期刊
JOURNAL OF NEUROTRAUMA
卷 20, 期 8, 页码 781-786出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/089771503767870005
关键词
child abuse; free radical; head injury; inflicted childhood trauma; oxidative stress; pediatric
It has been hypothesized that oxidative stress plays an important role in mediating secondary damage after traumatic brain injury (TBI). To study the relationship between lipid peroxidation, clinical variables, and neuronal damage in pediatric TBI, we measured levels of F-2-isoprostane, a marker of lipid peroxidation, and neuron-specific enolase (NSE), a marker of neuronal damage, in serial cerebrospinal fluid (CSF) samples from 23 infants and children with severe TBI (Glasgow Coma Scale score < 8). These were compared to CSF samples from 10 uninjured pediatric controls. On d1 after injury, F2-isoprostane was increased 6-fold vs. control (36.59 +/- 8.96 pg/ml vs. 5.64 +/- 8.08 pg/ml, p = 0.0035) and NSE was increased 10-fold (100.62 +/- 17.34 ng/ml vs. 8.63 +/- 2.76 ng/ml, p = 0.0002). Multivariate analysis of F-2-isoprostane levels and selected clinical variables showed a trend toward an inverse association with time after injury (p = 0.0708). Multivariate analysis of NSE levels and selected variables showed a positive association between d1 NSE and F-2-isoprostane (P = 0.0426). CSF F-2-isoprostane increases early after TBI in infants and children and is correlated with NSE, supporting a role for oxidative stress in the evolution of secondary damage early after severe TBI in infants and children.
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