重度妊高征胎盘的形态计量学观察

为探讨妊高征胎盘形态计量学特点，应用图像分析系统对２９例重度妊高征（妊高征组）和２９例正常妊娠（对照组）的胎盘床血管的胎盘绒毛进行形态计量学检测。结果：妊高征组胎盘绒毛具有合体细胞结节、细胞滋养细胞增生、绒毛基底膜增厚、纤维素样坏死和血管合体细胞膜的绒毛与对照组相比差异显著（Ｐ〈０．０５）。妊高征组胎盘绒毛直径、周长和面积参数均显著低于对照组（Ｐ〈０．０５）。妊高征组胎盘床螺旋动脉妊娠生理性改变缺     

延期妊娠并发羊水过少66例临床分析

目的 探讨延期妊娠并发羊水过少对母婴的影响。方法 采用回顾性分析方法,对延期妊娠分娩的产妇羊水正常组２３１例及羊水过少组６６例进行对比分析。结果 羊水过少组中羊水Ⅱ组度以上粪染、胎盘成熟度Ⅲ＾＋级及胎盘钙化、胎儿窘迫、新生儿窒息率、引产率、产后出血率及剖宫产率均显著高于羊水正常组。结论 羊水过少是胎和宫内慢性缺氧最敏感的特异性指标,不论是延期妊娠还是过期妊娠,一经确诊应积极引产,估计短时间内不能分     

过期妊娠胎盘等部位雌,孕激素受体水平的测定

采用荧光激素结合法，分别对３０例过期妊娠（过期妊娠组）和２７例足月妊娠妇女（对照组）有关的靶组织（胎盘、胎膜、子宫胎盘床和子宫下段肌层）的雌激素受体（ＥＲ）和孕激素受体（ＰＲ）进行了定性和定量分析。结果：过期妊娠组子宫胎盘床及胎膜ＥＲ水平较对照组明显减少，而ＰＲ却无明显差异；过期妊娠组各靶组织内ＥＲ与ＰＲ的比值（ＥＲ／ＰＲ）都明显低于对照组；各靶组织ＥＲ与ＰＲ水平呈明显的正相关；有宫缩者子这吕下段     

妊高征患者子宫、胎盘血管病变及其与妊娠结局的关系

目的 探讨妊高征患者子宫胎盘床、胎盘血管病变及其与妊娠结局的关系。方法 应用免疫组化技术对２９例重度妊高征（妊高征组）和２９例正常妊娠妇女（对照组）的子宫胎盘床、胎盘血管壁ＩｇＡ、ＩｇＧ、ＩｇＭ和Ｃ３的表达进行检测。结果 妊高征组胎盘绒毛和子宫盘床血管壁ＩｇＡ、ＩｇＧ、ＩｇＭ和Ｃ３的阳性表达率（胎盘绒毛：２０．１％,２４．１％,７２．４％和６５．５％;胎盘床：２０．０％,２０．０％,７０．０％和６     

妊娠高血压综合征合并胎儿宫内发育迟缓胎盘病理改变

目的 :通过对妊娠高血压综合征 (妊高征 )合并胎儿宫内发育迟缓的胎盘光镜和电镜观察 ,了解妊高征合并IUGR的胎盘病理改变 ,从而探讨妊高征引起 IU GR的原因。方法 :选取妊高征合并 IU GR患者、正常妊娠妇女胎盘各 30例 ,常规 HE染色及 PAS染色 ,观察胎盘形态学变化。另取妊高征合并 IUGR及正常胎盘各 5例 ,5 0 0 H型透射电镜观察。结果 :观察组绒毛间质纤维化及纤维素样坏死 >3%、绒毛间质白细胞浸润、合体滋养细胞结节 >30 %、绒毛血管减少瘀血、细胞滋养细胞增生 >2 0 %、滋养细胞基底膜增厚 >3%的数量均明显高于对照组 ,电镜发现合体滋养细胞超微结构改变明显 ,蜕膜螺旋动脉内皮损伤 ,管腔狭窄 ,部分动脉末端闭塞。结论 :妊高征引起 IUGR的病理改变主要有三方面 :绒毛毛细血管减少、瘀血 ;血管合体膜增厚 ;蜕膜螺旋动脉狭窄、闭塞。这也是妊高征造成 IU GR的病理学原因     

