Maternal diabetes constitutes an unfavorable environment for embryonic and fetoplacental development. Despite current treatments, pregnant women with pregestational diabetes are at increased risk for congenital malfor...Maternal diabetes constitutes an unfavorable environment for embryonic and fetoplacental development. Despite current treatments, pregnant women with pregestational diabetes are at increased risk for congenital malformations, materno-fetal complications, placental abnormalities and intrauterine malprogramming. The complications during pregnancy concern the mother (gravidic hypertension and/or preeclampsia, cesarean section) and the fetus (macrosomia or intrauterine growth restriction, shoulder dystocia, hypoglycemia and respiratory distress). The fetoplacental impairment and intrauterine programming of diseases in the offspring's later life induced by gestational diabetes are similar to those induced by type 1 and type 2 diabetes mellitus. Despite the existence of several developmental and morphological differences in the placenta from rodents and women, there are similarities in the alterations induced by maternal diabetes in the placenta from diabetic patients and diabetic experimental models. From both human and rodent diabetic experimentalmodels, it has been suggested that the placenta is a compromised target that largely suffers the impact of maternal diabetes. Depending on the maternal metabolic and proin ammatory derangements, macrosomia is explained by an excessive availability of nutrients and an increase in fetal insulin release, a phenotype related to the programming of glucose intolerance. The degree of fetal damage and placental dysfunction and the availability and utilisation of fetal substrates can lead to the induction of macrosomia or intrauterine growth restriction. In maternal diabetes, both the maternal environment and the genetic background are important in the complex and multifactorial processes that induce damage to the embryo, the placenta, the fetus and the offspring. Nevertheless, further research is needed to better understand the mechanisms that govern the early embryo development, the induction of congenital anomalies and fetal overgrowth in maternal diabetes.展开更多
目的探讨晚孕期多普勒超声技术测定多血管血流参数联合胎盘功能标评估胎儿生长受限(FGR)的价值。方法选择FGR孕妇42例作为FGR组,年龄23~35岁,平均年龄28.8岁(标准差3.35岁);孕周28~37+4周,平均孕周32+6.5周(标准差2+4.5周);孕前身体质...目的探讨晚孕期多普勒超声技术测定多血管血流参数联合胎盘功能标评估胎儿生长受限(FGR)的价值。方法选择FGR孕妇42例作为FGR组,年龄23~35岁,平均年龄28.8岁(标准差3.35岁);孕周28~37+4周,平均孕周32+6.5周(标准差2+4.5周);孕前身体质量指数(BMI)18.6~23.8 kg/m^(2),平均BMI 21.5 kg/m^(2)(标准差1.43 kg/m^(2))。产前检查正常孕妇61例作为对照组,年龄23~36岁,平均年龄29.3岁(标准差3.49岁);孕周28^(+2)~38周,平均孕周31^(+4.5)周(标准差3^(+2.7)周);孕前BMI 18.2~23.6 kg/m^(2),平均BMI 21.4 kg/m^(2)(标准差1.39 kg/m^(2))。通过多普勒超声检测各组多血管参数,包括脐动脉(UA)、大脑中动脉(MCA)、子宫动脉(UtA)的搏动指数(PI)、阻力指数(RI)及收缩期最大血流速度与舒张末期血流速度之比(S/D),计算脑-胎盘比(CPR)。定量检测母体血清雌三醇(E3)、胎盘泌乳素(HPL),评估胎盘功能,分析多血管血流参数及母体血指标与FGR的相关性,采用受试者工作特性(ROC)曲线评价不同指标对FGR的诊断预测价值。结果FGR组不良妊娠结局的发生率显著高于对照组(61.9%vs 11.5%。P<0.001)。FGR组UA-PI高于对照组(1.06±0.33 vs 0.94±0.19。P<0.05),而两组UA-S/D及RI比较,差异无统计学意义(P>0.05);FGR组MCA各参数[(PI:1.53±0.33 vs 1.75±0.32;S/D:4.26(3.43~5.24)vs 5.12(4.25~6.72);RI:0.76±0.07 vs 0.81±0.06]、CPR(1.59±0.59 vs 1.91±0.44)及母体血清E3[7.79(4.91~11.30)ng/mL vs 12.00(10.20~13.95)ng/mL]和HPL[(9.00±2.80)mg/L vs(11.91±2.27)mg/L]水平低于对照组,FGR组UtA各参数高于对照组[PI:0.75(0.66~1.07)vs 0.56(0.50~0.67);S/D:2.11(1.80~2.78)vs 1.86(1.70~2.19);RI:0.55±0.12 vs 0.47±0.08。均P<0.05]。多普勒超声检测单一血管参数预测FGR的诊断效能普遍较低(AUC<0.7),多普勒超声检测多血管参数联合母体血指标评估FRG(AUC=0.883),可显著提高诊断效能。结论单一血管的多普勒血流参数预测FGR的准确性较低,联合多血管血流参数与胎盘功能�展开更多
