Pediatrics international : official journal of the Japan Pediatric Society · 2008
Neurokinin A level in hypoxic-ischemic encephalopathy.
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Nassar May F, El-Sayed Hoda L, Fouad Nermine T, El-Toukhy Hazem I
Аннотация
BACKGROUND: The present study was performed to investigate the effect of neonatal hypoxic-ischemic encephalopathy (HIE) on the neurotransmitter neurokinin A (NKA) and determine its relation to the severity of neonatal hypoxia.
METHODS: Eighteen neonates suffering from HIE were compared to 10 clinically healthy full-term neonates acting as the control group. Maternal history of each neonate was collected, then deliveries were attended, resuscitation details including the Apgar score and thorough clinical examination of the neonates were performed. Routine laboratory work-up was done for the enrolled neonates, including complete blood count and C-reactive protein as well as estimation of NKA by enzyme-linked immunosorbent assay in the cord blood and after clinical stabilization.
RESULTS: NKA was significantly lower in HIE patients compared to the controls at delivery with improvement in the follow-up sample. Additionally, the maximum decrease was detected in the neonates who suffered severe hypoxia compared to those who suffered mild hypoxia. Significant positive correlations were demonstrated between NKA at birth and Apgar scores at the 10th and 15th min. Regression showed that stage of HIE was the strongest determinant factor for the level of NKA at birth.
CONCLUSION: NKA levels are decreased in HIE and this is more profound in the severe degrees of hypoxia compared to the mild ones. This emphasizes its role in pathogenesis of HIE and further proves that an imbalance in the central neuropeptide system results from HIE in the neonatal period.
METHODS: Eighteen neonates suffering from HIE were compared to 10 clinically healthy full-term neonates acting as the control group. Maternal history of each neonate was collected, then deliveries were attended, resuscitation details including the Apgar score and thorough clinical examination of the neonates were performed. Routine laboratory work-up was done for the enrolled neonates, including complete blood count and C-reactive protein as well as estimation of NKA by enzyme-linked immunosorbent assay in the cord blood and after clinical stabilization.
RESULTS: NKA was significantly lower in HIE patients compared to the controls at delivery with improvement in the follow-up sample. Additionally, the maximum decrease was detected in the neonates who suffered severe hypoxia compared to those who suffered mild hypoxia. Significant positive correlations were demonstrated between NKA at birth and Apgar scores at the 10th and 15th min. Regression showed that stage of HIE was the strongest determinant factor for the level of NKA at birth.
CONCLUSION: NKA levels are decreased in HIE and this is more profound in the severe degrees of hypoxia compared to the mild ones. This emphasizes its role in pathogenesis of HIE and further proves that an imbalance in the central neuropeptide system results from HIE in the neonatal period.