延期妊娠终止妊娠时机及方式探讨

目的探讨延期妊娠终止妊娠时机，以确定适当的处理措施。方法回顾性分析我院产科2005年10月-2007年9月分娩的妊娠41-41州周且无妊娠合并症的初产妇278例的临床资料。结果延期妊娠组羊水过少、羊水Ⅲ度污染、胎儿窘迫、新生儿窒息、巨大儿和剖宫产率均较足月分娩组高（P〈0．05）；延期妊娠引产干预组羊水Ⅲ度污染、剖宫产率均较延期妊娠自然临产组高，而阴道自然分娩率低（P〈0．05）；用地诺前列酮做引产前预处理＋催产素引产较直接催产素静点引产组有较高的自然分娩率和较低的剖宫产率及引产失败率（P〈0．05）。结论延期妊娠属于高危妊娠，在综合监测提示胎盘功能良好状态下仍可继续妊娠，不适当的干预可增加难产率，引产前的预处理可增加自然分娩机会。     

延期妊娠141例临床分析及对策

目的 :探讨延期妊娠对胎儿的危害及临床处理措施。方法 :回顾分析 1998年 1月至 2 0 0 0年 12月 3年间我院收治的 14 1例延期妊娠的临床资料。结果 :延期妊娠使胎儿宫内窘迫、羊水过少、羊水粪染、脐带缠绕、手术产等发生率增高。结论 :延期妊娠时胎盘功能逐渐降低 ,胎儿高危程度逐渐增加 ,产前、产时严密监护 ,及时处理 ,可减少过期妊娠的发生 ,并确保母婴安全     

彩色和能量多普勒超声对高危妊娠胎盘绒毛动脉的血流监测及与妊娠结局的关系

目的　研究高危妊娠胎盘循环的病理生理变化及与其妊娠结局的关系。方法　将研究对象根据脐血流S/D值和临床症状将 1 0 2例研究对象分为三组 :脐血流S/D≥ 95 th%者 37例为胎儿 -胎盘供血不足组 ;脐血流S/D <95 th%者同时有妊娠合并症及并发症者 4 2例为妊娠合并症和并发症组 ;无任何妊娠合并症和并发症2 3例作为正常妊娠对照组。经彩色和能量多普勒超声检测三组脐动脉、胎盘内绒毛动脉的阻力及计数胎盘内绒毛血管的条数并与妊娠结局相比较。结果　脐血流S/D≥ 95 th%的孕妇胎盘内绒毛血管的数量明显低于正常妊娠组和妊娠合并症、并发症组 ,胎盘内绒毛动脉的S/D值均显著高于其他两组。虽然正常组和妊娠合并症及并发症组脐动脉血流S/D值均小于 95 th% ,但妊娠合并症和并发症组胎盘内绒毛血管的数量显著低于正常组 ,胎盘内绒毛动脉S/D值显著高于正常组。三组中胎儿 -胎盘供血不足组妊娠结局最差 ;妊娠合并症和并发症组胎儿体重和胎盘重量居中 ;正常妊娠无不良围产儿结局。结论　彩色和能量多普勒超声可监测胎盘内绒毛血管数量及绒毛动脉的阻力 ,其血流动力学的变化为进一步洞察高危妊娠胎盘循环提供了直接依据     

重度妊娠高血压综合征患者子宫胎盘病理变化及其临床意义

目的 探讨重度妊娠高血压综合征（妊高征）患者子宫胎盘病理变化及其对孕产妇和围产儿结局的影响。方法 选择正常晚孕妇女（对照组）和重度妊高征患者（观察组）各１１７例,常规ＨＥ染色观察胎盘形态学变化,并对两组孕妇进行血液分析、生化检查及肝肾功能检查。结果 观察组胎盘重量明显减轻,细胞滋养细胞增殖,合体滋养细胞结节增多,基底膜增厚,基质纤维素样坏死,绒毛间隙水肿,绒毛内血管数目减少、淤血严重等,蜕膜内血管生理性改变消失,与对照组上述各指标比较,差异均有极显著性（Ｐ〈０．０１）;观察组合并严重贫血、重度血小板减少症、血液高粘度、低蛋白血症、大量腹水、眼底动脉并挛性改变等多于对照组,差异具有极显著性（Ｐ〈０．０１）。结论 重度妊高征患者胎盘形态学病理变化明显,且与病情严重程度呈平行关系。     

