| Objective:Brain injury in premature infants is a common complication. With therapid development of perinatal medicine and neonatal intensive caretechnology, the survival rate of premature infants is higher than before,however10%-20%of the preterm infants have different degree ofneurological sequelae, that caused heavy burden to society and family. Soearly diagnosis and early control are urgent. In addition to the associated withpremature own factors, a common cause of premature brain injure includeperinatal hypoxia ischemia，infection，oxidative stress or inflammation. Inrecent years, a lot of researches have shown that a variety of inflammatorymediators and cytokines involved in the pathophysiological process of braindamage, the role of inflammatory factors in brain damage course is paid moreand more attention. neurons in the brain and cerebral vascular endothelial cellshave a large number of visfatin.In recent years,it is considered a beforinflammatory factor, Hypoxia can lead the level of visfatin to increase，thatcan damage vascular endothelial and increase IL-1β, IL-6, and the level ofTNF-A, thus start the brain damage in the inflammatory cascade reaction.High mobility protein1(HMGB1) is a kind of important inflammatorymediators. It expressed in the brain tissue widely. When hypoxia ischemiadamage brain, the serum HMGB1is released by damaged neurons orastrocytes passive in early and amplifies the delay phase of nerveinflammation, aggravate the brain damage. This study will observe theexpression of serum visfatin and high mobility group protein1in prematurebrain damage disease dynamically.To evaluate the dynamic changes of serumvisfatin and high mobility group box-1(HMGB1) levels in premature braininjure，and try to find the relationship between their levels and the severity of premature brain injure, it will reveal secondary inflammatory reaction in therole of brain damage, In order to further reveal the pathogenesis of prematureinfant brain injury to provide clinical trial basis.Methods:From the fourth hospital of Hebei medical university neonatal obstetricand intensive care unit，chose80premature infants from march2013tillJanuary2014who had perinatal hypoxic ischemic risk factors. Perinatalhypoxic ischemic risk factors was including pregnancy-induced hypertensionsyndrome, Perinatal asphyxia，abnormal placenta, umbilical cord abnormality,and maternalanemia. According to clinical manifestations and ultrasound forthe diagnosis and differential diagnosis of premature infant brain injurydegree: no brain injury group50cases,30cases of brain injury group,16cases with mild brain injury group, moderate-severe brain injury14cases ofthe group; statistieally. The umbilical cord blood(2ml) were collectedimmediately after the newborns delivered. In addition, blood samples werecollected from venous blood of all cases in24-48hours and7days after birth,then divided into dry tubes, centrifuged5minutes with3000r/min and extractserum (1ml)-70℃refrigerator storage under test. The levels of serumHMGB1and visfatin were detected by ELISA technique. SPSS13.0statisticssoftware was used to carry on statistics processing. Qauntitiative variableswere describled as Mean±SD, Comparising two groups using T-text，Comparison among groups using single factor analysis of variance (one-wayANOVA), and SNK-q method was used between two group; To compare therelationship using linear correlation analysis;Chi-Square was used to comparecategorical variables. P-value<0.05(double side) had statistical significance.Results:1The clinical data of the selected children：Differences comparedbetween the two groups of neonates, gestational age, gender, weight, et al. theresult of the Equilibrium Analysis is they have no statistical difference(P>0.05).2The relationship between hypoxic ischemic risk factors in perinatal period and premature brain injury：Mother pregnancy hypertension syndrome,perinatal asphyxia, abnormal umbilical cord and placental abnormalities haddramatically increased the incidence of brain injury, and difference comparingwith no brain injury group was statistically significant(P<0.05); comparing thebrain injury groups who had maternal anemia with no brain injury group wasno significant difference(P>0.05).3Comparing the levels of visfatin and HMGB1between no brain injurygroup and brain injury group on cord blood,1-2day,7day after birth：On cordblood,1-2day,7day after birth point，the level of visfatin (63.68±12.572.37±11.9557.34±9.7)and HMGB1(66.44±12.2575.93±13.371.93±12.05)inbrain injury group were obviously higher than those in the no brain injurygroup (P<0.05).4Comparing the levels of visfatin and HMGB1among different degreebrain injury groups：On cord blood,1-2days after birth point,7day after birthpoint， the levels of visfatin(68.58±11.5777.15±12.0460.73±7.58）andHMGB1（70.97±13.2182.85±10.4676.65±11.71）in severe brain damagegroup were higher than the levels visfatin （59.40±12.0268.18±10.5054.38±10.58）and HMGB1（67.47±10.1469.85±12.7567.81±11.07） in mildbrain injury group (P<0.05). On７day after birth point， the levels ofvisfatin(54.38±10.5852.28±9.77) between mild brain injury group and nobrain injury group was no difference(P>0.05); the levels of HMGB1（67.81±11.07，40.61±7.34） was higher than those in no brain injury group(P<0.05).5The dynamic change of visfatin and HMGB1between brain damagegroup and no brain injury group：Umbilical cord blood the level of visfatin andHMGB1in brain injury group were high level；The1-2day after birth thelevel of visfatin and HMGB1continue to increase，and it was higher thanthose on cord blood point (P<0.05). The7day after birth, the level of visfatinwas lower than those on1-2day after birth (P<0.05), the mild group back tothe level of no brain damage group,with no obvious difference compared tothe no brain damage group (P>0.05).The severe brain damage group still higher than those in the no brain damage group and mild brain damage group(P<0.05). Comparing1-2day after birth, the level of HMGB1was no fallingon the7day after birth (P>0.05). The level of visfatin and HMGB1in nobrain injury group were no difference on cord blood,1-2days after birthpoint,7day after birth point (P>0.05).6The correlation with visfatin and HMGB1：The visfatin and HMGB1’slevels on cord blood and1-2days after birth was positively correlated (cordblood r1=0.529, P1=0.003；1-2day r2=0.634，P2=0.000)，On7days after birthpoint， the visfatin and HMGB1’s levels were no correlation（7day r7=-0.008，P7=0.882）.Conclusion:1Mother pregnancy-induced hypertension syndrome, perinatalasphyxia，abnormal umbilical cord and placental abnormalities are high riskfactors of premature infant brain injury, and they are closely related topremature infant brain injury.2The levels visfatin and HMGB1increase significantly in brain damagegroup，and they associate with the degree of brain injury closely.3The change of the level of visfatin and HMGB1in cord blood and1-2day after birth has correlation,especially in1-2day.The change of it suggestthat the tendency of the two index is agreement in brain damage,which likelywork together in the secondary brain injury. Monitoring visfatin and HMGB1can forecast the incidence of brain damage. |
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