABER and TEOAEs in hyperbilirubinemic newborns to avoid the auditory neuropathy. Biochemical index of neuronal damage [e.g. NSE] and ABERs can be used to evaluate the neurological sequels of neonatal hyperbilirubinemia like auditory neuropathy. For appropriate results to demonstrate the role of NSE and ABER for diagnosis of auditory neuropathy in neonatal hyperbilirubinemia, we must test a much larger sample of subjects in the future