妊娠中晚期乙型肝炎表面抗原阳性妇女胎盘感染的研究

目的 探讨乙型肝炎表面抗原（ＨＢｓＡｇ）阳性妇女妊娠中晚期胎盘各层细胞的乙型肝炎病毒感染状况。方法 收集太原市传染病医院妇产科ＨＢｓＡｇ阳性产妇胎盘１６７例（其中足月分娩胎盘１５８例,中期引产胎盘９例）,用免疫组织化学ＡＢＣ染色法检测胎盘蜕膜细胞、滋养层细胞、绒毛间质细胞和绒毛毛细血管内皮细胞ＨＢｓＡｇ和乙型肝炎核心抗原（ＨＢｃＡｇ）。结果 （１）足月分娩胎盘蜕膜细胞、滋养层细胞、绒毛间质细胞和绒毛毛细血管内皮细胞均感染乙型肝炎病毒,以胞浆分布为主,局灶性分布多见。从蜕膜细胞、滋养层细胞、盈盘间质细胞至绒毛毛细血管内皮细胞,乙型肝炎病毒感染率呈下降趋势,总感染率分别为６６．４６％（１０５／１５８）、５８．２３％（９２／１５８）、２７．２２％（４３／１５８）和１２．６６％（２０／１５８）。（２）中期引产胎盘有１例     

Decrease of uteroplacental blood flow after feticide during second-trimester pregnancy termination with complete placenta previa: Quantitative analysis using contrast-enhanced ultrasound imaging

Contrast enhanced ultrasound (CEUS) was used to quantify the dynamic changes in uteroplacental blood flow before and after the interruption of fetal villus circulation resulting from feticide during a second trimester pregnancy termination in a patient with complete placenta previa. Quantitative analysis was performed on time–intensity curves acquired 24 h before and 48 h and 120 h after feticide and demonstrated the persistence of utero-placental blood flow with a progressive and two-step reduction in intervillous space and uteroplacental blood flow. Our results suggest that placental blood flow reduction after interruption of fetal circulation is a progressive and delayed mechanism.     

血红素氧化酶-1、2及内皮素-1在妊娠高血压综合征患者胎盘组织中的表达及作用

目的:通过观察妊娠高血压综合征(简称妊高征,PIH)患者胎盘组织血红素氧化酶-1、2(HO-1、2)及内皮素-1(ET-1)的表达,探讨PIH发病机制。方法:采用免疫组化SABC法,检测20例PIH患者及正常孕妇的胎盘绒毛组织中的HO-1、2及ET-1,利用免疫组化图象分析软件测量胎盘大绒毛、微绒毛合体滋养细胞及血管的平均吸光度。结果:妊高征组大绒毛、微绒毛合体滋养细胞及血管部位的HO-2表达显著低于正常孕妇组(P<0.001),HO-1在胎盘合体滋养细胞的表达显著低于正常孕妇组(P<0.001),而妊高征组大绒毛、微绒毛合体滋养细胞及血管部位的ET-1表达显著高于正常孕妇组(P<0.001);且H0-1、2在胎盘大绒毛、微绒毛合体滋养细胞的表达与平均动脉压呈负相关,而ET-1在胎盘大绒毛、微绒毛合体滋养细胞的表达与平均动脉压呈正相关。结论:妊高征患者胎盘组织血红素氧化酶的表达减少可能在妊高征的发生、发展过程中起着重要的作用。     

