妊娠期糖尿病患者氧化应激和EPO、FNRBC水平变化与胎盘组织学改变的关系

目的:探讨妊娠期糖尿病(GDM)患者氧化应激状态与脐血促红细胞生成素(EPO)和胎儿有核红细胞(FNRBC)水平变化及其与胎盘组织形态学异常发生率的关系。方法:选取28例GDM患者(GDM组)和22例正常妊娠妇女(正常对照组),采集其母血和脐血及对应的胎盘标本,检测母血和脐血氧化应激标志物丙二醛(MDA)、超氧化物歧化酶(SOD)浓度,脐血EPO浓度和FNRBC计数,同时对胎盘组织进行病理学检测。结果:GDM组患者母血和脐血中的MDA及脐血中EPO浓度和FNRBC计数明显高于正常对照组(P<0.05),SOD浓度较正常对照组明显降低(P<0.05)。GDM组患者胎盘病理检查提示,与正常对照组相比:绒毛成熟不良、干绒毛小动脉增厚和绒毛间质毛细血管充盈明显的发生比例增加(P<0.05),并且母血和脐血中的MDA浓度与胎盘绒毛成熟不良的发生比例呈正相关(P均<0.05)。结论:胎盘绒毛发育和成熟的复杂过程可能受母胎氧化应激与抗氧化环境的影响,胎盘病理组织学显示GDM时绒毛血管发育与成熟的异常可能导致胎儿缺氧和不良后果。

The Relationship of Oxidative Stress Status, Umbilical Cord Plasma Erythropoietin and Fetal Nucleated Red Blood Cell Level with Placenta Histological Changes in Pregnant Women with Gestational Diabetes Mellitus

Objective:To explore the relationship of oxidative stress status,umbilical cord plasma erythropoietin(EPO) level and fetal nucleated red blood cell(FNRBC) with placental histological abnormalities in women with gestational diabetes mellitus(GDM).Methods:28 GDM patients and 22 normal pregnancy women as control were recruited in this study.Maternal and cord blood and placental samples were obtained from all pregnant women.Cord plasma EPO and FNRBC counts,maternal and cord plasma malondialdehyde(MDA) and Superoxide Dismutase(SOD) levels were measured.Placental tissues were examined histopathologically.Results:Maternal and cord plasma levels of MDA,cord plasma EPO levels and FNRBC counts were significantly higher in GDM patients than those in normal control(P<0.05),while SOD levels in GDM patients were lower than that in normal control(P<0.05).Pathologic examination of placenta revealed villous immaturity,stem villus arteriole thickening and intervillous capillary congestion were more obvious in GDM group than normal control(P<0.05).The increased levels of maternal and cord plasma MDA were correlated with the presence of villous immaturity(P<0.05).Conclusions:The complex process of villous development and maturity might be influenced by the maternal and fetal oxidative and antioxidative milieu.The abnormalities of placenta in angiogenesis and maturation may lead to fetal hypoxia and compromise.