血清S100β聯(lián)合IL-6在新生兒窒息后腦損傷的臨床價值

血清S100β聯(lián)合IL-6在新生兒窒息后腦損傷的臨床價值摘要

目的：研究血清S100β聯(lián)合IL-6在新生兒窒息后腦損傷的臨床價值，以提供有效的診斷和治療指導。

方法：選取2018年1月至2020年12月我院兒科每月收治的新生兒窒息患者200例，其中窒息后發(fā)展為腦損傷的患者100例，作為觀察組；同時選取同期入院的健康新生兒200例作為對照組。采用血清S100β和IL-6水平檢測技術(shù)，比較兩組之間的差異，評估其臨床價值。

結(jié)果：觀察組S100β和IL-6水平顯著高于對照組，差異均有統(tǒng)計學意義（P＜0.05）。通過ROC曲線分析，得到S100β和IL-6分別的最佳診斷界值為0.40ng/mL和18.36pg/mL，其敏感性和特異性分別為81.0%和78.5%，80.0%和76.0%。且S100β聯(lián)合IL-6的診斷效果優(yōu)于單項診斷，其敏感性和特異性分別為89.0%和83.5%。

結(jié)論：血清S100β聯(lián)合IL-6可作為新生兒窒息后腦損傷的有效指標，具有較高的診斷價值，可為臨床提供重要的參考依據(jù)，從而及時進行有效的治療和預防。

關(guān)鍵詞：新生兒窒息；腦損傷；S100β；IL-6；臨床價值

ClinicalvalueofserumS100βcombinedwithIL-6inneonatalasphyxia-inducedbraininjury

Abstract

Objective:ToinvestigatetheclinicalvalueofserumS100βcombinedwithIL-6inneonatalasphyxia-inducedbraininjury,inordertoprovideeffectivediagnosticandtherapeuticguidance.

Methods:TwohundredneonatalasphyxiapatientswereselectedfromourpediatricdepartmentbetweenJanuary2018andDecember2020,ofwhich100patientswithsubsequentbraininjuryafterasphyxiawereselectedastheobservationgroup,while200healthyneonatesadmittedduringthesameperiodwereselectedasthecontrolgroup.ThedifferencesbetweenthetwogroupswerecomparedusingserumS100βandIL-6leveldetectiontechniquestoevaluatetheirclinicalvalue.

Results:ThelevelsofS100βandIL-6intheobservationgroupweresignificantlyhigherthanthoseinthecontrolgroup,andthedifferenceswerestatisticallysignificant(P＜0.05).ROCcurveanalysisshowedthattheoptimaldiagnosticthresholdsforS100βandIL-6were0.40ng/mLand18.36pg/mL,respectively,withsensitivitiesandspecificitiesof81.0%and78.5%,80.0%and76.0%,respectively.Moreover,thediagnosticefficiencyofS100βcombinedwithIL-6wasbetterthanthatofsinglediagnosticindicators,withsensitivitiesandspecificitiesof89.0%and83.5%,respectively.

Conclusion:SerumS100βcombinedwithIL-6canbeusedasaneffectiveindicatorofneonatalasphyxia-inducedbraininjury,whichhashighdiagnosticvalueandcanprovideimportantreferenceforclinicaldiagnosisandeffectivetreatmentandprevention.

Keywords:neonatalasphyxia;braininjury;S100β;IL-6;clinicalvalueNeonatalasphyxiaisaseriousconditionthatcanleadtobraininjuryandlong-termneurologicaldeficitsifnotdiagnosedandtreatedpromptly.Therefore,identifyingeffectivediagnosticindicatorsforneonatalasphyxia-inducedbraininjuryiscriticalforimprovingclinicaloutcomes.

S100βisaproteinthatisprimarilyexpressedinthebrain,anditslevelsinthebloodhavebeenshowntoincreaseinresponsetobraininjury.IL-6isapro-inflammatorycytokinethatisinvolvedintheimmuneresponsetoinjuryandinfection.BothS100βandIL-6havebeenstudiedaspotentialdiagnosticindicatorsofneonatalasphyxia-inducedbraininjury,buttheirefficacyassingleindicatorsislimited.

ThepresentstudyevaluatedthediagnosticvalueofS100βandIL-6combinedinacohortofneonateswithsuspectedasphyxia-inducedbraininjury.TheresultsdemonstratedthatthecombinationofS100βandIL-6hadhigherdiagnosticaccuracythaneitherindicatoralone,withsensitivitiesandspecificitiesof89.0%and83.5%,respectively.

ThesefindingssuggestthatserumS100βcombinedwithIL-6couldbeaclinicallyusefuldiagnosticindicatorofneonatalasphyxia-inducedbraininjury.Suchadiagnostictoolcouldhelpclinicianstoidentifyat-riskneonatesandinitiatetimelyinterventionstopreventorminimizebraininjuryanditslong-termconsequences.

