脐血生物学标志物与早产儿脑损伤的关系
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摘要
目的探讨脐血血浆白介素-6 (IL-6)、降钙素原(PCT)和S100B蛋白与早产儿脑损伤之间的关系。方法选取2014年12月-2016年12月厦门市妇幼保健院NICU符合入组条件的244例胎龄≤34周的早产儿,于分娩时留取脐血,测定脐血血浆中IL-6、PCT、S100B水平;送胎盘病理检查;所有病例在出生后定期行头颅B超筛查,并在纠正胎龄36～42周时行颅脑磁共振(MRI)检查。结果头颅B超和MRI检查显示:早产儿脑损伤发生率38. 1%,其中出血性损伤发生率20. 1%、白质损伤发生率12. 7%,出血+白质损伤发生率4. 92%。母亲有绒毛膜羊膜炎的早产儿脑损伤的发生率为48. 94%,而母亲无绒毛膜羊膜炎的早产儿脑损伤发生率为23. 30%,两组比较差异有统计学意义(P=0. 000);按绒毛膜羊膜炎的分级(0、1、2、3级)分析,胎盘炎症程度越重,早产儿脑损伤发生率越高(P=0. 000)。脐血血浆IL-6、S100B水平在有、无脑损伤两组间差异有统计学意义(P<0. 05);进一步分析显示,脐血血浆S100B水平在出血性损伤组和白质损伤组、出血性损伤组和出血+白质损伤组之间差异有统计学意义(P<0. 05),在白质损伤组和出血+白质损伤组之间比较差异无统计学意义(P=0. 324);脐血血浆IL-6水平在3组间比较差异无统计学意义(P=0. 505)。分析脐血血浆IL-6、S100B水平与母亲绒毛膜羊膜炎、早产儿脑损伤之间的关系,结果显示脐血血浆IL-6水平在HCA+脑损伤和非HCA+非脑损伤组间比较差异有统计学意义(P=0. 040),其余各组差异无统计学意义(P>0. 05);脐血血浆S100B水平在HCA+脑损伤和HCA+非脑损伤、HCA+脑损伤和非HCA+非脑损伤、非HCA+脑损伤和非HCA+非脑损伤3组间两两比较,差异有统计学意义(P<0. 05);其余3组两两比较差异无统计学意义(P>0. 05)。脐血血浆S100B水平与胎龄呈负相关(r=-0. 150,P=0. 019);脐血血浆IL-6水平与胎龄无相关性(r=-0. 112,P=0. 081)。结论早产儿脑损伤的发生率仍高,与母亲有绒毛膜羊膜炎密切相关;存在脑损伤的早产儿,出生时脐血血浆IL-6、S100B水平明显升高,而且在白质损伤时脐血血浆S100B水平明显高于出血性损伤;相比IL-6,脐血血浆S100B水平对于早期预测早产儿脑损伤更具特异度。
引文
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[15] Sen J,Belli A. S100B in neuropathologic states:the CRP of the brain?[J]. J Neurosci Res,2007,85(7):1373-1380.
[16] Tiu SC,Chan WY,Heizmann CW,et al. Differential expression of S100B and S100A6 in the human fetal and aged cerebral cortex[J]. Brain Res,2000,119(2):159-168.
[2] Glass HC,Costarino AT,Stayer SA,et al. Outcomes for extremely premature infants[J]. Anesth Analg, 2015, 120(6):1337-1351.
[3] Hecht JL,Fichorova RN,Tang VF,et al. The relationship between neonatal blood protein profiles and placenta histologic characteristics in extremely low gestation age newborns[J]. Pediatr Res,2011,69(1):68-73.
[4]周丛乐,邵肖梅,叶鸿瑁,等.实用新生儿学[M].第4版,北京:人民卫生出版社,2012:706-715.
[5]刘畅,富建华,薛辛东,等.早产儿脑白质损伤的早期影像学改变及其对预后的影响[J].中华儿科杂志,2012,50(10):762-766.
[6] O'shea TM,Counsell SJ,Bartels DB,et al. Magnetic resonance and ultrasound brain imaging in preterm infants[J]. Early Hum Dev,2005,81(3):263-271.
[7] Volpe JJ. Cerebral white matter injury of the premature infant-more common than you think[J]. Pediatrics,2003,112(1Pt 1):176-180.
[8] Veyrac C,Couture A,Saguintaah M,et al. Brain ultrasonography in the premature infant[J]. Pediatr Radiol,2006,36(7):626-635.
[9]中华医学会儿科学分会新生儿学组,《中华儿科杂志》编辑委员会.早产儿脑室周围—脑室内出血与脑室周围白质软化的诊断建议[J].中华儿科杂志,2007,45(1):34-36.
[10]袁日明,俞惠民.重新认识早产儿脑损伤[J].中华围产医学杂志,2014,17(5):289-292.
[11] Rees S,Harding R,Walker D. The biological basis of injury and neuroprotection in the fetal and neonatal brain[J]. Int J Dev Neurosci,2011,29(6):551-563.
[12]詹险峰,梅梅.细胞因子与围产期脑损伤[J].中华围产医学杂志,2014,17(5):302-306.
[13] Lehnardt S. Innate immunity and neuroinflammation in the CNS:the role of microglia in Toll-like receptor-mediated neuronal injury[J]. Glia,2010,58(3):253-263.
[14]陈珊,李薇,瞿柳红,等.血浆S100B蛋白和髓鞘碱性蛋白与早产儿脑损伤的关系[J].中华实用儿科临床杂志,2014,29(12):902-906.
[15] Sen J,Belli A. S100B in neuropathologic states:the CRP of the brain?[J]. J Neurosci Res,2007,85(7):1373-1380.
[16] Tiu SC,Chan WY,Heizmann CW,et al. Differential expression of S100B and S100A6 in the human fetal and aged cerebral cortex[J]. Brain Res,2000,119(2):159-168.