胎盘表皮生长因子受体的表达改变与胎儿宫内生长迟缓 …

目的 研究胎儿宫内生长迟缓（ＩＵＧＲ）患者胎盘表皮生长因子受体（ＥＧＦＲ）的表达与正常妊娠及巨大儿胎盘之间是否有差异,并分析其变化与胎盘绒毛发育是否有关。方法 取足月分娩胎盘组织标本６３例,于分娩后立即置于４％中性甲醛缓冲液固定。用免疫组织化学ＳＰ法进行胎盘ＥＧＦＲ检测。同时对肖绒毛血管大小、面积及绒毛面密度等进行分析测量。结果 ＩＵＧＲ组胎盘ＥＧＦＲ的表达较正常对照组和巨大儿组明显增加,ＩＵＧＲ     

胎儿生长迟缓孕妇胎盘微绒毛的体视学研究

对１２例胎儿生长迟缓及１０例正常胎儿（对照组）的盘组织进行光镜水平和电镜水平的定量观测。ＩＵＧＲ组中，胎盘正常重量指数的有６例，低重量的指数的有６例。结果：ＩＵＧＲ组胎盘重量、胎盘容积、绒毛表面积及绒毛毛细血管表面积均小于对照组，ＮＰＩ组胎盘重量、胎盘容积、绒毛表面积、绒毛毛细血管表面积、微绒行间腔表面积密度和微绒毛表面积绝驿值小于对照组及ＬＰＩ组。     

胎儿宫内生长迟缓患者脐动脉波形异常与胎盘病理改变的关系

目的　探讨胎儿宫内生长迟缓（IUGR）患者胎儿脐动脉波形异常与胎盘重量、体积及各级绒毛血管数量的关系。方法　选择分娩前1周内,患IUGR或B超检查有胎儿脐动脉波形异常的患者40例,分为脐动脉波形异常伴IUGR10例为研究组;脐动脉波形异常不伴IUGR（AN）;脐动脉波形正常伴IUGR（NA）,脐动脉波形正常不伴IUGR（NN）各10例为对照组。用免疫组织化学SP法,检测以上各组胎盘干血管中α-平滑肌肌动蛋白（α-smoothmuscleactin,α-SMA）表达,以确定各级绒毛和各级血管,比较研究组和各对照组间胎盘重量、体积大小、各级绒毛及血管数量。结果　（1）研究组胎盘重量、体积分别为（283.40±23.82)g及（234.60±52.08)cm     

胎儿宫内发育迟缓胎盘的组织计量观察

对妊高征合并胎儿宫内发育迟缓（ＩＵＧＲ）１１例、ＩＵＧＲ１３例、正常妊娠分娩１５例患者的胎盘组织进行了形态测定及观察。结果表明：ＩＵＧＲ患者胎盘中代表胎儿循环的三级绒毛干动脉总数、正常动脉比例数及百分比明显低于对照组（Ｐ〈０．０１）。代表母儿交换能力的血管合体膜（ＶＳＭ）百分比及绒毛间隙容积百分比也明显低于对照组（Ｐ〉０．０５）。而标志着胎盘缺氧的合体结节绒毛百分比则显著增高。提示：有ＩＵＧＲ时胎     

胎儿生长迟缓胎盘病理检查与病原体检测的对比研究

目的：研究胎儿宫内生长迟缓胎盘病理变化与胎盘石蜡包埋组织有关病原体检测结果的相关性。方法：对１９８６～１９９３年５３例胎儿宫内生长迟缓胎盘进行病理检查，并用ＰＣＲ技术对石蜡包埋的胎盘组织进行弓形体、巨细胞病毒及Ⅱ型单纯疱疹病毒检测。结果：５３例中１９例检出病原体，感染率３５．８５％。胎盘有绒毛炎的１８例中１０例病原体阳性，以绒毛发育迟缓为主要病变的１１例中７例病原体阳性，绒毛间隙炎的３例中２例病原体阳性。胎盘有上述病理性改变者，血行性感染发生率达５９．３８％。结论：本研究显示某些原因不明的胎儿宫内生长迟缓系胎盘血行性感染所致。而绒毛炎、绒毛成熟障碍的形态学变化则提示胎盘的血行性感染。     