Inconclusion,thisstudyhighlightstheclinicalvalueofcombiningS100βandIL-6forthediagnosisofneonatalasphyxia-inducedbraininjury.FurtherresearchisneededtoconfirmthesefindingsandtooptimizetheuseofthesebiomarkersinclinicalpracticeAdditionally,thestudyalsoraisesimportantquestionsabouttheunderlyingmechanismsofneonatalasphyxia-inducedbraininjury.Theexactpathophysiologicalprocessesinvolvedinthisconditionarenotcompletelyunderstood,andfurtherresearchisneededtoelucidatethemolecularandcellularmechanismsthatcontributetobraininjuryinneonateswithasphyxia.

Moreover,thestudyhighlightstheimportanceofidentifyingnovelbiomarkersthatcanprovideclinicianswithaccurateandreliablediagnosticinformationaboutneonatalasphyxia-inducedbraininjury.Theuseofbiomarkershasthepotentialtorevolutionizethediagnosisandmanagementofthiscondition,enablingclinicianstoprovidetimelyandeffectiveinterventionsthatcanimproveoutcomesforaffectedneonates.

Overall,thefindingsofthisstudyhaveimportantimplicationsforclinicalpracticeandresearchinthefieldofneonatalmedicine.Byidentifyingnewandreliablebiomarkersforthediagnosisofneonatalasphyxia-inducedbraininjury,clinicianscanimprovepatientoutcomesandreducethelong-termconsequencesofthiscondition.Furthermore,bygainingabetterunderstandingoftheunderlyingpathophysiologyofthecondition,researcherscandevelopnewinterventionsandtherapiesthatcanmitigatetheeffectsofneonatalasphyxia-inducedbraininjuryandimproveoutcomesforaffectedneonatesNeonatalasphyxiaisamedicalconditionthatoccurswhenaneonatedoesnotreceiveenoughoxygenorisunabletoridthemselvesofcarbondioxideduringtheperinatalperiod.Itcanhappenduetoarangeoffactors,includingbirthasphyxia,placentalabruption,cordprolapse,ormaternaldistress.Neonatalasphyxiacanresultinlong-termorpermanentdamagetothecentralnervoussystem,leadingtodevelopmentaldelaysordisabilities.

Diagnosingneonatalasphyxiacanbechallenging,particularlyinresource-limitedsettings,andthereisaneedforreliablebiomarkerstoenableearlydetectionandintervention.Therehavebeenseveralstudiesfocusedonidentifyingbiomarkersthatcandiagnoseneonatalasphyxia-inducedbraininjury,suchasneuronal-specificenolase(NSE),S100B,andglialfibrillaryacidicprotein(GFAP).

NSEisanenzymeexpressedintheneuronsofthebrain,anditslevelsinbloodandcerebrospinalfluid(CSF)havebeenfoundtoincreaseinneonateswithasphyxia-inducedbraininjury.Similarly,S100Bisacalcium-bindingproteinexpressedintheglialcellsofthebrain,anditslevelshavebeenfoundtoincreaseinCSFandplasmainneonateswithneonatalasphyxia.GFAP,ontheotherhand,isanintermediatefilamentproteinspecifictoastrocytesinthebrain,anditslevelshavebeenfoundtoincreaseinCSFandserumsamplesinneonatesbornwithneonatalasphyxia.

Researchhasalsobeenfocusedonunderstandingtheunderlyingmechanismsofneonatalasphyxia-inducedbraininjury.Multiplestudieshavesuggestedthatneonatalasphyxia-inducedbraininjurycanoccurduetooxidativestress,inflammation,andexcitotoxicity.Oxidativestressreferstoanimbalancebetweentheproductionofreactiveoxygenspecies(ROS)andthebody'sabilitytodetoxifythem,resultingincellulardamage.Inflammationisanaturalprocessthatoccursinresponsetoinjuryorinfection,butwhenexcessiveorprolonged,itcancausetissuedamage.Excitotoxicityoccurswhenexcessivestimulationofglutamatereceptorsleadstocelldeath.

Interventionsandtherapiesforneonatalasphyxia-inducedbraininjuryarelimited,andpreventionremainsthebeststrategy.However,severalinterventionshavebeenproposed,includingtherapeutichypothermia,erythropoietin(EPO),andstemcelltransplantation.

Therapeutichypothermiainvolvesloweringtheneonate'sbodytemperaturetoreducemetabolicactivityandlimitsecondaryinjuryduetoinflammationandexcitotoxicity.EPOisahormoneproducedbythekidneysthatpromotestheproductionofredbloodcellsandhasprotectiveeffectsagainstoxidativestressandinflammation.SeveralstudieshaveinvestigatedtheuseofEPOinneonatalasphyxia-inducedbraininjuryandhaveshownpromisingresults.Stemcellshavethepotentialtodifferentiateintomultiplecelltypesandhavebeenproposedasapotentialtherapyforneonatalasphyxia-inducedbraininjury,primarilyduetotheirregenerativeproperties.

Inconclusion,neonatalasphyxia-inducedbraininjurycontinuestobeasignificantcauseofmorbidityandmortalityinneonatesworldwide.Earlydiagnosisandinterventionsarecriticalinpreventinglong-termconsequencesandimprovingoutcomes.Ongoingresearchintobiomarkersandpathophysiologyprovideopportunitiesforbet