胎盘早剥并发子宫胎盘卒中的危险因素分析

目的 探讨胎盘早剥并发子宫胎盘卒中的发病危险因素、临床特征及母儿结局.方法 收集2002年1月至2006年12月上海交通大学医学院附属国际和平妇幼保健院住院分娩的52例胎盘早剥产妇的临床资料,按是否并发子宫胎盘卒中分为两组:胎盘早剥并发子宫胎盘卒中17例为观察组,未并发子宫胎盘卒中的35例为对照组.采用回顾性研究方法对观察组子宫胎盘卒中的发病危险因素、临床特征及母儿结局进行分析,并与对照组进行比较.结果 (1)发生率:2002年1月至2006年12月共分娩35 049人次,胎盘早剥发生率为0.15%(52/35 049),胎盘早剥并发子宫胎盘卒中的发生率为0.05%(17/35 049),其中胎盘早剥产妇中子宫胎盘卒中的发生率为33%(17/52).(2)一般情况及分娩方式、分娩孕周:两组产妇的平均年龄、体重指数比较,差异无统计学意义(P>0.05).观察组产妇均以剖宫产结束分娩,而对照组产妇经阴道及剖宫产分娩为14及21例,比较两组分娩方式及分娩孕周,差异有统计学意义(P<0.01).观察组产妇早产发生率为88%(15/17),而对照组为49%(17/35),两组比较,差异有统计学意义(P<0.01).(3)发病危险因素:观察组产妇子痫前期发生率及发病持续时间分别为71%(12/17)及6.4 h,对照组分别为20%(7/35)及4.2 h,两组比较,差异均有统计学意义(P<0.01);两组产妇胎膜早破、羊水过多及其他因素比较,差异均无统计学意义(P>0.05).(4)临床特征:观察组产妇血性羊水、胎儿窘迫、宫腔积血及产后出血的发生率分别为82%(14/17)、65%(11/17)、35%(6/17)及59%(10/17),对照组分别为26%(9/35)、29%(10/35)、6%(2/35)及11%(4/35),两组比较,差异均有统计学意义(P<0.01).而两组产妇在主诉腹痛、阴道流血及腹肌张力高的发生率比较,差异均无统计学意义(P>0.05).(5)胎盘附着部位、剥离面积比较:观察组胎盘附着部位在子宫的前、后壁5例(5/17),宫底宫角12例(12/17);对照组胎盘附着部位在子宫的前、后壁24例(24/35),宫底宫角11例(11/35),两组胎盘附着宫底宫角部位发生例数比较,差异有统计学意义(P<0.01).观察组胎盘剥离面积均超过1/3,其中有9例患者剥离面积≥2/3;而对照组胎盘剥离面积≤1/3者27例,剥离面积在1/3～2/3者8例,两组比较,差异均有统计学意义(P<0.01).(6)母儿并发症及预后比较:观察组产妇发生失血性休克3例、DIC3例、子宫切除1例、死胎3例、新生儿窒息8例及新生儿死亡1例,而对照组除新生儿窒息5例及死胎2例外,其余指标均为0,两组比较,差异有统计学意义(P<0.01).结论 胎盘早剥并发子宫胎盘卒中发病的危险因素主要是子痫前期、发病持续时间长和胎盘附着宫角宫底部.胎盘早剥并发子宫胎盘卒中患者的母儿结局不良.     

Influence of inflammatory infiltrate and alterations of the blood flow in the etiopathogenesis of the basement membrane of the amniotic epithelium (BMAE) thickening in patients with hypertensive syndromes in pregnancy

Purpose

To evaluate the mechanisms involved in the etiology of the basement membrane of the amniotic epithelium (BMAE) thickening in patients with hypertensive syndromes in pregnancy (HSP).

Methods

Eighty placentas from patients presenting HSP were morphologically examined in staining through hematoxylin–eosin and periodic acid Schiff method. Placental morphological changes were classified into: diagnostic of low placental blood flow, characterized by a larger number of syncytial knots, fibrin deposits, and a larger number of vessels in terminal villi; and placentas with inflammation that presented inflammatory infiltrate in membranes or placental villi. Measurements of thickness were made with an automatic image analyzing software.

Results

BMAE thickness was higher in the group with HSP, particularly in cases with gestational hypertension and pre-eclampsia superimposed on chronic hypertension (PSCH). In the placentas of the HSP group, the thickness of the BMAE was higher in cases with inflammatory infiltrate. There was a positive and significant correlation between the BMAE thickness and the thickness of the amniotic epithelium. The BMAE thickening areas were associated with hyperplasia and edema of the amniotic epithelium.

Conclusions

BMAE thickening in cases with HSP is more evident when there is an interaction between the severe effects of uteroplacental hypoxia, with consequent death and remodelling of the amniotic epithelium cells, as in PSCH, with local inflammatory processes that make this thickening much more evident.     