目的:探讨三维彩色能量成像(three-dimensional color power angiographic,3D-CPA)联合彩色多普勒血流成像(color Doppler flow imaging,CDFI)对妊高症孕妇胎盘功能评定的可行性。方法:回顾性收集某院2018年1月至2020年6月期间就诊的孕...目的:探讨三维彩色能量成像(three-dimensional color power angiographic,3D-CPA)联合彩色多普勒血流成像(color Doppler flow imaging,CDFI)对妊高症孕妇胎盘功能评定的可行性。方法:回顾性收集某院2018年1月至2020年6月期间就诊的孕周为30~42周的180例孕妇的临床资料,根据是否存在妊高症将180例孕妇分为实验组(100例)和对照组(80例),并根据实验组孕妇临床表现严重程度分为轻度子痫前期组(A组,78例)和重度子痫前期组(B组,22例),实验组和对照组均行3D-CPA联合CDFI检查,记录胎儿脐动脉、胎儿大脑中动脉、子宫动脉的收缩末期峰值/舒张末期峰值(systolic/diastolic,S/D)、搏动指数(pulsatile index,PI)、阻力指数(resistance index,RI)及胎盘血管化指数(vascularization index,VI)、血流指数(flow index,FI)和血管化血流指数(vascularization-flow index,VFI)值。采用SPSS 18.0软件进行统计学分析。结果:B组孕妇年龄明显大于对照组及A组(P均<0.05),A组孕妇年龄大于对照组(P<0.05);实验组和对照组孕妇的孕次、产次无明显差异(P均>0.05);B组孕妇胎儿脐动脉血流参数S/D、PI、RI值明显高于对照组及A组(P均<0.05);B组、A组孕妇子宫动脉血流参数S/D、PI、RI值均高于对照组(P均<0.05);B组、A组胎盘三维能量指数VI、FI、VFI值均明显低于对照组(P均<0.05);对照组、实验组孕37周+孕妇血流参数S/D、PI、RI值均低于孕30~37周孕妇(P均<0.05),实验组孕37周+血流参数S/D、PI、RI值均低于对照组孕37周+孕妇(P均<0.05)。结论:3D-CPA联合CDFI可对子宫动脉、脐动脉以及胎儿大脑中动脉相关血流参数及胎盘三维能量指数进行量化分析,在妊高症孕妇胎盘功能评估方面具有重要意义,可为临床医师评估孕妇胎盘功能提供参考。展开更多
文摘Maternal diabetes constitutes an unfavorable environment for embryonic and fetoplacental development. Despite current treatments, pregnant women with pregestational diabetes are at increased risk for congenital malformations, materno-fetal complications, placental abnormalities and intrauterine malprogramming. The complications during pregnancy concern the mother (gravidic hypertension and/or preeclampsia, cesarean section) and the fetus (macrosomia or intrauterine growth restriction, shoulder dystocia, hypoglycemia and respiratory distress). The fetoplacental impairment and intrauterine programming of diseases in the offspring's later life induced by gestational diabetes are similar to those induced by type 1 and type 2 diabetes mellitus. Despite the existence of several developmental and morphological differences in the placenta from rodents and women, there are similarities in the alterations induced by maternal diabetes in the placenta from diabetic patients and diabetic experimental models. From both human and rodent diabetic experimentalmodels, it has been suggested that the placenta is a compromised target that largely suffers the impact of maternal diabetes. Depending on the maternal metabolic and proin ammatory derangements, macrosomia is explained by an excessive availability of nutrients and an increase in fetal insulin release, a phenotype related to the programming of glucose intolerance. The degree of fetal damage and placental dysfunction and the availability and utilisation of fetal substrates can lead to the induction of macrosomia or intrauterine growth restriction. In maternal diabetes, both the maternal environment and the genetic background are important in the complex and multifactorial processes that induce damage to the embryo, the placenta, the fetus and the offspring. Nevertheless, further research is needed to better understand the mechanisms that govern the early embryo development, the induction of congenital anomalies and fetal overgrowth in maternal diabetes.