胎盘表皮生长因子受体的表达改变与胎儿宫内生长迟缓的关系研究

目的　研究胎儿宫内生长迟缓 (IUGR)患者胎盘表皮生长因子受体 (EGFR)的表达与正常妊娠及巨大儿胎盘之间是否有差异 ,并分析其变化与胎盘绒毛发育是否有关。方法　取足月分娩胎盘组织标本 6 3例 ,于分娩后立即置于 4%中性甲醛缓冲液固定。用免疫组织化学SP法进行胎盘EGFR检测。同时对末梢绒毛血管大小、面积及绒毛面密度等进行分析测量。结果　IUGR组胎盘EGFR的表达较正常对照组和巨大儿组明显增加 (P <0 0 1) ,IUGR胎盘末梢绒毛血管数及血管占绒毛横面积比均明显减少 (P均 <0 0 5 ;P均 <0 0 0 1) ;而巨大儿组与对照组比较无显著性差异。三组胎盘绒毛面密度无显著性差异 (P >0 0 5 )。结论　IUGR儿胎盘EGFR表达增加与其胎盘绒毛发育不良有关 ,EGFR在胎儿胎盘的生长发育及IUGR的发生中起重要调节作用。     

胎儿宫内发育迟缓的胎盘病理变化

孕妇、胎盘和胎儿三方面间的功能有着复杂的关系 ,导致胎儿宫内发育迟缓 (ＩＵＧＲ)的母体或胎儿因素往往可反映在胎盘的形态学 (包括孕期胎盘的血行性感染 )、胎盘组织光镜与电镜的体视学 (ＩＵＧＲ胎盘绒毛的组织计量检测、不同重量指数ＩＵＧＲ胎盘绒毛光镜与电镜的体视学、不同重量指数ＩＵＧＲ胎盘微绒毛的体视学 )上 ,且胎盘本身的变化及胎盘床的变化亦可导致ＩＵＧＲ。现将常见的直接或间接与胎盘及其附属物有关的病理变化分述如下。1　胎盘发育异常1.1　胎盘成熟障碍的光镜表现　　正常妊娠时 ,随着孕周的增加 ,胎盘也不断发育和成…     

胎儿宫内发育迟缓时胎盘病理改变与孕妇血及脐血中一氧化氮水平的关系

目的了解胎儿宫内发育迟缓（ＩＵＧＲ）时胎盘病理改变与母血及脐血中一氧化氮（ＮＯ）水平的关系。方法对１９９７年１１月～１９９８年１０月３８例妊娠合并胎儿宫内发育迟缓（ＩＵＧＲ组）及３０例正常孕妇（对照组）分娩后的胎盘及胎儿附属物进行分析。用隔还原显色法测定母血及脐血ＮＯ水平。结果ＩＵＧＲ组中２６例有胎盘、脐带病理改变（６８．４２％）。主要表现为绒毛发育迟缓及绒毛炎;对照组中５例有胎盘病理改变（１６．６７％）,两组比较差异有极显著性（Ｐ＜０．０１）;ＩＵＧＲ组中母血及脐血ＮＯ水平均低于对照组（Ｐ＜０．０５,Ｐ＜０．０１）;ＩＵＧＲ组中２６例胎盘病理改变明显,其母血及脐血ＮＯ水平低于胎盘无明显病理改变者（Ｐ＜０．０５,Ｐ＜０．０５）;两组脐血ＮＯ水平均高于母血ＮＯ水平（Ｐ＜０．０１,Ｐ＜０．０５）,两组脐血与母血ＮＯ水平均有相关性（ｒ＝０．５４７５,ｒ＝０．８５０６）;脐血ＮＯ水平与新生儿体重在ＩＵＧＲ组未发现明显相关性（ｒ＝０．２８３８）。结论ＩＵＧＲ时,胎盘发生明显病理变化,导致母血及脐血中ＮＯ的水平降低。     

胎盘绒毛滋养层细胞MMP-9表达与胎儿宫内发育迟缓的关系

目的:研究胎盘绒毛滋养层细胞基质金属蛋白酶-9(MMP-9)的表达,探讨MMP-9在胎儿宫内发育迟缓(IUGR)发病中的作用。方法:用免疫组化两步法测定30例妊高征合并IUGR患者和28例非妊高征IUGR及30例正常妊娠患者胎盘组织中滋养层细胞MMP-9的表达。结果:正常妊娠组滋养细胞MMP-9表达阳性率为73.3％,明显高于妊高征合并IUGR组及非妊高征IUGR组(分别为23.3％和21.4％,P<0.001),而后两者差异无显著性(P>0.05)。随妊高征病情的加重,MMP-9的表达有减少的趋势。结论:在妊高征合并IUGR及非妊高征IUGR患者胎盘中,滋养细胞基质金属蛋白酶表达均减少,与IUGR发生有密切关系。     

食用蚂蚁治疗胎鼠宫内发育迟缓的研究

目的 了解蚂蚁对大鼠胎鼠的生长促进作用。方法 将交配后的大鼠分为３组,Ａ组,１４只,为不吸烟空白对照组,Ｂ组１８只,为只吸烟,不治疗的宫内发育迟缓（ＩＵＧＲ）对照组,Ｃ组为１６只,为吸烟,食用蚂蚁治疗ＩＵＧＲ组,观察各组胎鼠生长发育的情况,以了解食用蚂蚁对胎鼠的生长促进作用。结果 蚂蚁治疗组胎鼠的平均体重,身长和尾长显著高于两个对照组（均为Ｐ〈０．０１）,蚂蚁治疗作用。结果 蚂蚁治疗组胎鼠的平均体     

胎儿宫内发育迟缓时孕妇及胎儿生长激素,胰岛素与甲状腺激素？…

目的 搪塞胎儿宫内发育迟缓（ＩＵＧＲ）时孕妇血清、脐血和羊水中生长激素、胰岛素及甲状腺激素的变化,方法 采用放射免疫和因相微球放射免疫法测定正常足月妊娠４２例（正常组）和足月妊娠ＩＵＧＲ２３例（ＩＵＧＲ）组）孕妇血清、脐血和羊水中生长激素、胰岛素、三碘甲腺原氨酸（Ｔ３）、甲状腺素（Ｔ４）和促甲状腺素（ＴＳＨ）水平。结果 ＩＵＧＲ组孕妇血清和脐血中生长激素显著下降,脐血和羊水中胰岛素水平与正常组比较     

血浆胎盘异铁蛋白在胎儿宫内发育迟缓发生机制中的作用

目的　探讨血浆胎盘异铁蛋白 (placentalisoferritin ,PLF)在胎儿宫内发育迟缓 (IUGR)发生机制中的作用。方法　对晚孕早期 (孕 2 434周 )最初正常的 43例孕妇 ,分别用ELISA法和Criess法对血浆胎盘异铁蛋白和一氧化氮 (NO)代谢产物亚硝酸基 /硝酸基 (NO2 -/NO3 -)的水平进行测定 ,根据随访妊娠结局分为IUGR组 (2 0例 )和正常组 (2 3例 )。结果　IUGR组晚孕早期PLF水平 (2 48 82± 5 8 37)mg/L低于正常组 (775 0 5± 95 0 2 )mg/L ,其差异具有极显著性意义 (P <0 0 1) ;而NO水平 (6 3 2 1± 48 4 9) μmol/L较正常组 (36 2 9± 2 4 5 8)μmol/L明显升高 ,其差异具有显著性意义 (P <0 0 5 ) ;血浆胎盘异铁蛋白水平与血浆一氧化氮水平呈负相关 (r=- 0 5 98,P <0 0 1)。结论　晚孕早期血浆胎盘异铁蛋白水平的降低与胎儿宫内发育迟缓的发生有密切关系 ,血管内皮细胞损伤可能是其作用机制之一。     

胎儿宫内生长迟缓孕妇静脉血及其新生儿脐血一氧化氮水平测定的临床意义

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Morphological characteristics of placentas associated with idiopathic intrauterine growth retardation: a clinicopathologic study

Objectives

To investigate histopathologic findings, placental diameters and characteristics of syncytial knots in the placentas from idiopathic intrauterine growth retardation (IUGR) pregnancies, and to compare them with a normal birth weight group.

Study design

Based on strict eligibility criteria, this prospective case-control study included 52 term placentas from idiopathic IUGR pregnancies and 69 term placentas from normal birth weight pregnancies. The study was carried out at the Clinical Hospital Centre, Split, where all placentas were collected and examined. For each placenta, diameters were measured and the following histopathologic findings were recorded: infarction, intervillous thrombosis, abruption, villous branching and maturation, chorioamnionitis, decidual vasculopathy and hemorrhagic endovasculitis for each placenta. In addition we assessed quantitative (number of syncytial knots and number of syncytial nuclei per syncytial knot) and qualitative (density and surface area) characteristics of syncytial knots in each placental sample. Statistical significance was tested using χ²-test, Student's t-test and Mann-Whitney U-test. Statistical significance was set at P ≤ 0.05.

Results

There was no difference in investigated histopathologic findings between idiopathic IUGR placentas and control group placentas. Placental diameters correlated significantly with neonatal birth weight (r = 0.64; P < 0.01); with higher birth weight there is an increase in placental diameters. Syncytial knots from idiopathic IUGR had significantly smaller surface area (Z = 2.637; P = 0.008) and higher density (Z = 3.225; P = 0.001) compared with the control group, while there is no difference in number of syncytial knots per individual villus, total number of syncytial knots in each placenta sample or number of syncytial nuclei per syncytial knot.

Conclusions

The investigated histopathologic findings in idiopathic IUGR placentas are incidental, with no higher frequency than in placentas from uncomplicated pregnancies, and should not be considered as possible causative factors for idiopathic IUGR. The demonstrated qualitative changes of syncytial knots in placentas associated with IUGR could represent a compensatory mechanism.     

Impact of transient period of metabolic adaptation on perinatal asphyxia in neonates with intrauterine growth retardation

Introduction: Temperature, glycemia and respiration make neonatal energy triangle (NET). In growth retardation (IUGR) neonates pathological metabolic adaptation exists in transient neonatal period.

Aim: The of this study was to examine the occurrence of pathological NET and check its impact on perinatal asphyxia during the transient period in IUGR neonates.

Material and methods: One hundred and fifty-nine neonates with IUGR were classified into – early preterm, late preterm and term neonates. By the presence of hypothermia, hypoglycemia and hypoxia in the first hour after birth neonates were classified into: group of pathological NET, group of unstable NET and group of stable NET. We analyzed distribution per body mass, gestational age, type of IUGR, gender and the frequency of perinatal asphyxia between the groups.

Results: The late preterm neonates were the most frequent in the group of pathological NET. Perinatal asphyxia was diagnosed in 52 (32.7%) neonates, with highest frequency in the group of pathological NET. Univariate binary logistic regression analysis showed that pathological NET in neonates with IUGR is significant predictor for perinatal asphyxia occurrence (OR?=?8.57; CI?=?4.05–18.12; p?R²?=?0.27).

Conclusion: Poor metabolic adaptation in neonates with IUGR in the first hour after birth is significant risk factor for the perinatal asphyxia.