彩色多普勒监测妊高征孕妇子宫胎盘血流变化

应用彩色多普勒血流显像技术监测了３１例妊高征孕妇及７４例正常孕妇子宫胎盘血流，同时测定血中雌三醇、胎盘泌乳素、血栓素代谢产物、前列环素代谢产物及ＴＸＢ２／６ＫＰ比值。结果表明：正常孕妇子宫动脉及胎儿脐动脉的时间平均血流速度及血流量明显高于妊高征孕妇。     

Concentration of placental protein 10 (PP10) in maternal serum and amniotic fluid throughout normal gestation and in pregnancy complicated by fetal growth retardation

PP10, a new placental glycoprotein, was studied by a specific and sensitive double-antibody radioimmunoassay in maternal serum and other body fluids throughout pregnancy. The mean value of serum PP10 in healthy nonpregnant individuals was approximately 10 microU/l. During normal pregnancy it rose to 3,500 microU/l. The rate of rise was obtained from 78 normal pregnancies with 279 single assay values from weeks 6-40. The shape of the curve resembled that for other placental proteins (HPL, SP1). PP10 levels in amniotic fluid were measured in 145 samples from weeks 13-55 of normal pregnancies and at term. The mean concentration was 500 microU/l until week 18 and then rose slowly. Cord blood contained only trace amounts. PP10 was not found in maternal urine. The concentration in maternal serum and amniotic fluid was higher in twin pregnancies than in singleton pregnancies. In 46 cases with low birth weights the PP10 levels in maternal serum were significantly lower than normal. Simultaneous measurements of PP10 and E3, HPL and SP1 were made in 17 individual follow-up's. PP10 was comparable with E3 and appeared to be better than HPL and SP1 in predicting intrauterine fetal growth retardation.     

Nutritional paradigms of ovine fetal growth restriction: implications for human pregnancy

Low birth weight and prematurity are associated with short inter-pregnancy intervals, low pre-pregnancy weights, insufficient maternal weight gains during pregnancy, multifetal pregnancies and a young maternal age. Improvements in maternal nutritional status are arguably imperative for ensuring an appropriate pregnancy outcome in these vulnerable groups, but ethical boundaries limit these investigations. Experimental paradigms using the pregnant sheep have been widely used to identify the nutritionally sensitive periods of conceptus development. In adult sheep, severe undernutrition during the periconceptual period accelerates maturation of the fetal hypothalamic-pituitary adrenal axis and results in pre-term delivery. Low pre-pregnancy weight, followed by undernutrition during mid-pregnancy, results in reduced placental growth and lower birth weights at term. Studies that have restricted nutrients during mid-gestation only reveal variable effects on the placental and fetal growth trajectory, however if undernutrition is prolonged during late-pregnancy, fetal growth is compromised, particularly in twin pregnancies. In contrast, overnourishing the adolescent sheep to promote rapid maternal growth, results in the premature delivery of low birth weight lambs. These effects are mediated by impaired placental growth, uteroplacental blood flows and fetal nutrient uptakes. At the other end of the nutritional spectrum, undernourishing the adolescent sheep to gradually deplete nutrient reserves, results in fetal growth restriction which is independent of alterations in placental mass.     

Thrombophilia and pregnancy complications

OBJECTIVE: This systematic review examines the strength of the association between thrombophilia and recurrent pregnancy loss and other serious obstetric complications.Study design Electronic databases and manual bibliography searches were used to identify studies evaluating the association between thrombophilia and pregnancy loss, preeclampsia, fetal growth retardation, and placental abruption. RESULTS: Thrombophilic disorders are associated with an increased risk of fetal loss in the majority of case control and cohort studies. The risk is increased throughout pregnancy, but may be higher in the second and third trimester. The common pathologic finding of placental infarction suggests unexplained fetal loss may result from uteroplacental insufficiency and thrombosis. Thrombophilic disorders are not consistently associated with preeclampsia, fetal growth retardation, or placental abruption. Preliminary data suggest prophylactic anticoagulation may improve outcome in thrombophilic women with unexplained recurrent fetal loss. CONCLUSION: Women with thrombophilia have an increased risk of pregnancy loss and possibly other serious obstetric complications, although definition of the magnitude of risk will require prospective longitudinal studies. Preliminary data suggesting prophylactic anticoagulation may improve gestational outcome provide a rationale for prospective randomized trials in thrombophilic women with unexplained recurrent fetal loss.