Document Type : Original Article
Department of Pediatrics, North Khorasan University of Medical Sciences, Bojnurd, Iran
Department of Obstetrics and Gynecology, School of Medicine, University of Texas Medical Branch, Texas, USA
Department of Pathobiology and Laboratory Sciences, North Khorasan University of Medical Sciences, Bojnurd, Iran
Background: Neonatal hypoxic-ischemic encephalopathy (HIE) is one of the most common causes of long-term neurological disabilities among children. Various types of cellular stress stimuli, including oxidative stress, inflammation, and hypoxia, induce heme oxygenase-1 (HO-1) enzyme for different kinds of tissues. The purpose of this study was to evaluate the plasma level of HO-1 enzyme in neonatal HIE patients and to determine the relationship between HO-1 enzyme level and clinical severity of HIE.
Methods: In this case-control study, the plasma level of HO-1 enzyme was measured through sandwich ELISA in 28 newborns with a proven diagnosis of HIE and 31 healthy full-term newborns admitted to Bentolhoda Hospital, Bojnourd, Iran. Newborns with HIE were classified according to the Sarnat staging to mild, moderate, and severe HIE. Maternal and neonatal data were recorded in checklists and compared between the two groups.
Results: The mean plasma level of HO-1 enzyme in HIE patients was significantly higher than that in the control group (104.0 ± 4.01 and 91.63± 2.67 pg/ml, respectively, P=0.011). We also found that plasma HO-1 levels were significantly higher in severe neonatal HIE patients compared to mild and moderate neonatal HIE patients (121.0 ± 8.48Vs. 91.23 ± 3.35 and 105.5 ± 5.76,
P ˂ 0.001).
Conclusion: Our findings suggested that HO-1enzyme may be associated with the pathophysiology and clinical severity of neonatal HIE. We suggest further research on the correlation of plasma level of HO-1 enzyme at birth with the multi-organ dysfunction and abnormal neurodevelopmental outcomes in full-term newborns with HIE.