Vasiljević Brankica, Maglajlić-Djukić Svjetlana, Gojnić Miroslava, Stanković Sanja
Clinic of Gynecology and Obstetrics, Clinical Centre of Serbia Visgradska 26, 11000 Belgrade, Serbia.
Srp Arh Celok Lek. 2012 Jan-Feb;140(1-2):35-41.
The pathogenesis of perinatal hypoxic-ischemic brain damage is highly complex.
The aim of this study was to assess the role of oxidative stress in hypoxic-ischemic brain injury and subsequent abnormal neurological outcome in infants with perinatal hypoxic-ischemic encephalopathy (HIE). We estimated perinatal oxidative brain damage measuring activity of glutathione peroxidase (GPX) in cerebrospinal fluid (CSF) as an indirect biomarker of free radical production during cerebral hypoxia-ischemia in correlation with the level of intracellular enzyme neuron specific enolase (NSE) in CSF as a biomarker of extend of brain injury.
Ninety neonates (>32 GA) with perinatal HIE were enrolled prospectively. HIE was categorized into three stages according Sarnat and Sarnat clinical scoring system and changes seen on amplitude integrated EEG. CSF for GPX analysis and NSE analysis was taken in the first 72 hours of life. Neurodevelopment outcome was assessed at 12 months of corrected gestational age.
GPX activity in CSF was in good relation with clinical stage of HIE (p < 0.0001) and GA (p < 0.0001) and significantly corresponded with subsequent neurodevelopment outcome (p < 0.001). GPX activity in CSF showed a strong correlation with NSE levels in CSF (p < 0.001) as the biomarker of extent of brain injury.
Our results suggest that oxidative stress might be important contributing factor in perinatal hypoxic-ischemic brain damage, particularly in preterm neonates.
围产期缺氧缺血性脑损伤的发病机制高度复杂。
本研究旨在评估氧化应激在围产期缺氧缺血性脑病（HIE）婴儿的缺氧缺血性脑损伤及随后异常神经学结局中的作用。我们通过测量脑脊液（CSF）中谷胱甘肽过氧化物酶（GPX）的活性来估计围产期氧化脑损伤，作为脑缺氧缺血期间自由基产生的间接生物标志物，并与CSF中细胞内酶神经元特异性烯醇化酶（NSE）的水平相关联，后者作为脑损伤程度的生物标志物。
前瞻性纳入90例孕周>32周的围产期HIE新生儿。根据Sarnat和Sarnat临床评分系统以及振幅整合脑电图上的变化，将HIE分为三个阶段。在出生后的前72小时内采集CSF用于GPX分析和NSE分析。在矫正胎龄12个月时评估神经发育结局。
CSF中的GPX活性与HIE的临床阶段（p<0.0001）和孕周（p<0.0001）密切相关，并且与随后的神经发育结局显著相关（p<0.001）。CSF中的GPX活性与CSF中作为脑损伤程度生物标志物的NSE水平密切相关（p<0.001）。
我们的结果表明，氧化应激可能是围产期缺氧缺血性脑损伤的重要促成因素，尤其是在早产儿中。