文摘目的探讨晚孕期多普勒超声技术测定多血管血流参数联合胎盘功能标评估胎儿生长受限(FGR)的价值。方法选择FGR孕妇42例作为FGR组,年龄23~35岁,平均年龄28.8岁(标准差3.35岁);孕周28~37+4周,平均孕周32+6.5周(标准差2+4.5周);孕前身体质量指数(BMI)18.6~23.8 kg/m^(2),平均BMI 21.5 kg/m^(2)(标准差1.43 kg/m^(2))。产前检查正常孕妇61例作为对照组,年龄23~36岁,平均年龄29.3岁(标准差3.49岁);孕周28^(+2)~38周,平均孕周31^(+4.5)周(标准差3^(+2.7)周);孕前BMI 18.2~23.6 kg/m^(2),平均BMI 21.4 kg/m^(2)(标准差1.39 kg/m^(2))。通过多普勒超声检测各组多血管参数,包括脐动脉(UA)、大脑中动脉(MCA)、子宫动脉(UtA)的搏动指数(PI)、阻力指数(RI)及收缩期最大血流速度与舒张末期血流速度之比(S/D),计算脑-胎盘比(CPR)。定量检测母体血清雌三醇(E3)、胎盘泌乳素(HPL),评估胎盘功能,分析多血管血流参数及母体血指标与FGR的相关性,采用受试者工作特性(ROC)曲线评价不同指标对FGR的诊断预测价值。结果FGR组不良妊娠结局的发生率显著高于对照组(61.9%vs 11.5%。P<0.001)。FGR组UA-PI高于对照组(1.06±0.33 vs 0.94±0.19。P<0.05),而两组UA-S/D及RI比较,差异无统计学意义(P>0.05);FGR组MCA各参数[(PI:1.53±0.33 vs 1.75±0.32;S/D:4.26(3.43~5.24)vs 5.12(4.25~6.72);RI:0.76±0.07 vs 0.81±0.06]、CPR(1.59±0.59 vs 1.91±0.44)及母体血清E3[7.79(4.91~11.30)ng/mL vs 12.00(10.20~13.95)ng/mL]和HPL[(9.00±2.80)mg/L vs(11.91±2.27)mg/L]水平低于对照组,FGR组UtA各参数高于对照组[PI:0.75(0.66~1.07)vs 0.56(0.50~0.67);S/D:2.11(1.80~2.78)vs 1.86(1.70~2.19);RI:0.55±0.12 vs 0.47±0.08。均P<0.05]。多普勒超声检测单一血管参数预测FGR的诊断效能普遍较低(AUC<0.7),多普勒超声检测多血管参数联合母体血指标评估FRG(AUC=0.883),可显著提高诊断效能。结论单一血管的多普勒血流参数预测FGR的准确性较低,联合多血管血流参数与胎盘功能�
