雌激素受体和孕激素受体在妊娠期高血压疾病胎盘组织中的表达

目的探讨雌激素受体(estrogen receptor,ER)和孕激素受体(progestwrone receptor,PR)在妊娠高血压疾病(HDCP)胎盘组织中的表达。方法应用免疫组化法和Western blotting法,以正常剖宫产分娩孕妇25例为对照,检测50例轻度子痫前期和重度子痫前期患者胎盘组织中ER及PR的表达情况。结果 SER和PR在轻度子痫前期和重度子痫前期患者胎盘组织中表达比正常剖宫产患者胎盘组织中表达显著降低(<0.05),并且ER在重度子痫前期患者胎盘组织中表达下降更为显著(<0.05)。结论 ER及PR在HDCP胎盘组织中低表达。     

晚期正常妊娠和子痫前期胎盘中组织蛋白酶B的表达

目的探讨组织蛋白酶B(cathepsin B)在晚期妊娠胎盘绒毛的表达及在子痫前期发病中可能的作用。方法分别取正常足月胎盘36例和子痫前期胎盘30例,免疫组化方法检测胎盘绒毛cathepsin B的表达情况,同时观察胎盘组织的病理变化。结果 cathepsin B在晚期妊娠胎盘绒毛细胞滋养细胞的细胞质中有高表达。正常足月胎盘cathepsin B表达阴性(-)1例(2.7%),弱阳性(+)16例(43.2%),阳性(～)20例(54.1%);子痫前期胎盘cathepsin B表达阴性(-)5例(16.7%),弱阳性(+)16例(53.3%),阳性(～)9例(30.0%),cathepsin B在子痫前期胎盘阴性率表达较正常足月胎盘高,而阳性率表达较低,两组比较差异有显著性(P0.05);结论cathepsin B在晚期妊娠胎盘中仍然有高表达,cathepsin B在正常足月妊娠和子痫前期胎盘表达的差异提示cathepsin B不仅参与了正常妊娠的维持,cathepsin B表达降低导致的滋养细胞侵袭能力下降,可能与子痫前期的发病有关。     

胎盘生长因子及受体在妊娠肝内胆汁淤积症患者胎盘中的表达及其意义

目的探讨胎盘生长因子(PLGF)及受体(F lt-1)在妊娠肝内胆汁淤积症患者胎盘中的表达及其意义。方法采用免疫组织化学方法测定30例妊娠肝内胆汁淤积症患者(ICP组)和30例正常晚期妊娠妇女(对照组)的胎盘组织及8例早孕绒毛组织中PLGF及F lt-1的表达。同时还用抗FⅧRA抗体标记ICP组和对照组孕妇胎盘中的血管密度。结果PLGF及F lt-1在早孕绒毛中主要分布于滋养叶细胞,在ICP患者和对照组胎盘中分布基本一致,主要分布于合体滋养细胞、细胞滋养细胞、血管内皮细胞和绒毛间质细胞。在ICP胎盘中PLGF、F lt-1表达强度及胎盘血管密度均明显低于对照组(P<0.01)。相关分析显示,胎盘组织中PLGF表达强度与胎盘血管密度呈正相关。结论妊娠肝内胆汁淤积症患者胎盘PLGF及F lt-1表达下降与胎盘滋养叶细胞侵入异常、胎盘血管形成异常、胎盘血管密度降低有关,可能是ICP胎儿妊娠结局不良的原因。     

白血病抑制因子及其受体在宫外孕胚胎组织中的表达及临床意义

目的探讨宫外孕胚胎组织中的白血病抑制因子(LIF)及其受体(LIFR)的表达。方法应用免疫组织化学方法检测白血病抑制因子(LIF)及其受体(LIFR)在30例宫外孕、30例人工流产以及30例足月妊娠胎盘组织中的表达。用卡方检验(Chi-Square Test)检测LIF、LIFR在宫外孕、人工流产及足月妊娠胎盘组织中的表达是否有差异。结果 LIF、LIFR在宫外孕胎盘组织中阳性率分别为93%和90%,在人工流产胎盘组织中阳性率分别为93%和90%,在足月妊娠胎盘组织中无阳性表达。结论白血病抑制因子(LIF)及其受体(LIFR)在早期妊娠中,对维持胎盘的功能和胚胎的生长发育具有重要意义,对晚期妊娠的临床意义还有待进一步研究。     

血清可溶性Fas与胎盘组织胎盘生长因子的表达在早发型重度子痫前期发病中的作用

目的:探讨血清可溶性Fas与胎盘组织胎盘生长因子在早发型重度子痫前期发病中的作用。方法:采用ELISA和免疫组化法分别检测20例早发重度子痫前期患者、35例晚发重度子痫前期患者和40例正常晚期妊娠患者血清可溶性Fas(Soluble Fas,sFas)和胎盘组织胎盘生长因子(placental growth factor,PlGF)的表达。结果:正常妊娠组、早发重度组、晚发重度组血清sFas水平分别为(1.17±0.53)、(6.68±0.97)和(3.17±0.74)mg/L,早发重度组、晚发重度组均显著高于正常对照组,差异有显著性(P<0.05)。早发重度组又明显高于晚发重度组,差异有显著性。正常妊娠组胎盘组织PlGF表达的平均灰度值显著高于早发型及晚发型重度子痫前期组,其中早发型子痫前期重度组表达最低。早发重度组中血清sFas与PlGF呈负相关,相关系数-0.748。结论:重度子痫前期患者血清sFas表达升高,且早发重度组表达显著高于晚发重度组,并与PlGF呈负相关,说明其异常表达可能是早发重度子痫前期发病的主要原因。     

HMGB1和NF-κBp65在葡萄胎、绒癌中的表达变化及意义

目的研究早期妊娠、晚期妊娠的胎盘组织、葡萄胎和绒癌组织中高迁移率族蛋白1(HMGB1)和核因子-κBp65(NF-κBp65)的表达变化及意义,探讨HMGB1和NF-κBp65与滋养细胞疾病的关系。方法选择2010年6月至2013年12月潍坊市中医院和潍坊市人民医院收治的流产、剖宫产、葡萄胎和绒癌标本,应用免疫组织化学方法检测HMGB1及NF-κBp65在早期妊娠、晚期妊娠的胎盘组织、葡萄胎和绒癌组织中的表达变化。结果 1.HMGB1阳性颗粒主要定位于细胞质和细胞核中,主要表达于绒毛滋养细胞和血管内皮细胞和间质细胞。与早期和晚期妊娠绒毛组织相比较,葡萄胎和绒癌组织中HMGB1阳性着色强度均明显增强,差异有统计学意义(P0.001)。2.NF-κBp65阳性颗粒主要定位在细胞质中,主要分布于绒毛滋养细胞、绒毛间质、血管内皮细胞。与早期和晚期妊娠绒毛组织相比较,葡萄胎和绒癌组织中NF-κBp65阳性着色强度均明显增强,差异有统计学意义(P0.001)。3.HMGB1与NF-κBp65平均光密度值在葡萄胎中表达强度呈正相关(r=0.7499,P=0.000);在绒癌组织中表达强度呈正相关(r=0.7338,P=0.000)。结论 HMGB1及NF-κBp65高表达与葡萄胎、绒癌的发生相关;HMGB1和NF-κBp65在葡萄胎和绒癌组织中的表达趋势一致,两者线性相关分析为正相关,提示HMGB1高表达可增强NF-κBp65的表达,与肿瘤细胞的生长有关。     

Apelin和APJ在绒毛及胎盘组织中的表达及意义

目的探讨血管活性肽Apelin及其受体APJ在早期妊娠绒毛和晚期妊娠胎盘组织中的表达和定位。方法分别取10例妊娠7-9w妇女（早孕组）的绒毛组织和15例妊娠37-41w妇女的胎盘组织,采用实时荧光定量逆转录聚合酶链反应法（FO-RT-PCR）及免疫组织化学染色分析法检测两组孕妇胎盘Apelin mRNA及其蛋白的表达情况,并用高清晰度彩色图文分析系统（HPIAS-1000）对其进行定量分析。结果FQ-RT-PCR结果显示,足月妊娠胎盘Apelin mRNA显著高于早孕绒毛组织（P〈0.05）。免疫组化及高清晰度彩色图文分析系统结果显示,Apelin-36和APJ蛋白在早孕绒毛组织和足月妊娠胎盘组织中均有表达,二者在早孕绒毛组织中的表达部位主要位于绒毛内滋养细胞：在足月妊娠胎盘组织中,主要表达于胎盘合体滋养细胞及血管内皮细胞Apelin在足月妊娠胎盘组织中的表达强度要高于早孕绒毛组织,有极显著性差异（P〈0.01）,而APJ在早孕绒毛组织和足月妊娠胎盘组织中的表达强度无明显差异（P〉0.05）。结论Apelin在晚孕胎盘组织中表达增强,Apelin/APJ可能在子宫-胎盘血管的发育及功能调控过程中发挥重要作用。     

TLR4在妊娠合并梅毒感染的胎盘与胎膜中表达

目的检测TLR4基因在妊娠合并梅毒感染人胎盘与胎膜中表达变化。方法取妊娠合并梅毒感染及正常足月分娩之胎盘与胎膜样本各5例;应用RTPCR技术对妊娠合并梅毒感染胎盘与胎膜组织上TLR4基因的mRNA表达的检测;应用免疫组化技术对妊娠合并梅毒感染胎盘与胎膜组织上TLR4基因的蛋白表达的检测。结果TLR4基因在妊娠合并梅毒感染人胎盘与胎膜中表达水平显著高于正常晚期妊娠胎盘与胎膜。在妊娠合并梅毒感染胎膜组织中TLR4基因表达较正常胎膜组织升高50%,P〈0.05;在妊娠合并梅毒感染胎盘组织中TLR4基因表达较正常胎盘组织升高120%,P〈0.05。TLR4在妊娠合并梅毒感染的胎盘合体滋养细胞、羊膜上皮细胞和胎膜中的平滑绒毛膜细胞滋养细胞上表达增强,与RT-PCR结果一致。结论TLR4基因在妊娠合并梅毒感染人胎盘与胎膜中表达水平显著增加,提示TLR4可能在妊娠合并梅毒感染的胎盘与胎膜分子病理中发挥作用。     

Calpain10基因在脂肪及胎盘组织中的表达与妊娠糖尿病的相关研究

目的检测钙蛋白酶10(Calpain10)mRNA在妊娠糖尿病患者脂肪及胎盘组织中的表达,以探求Calpain10在妊娠糖尿病发病机制中的意义。方法用半定量逆转录聚合酶链反应(RT-PCR)技术检测正常妊娠(60例),妊娠糖尿病患者(60例)剖宫产后脂肪及胎盘中Calpain10基因在转录水平的表达。结果妊娠糖尿病组脂肪组织中Calpain10mRNA表达量较正常妊娠组显著下降(P0.01),并与妊娠糖尿病胰岛素抵抗指标相关(P0.01);而胎盘组织中Calpain10mRNA表达则无差异。结论脂肪组织Calpain10表达的减少可能是GDM患者胰岛素抵抗的重要原因。胎盘Calpain10的表达与GDM及其胰岛素抵抗的关系不明显。     

p53在妊娠滋养细胞和肿瘤中的表达

目的：分析Ｐ５３过度表达与葡萄胎、恶性葡萄胎（恶葡）、绒毛膜癌（绒癌）的恶性程度及预后关系。方法：采用单克隆抗体免疫组化技术，对正常胎盘绒志及妊娠滋养细胞肿瘤组织，进行肿瘤抑制基因Ｐ５３表达检测。其中包括早期妊娠１０例，中期妊娠１０例，晚期妊娠１３例，葡萄胎４０例，恶葡９例，绒癌２０例；结果：正常胎盘Ｐ５３异常表达阴性，葡萄胎、恶葡、绒癌阳性表达率分别为４２．５％（１７／４０）、５５．５％（５／９     

妊娠期高血压疾病患者孕中期血管内皮功能变化

目的探讨妊娠期高血压疾病患者在孕中期临床发病前的血管内皮功能的变化。方法对340例孕中期孕妇用超声行肱动脉血流介导的舒张功能（FMD）,血清内皮素（ET）、一氧化氮（NO）测定,并根据其随访的妊娠结局分为妊娠期高血压疾病组（妊高征组）和正常组,比较两组的FMD,ET,NO结果。结果 340例中有41例孕晚期发生妊娠期高血压疾病（妊高征组）,而其余299例未发生妊娠期高血压疾病（正常组）。孕中期妊高征组FMD、血清NO显著低于正常组,而血清ET显著高于正常组,差异均有显著性（P〈0.05）。在妊高征组内,重度子痫前期组FMD、血清NO显著低于轻度子痫前期组,而血清ET显著高于轻度子痫前期,差异有显著性（P〈0.05）。结论孕中期妊娠期高血压疾病潜在患者虽然血压正常,但已存在血管内皮损伤,可被超声、实验室等检出。     

Activation of the novel prothrombinase, fg12, as a basis for the pregnancy complications spontaneous abortion and pre-eclampsia

PROBLEM: Impaired trophoblast invasion during the first trimester of pregnancy is linked to spontaneous abortion, and defective invasion in the second trimester to hypertension + proteinuria (pre-eclampsia). Hypertension developing during the third trimester of human pregnancy represents, in part, a corrective response in the mother to provide adequate placental perfusion for fetal growth when trophoblast has not to invaded and converted the myometrial porprtion of maternal spiral arteries into to low resistance-high capacitance conduits. Deportation of vesicles from hypoxemic trophoblast is thought to cause hypertension plus proteinuria, vascular damage and a systemic coagulopathy. Trophoblast invasion may be inhibited by local cytokines, such as TGF-betas but Thl-type cytokines associated with pre-eclapmsia and spontaneous abortions (e.g., IL-1, TNF-alpha, IFN-gamma) are not known to inhibit migration at in situ concentrations. Trophoblast invasion is also inhibited by the binding of surface integrins to fibronectin and fibrin, and fibrin production is stimulated by these Th1 cytokines via up-regulation of prothrombinases(s) such as fg12 which directly and via TNF-alpha-facilitated inflamation compromise trophoblast cell integrity. We, therefore, asked if fg12 expression and TNF-alpha are increased in first trimester human miscarriage and in third trimester pre-eclampsia. METHODS: fg12 mRNA was detected using in situ hybridization and fg12 protein by immunohistochemistry. TNF-alpha mRNA and protein were similarly tested. The techniques were validated using uterine sections from day 8.5 of CBA x DBA/2 pregnancies, and then were applied to sections of placentae from normal and pre-eclamptic pregnancies with and without intrauterine fetal growth restriction (IUGR). Fibrin was detectectd by immunohistochemistry. RESULTS: Expression of fg12 protein correlated with fg12 mRNA expression in mouse uteri and in placentae from normal human pregnancies. Increased expression of fg12 and TNF-alpha mRNA and protein, and increased fibrin deposition was detected in placental trophoblast. CONCLUSIONS: Activation of fg12 prothrombinase by Th1-type cytokines in pregnancy may lead to spontaneous abortion, or in ongoing pregnancy, to pre-eclampsia and/or IUGR.     

南昌地区正常孕产妇血液流变学指标测定

南昌地区正常孕产妇血液流变学指标测定１黄维新２郭丹２刘淮２徐晓兰２习斌蓉２过去血液流变学的研究主要集中在内科疾病的诊断与治疗方面，在产科方面的研究较少，但孕妇的机体为适应妊娠的需要而会发生一系列生理变化，因而其血液流变性也会随之发生改变。为了探明正常...     

Coelomic cells show apoptosis via Fas/FasL system: a comparative study between healthy human pregnancies and missed miscarriages

BACKGROUND: The Fas/Fas ligand (FasL) system represents one of the mainapoptotic pathways controlling placental apoptosis throughoutgestation. In the current study, we have examined the Fas/FasLprotein expression and the apoptotic incidents of coelomic cells,amniotic cells and trophoblastic tissue in first trimester humanpregnancies and missed miscarriages (MM). METHODS: Protein expression was determined by immunofluoresence, westernblotting analysis, immunohistochemistry and indirectly by RT–PCR,whereas apoptotic cell death was assessed by in situ DNA fragmentationanalysis. RESULTS: Coelomic cells express Fas/FasL proteins, can undergo apoptosisand were the only cells in which apoptosis, Fas protein expressionand FasL protein expression were accordingly increased alongwith gestational age (P = 0.001, P = 0.008; P = 0.012, respectively).In contrast, amniotic cells and trophoblast showed a consistencyin the expression levels of Fas/FasL proteins in healthy pregnancies.MM were accompanied by increased Fas/FasL protein expressionin all examined samples (P < 0.001). The increase of Fas/FasLprotein expression was accompanied by proportional increaseof apoptotic incidents among the coelomic cell population (P= 0.023, P = 0.009, respectively), whereas amniotic cells andtrophoblast appeared to be resistant to Fas-induced apoptosis.The lowest expression of Fas/FasL proteins and the minimum occurrenceof apoptotic incidents were detected in the trophoblast. CONCLUSIONS: These data suggest that there is a different regulation andfunction of the Fas/FasL system in early human pregnancies.Aberration of the Fas-mediated apoptosis may represent one ofthe execution-step necessary for pregnancy loss in MM cases.     

Expression of intracellular Th1 and Th2 cytokines in women with recurrent spontaneous abortion,implantation failures after IVF/ET or normal pregnancy

PROBLEM: We aimed to investigate absolute counts of intracellular T helper 1 (Th1) and Th2 cytokine expressing T-cell subpopulations in women with three or more recurrent spontaneous abortions (RSA), multiple implantation failures after in-vitro fertilization and embryo transfer (IVF/ET) (three or more) or during normal pregnancy. METHOD OF STUDY: Absolute cell counts and percentages of CD3+, CD3+/CD4+, and CD3+/CD8+ T-cell populations expressing intracellular cytokines [interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-4 and IL-10] was studied by four-color flow cytometry in 15 RSA and 13 implantation failure patients. Eighteen fertile non-pregnant and 47 normal pregnant women were also compared with regard to intracellular cytokine expression. RESULTS: Interleukin-10 producing CD3+/CD8+ T-cell counts were significantly lower in women with RSA (P < 0.05) and implantation failures (P < 0.05), and TNF-alpha producing CD3+/CD4+ T-cell counts were higher in women with RSA (P < 0.05) and implantation failures (P < 0.005) than those of non-pregnant fertile controls. During normal pregnancies, first trimester IL-4 expressing CD3+, CD3+/CD4+ T-cell counts (P < 0.05) and IFN-gamma expressing CD3+ T-cell counts (P < 0.05) were significantly higher than those of third trimester (P < 0.05). First trimester TNF-alpha expressing CD3+/CD8+ T-cell counts were significantly higher than those of second and third trimester women (P < 0.05). However, there are no differences in cytokine expression between non-pregnant and first trimester pregnant women. CONCLUSION: Absolute counts of IFN-gamma, IL-4, and TNF-alpha expressing T cells decrease with the progress of gestation (third trimester) during normal pregnancies. In women with implantation failures, absolute cell counts of TNF-alpha expressing CD3+/ 4- cells reflects the presence of dominant Th1 immune response. A significantly increased Th1 cytokine expression may be the underlying immune etiology for reproductive failures.     

Regulatory Mechanisms for Apoptosis in Placental Tissue during Normal Pregnancy and Gestosis-Complicated Pregnancy

The localization of apoptosis and expression of proapoptotic and antiapoptotic factors by the placental tissue were compared during normal pregnancy and gestosis-complicated pregnancy. The degree of apoptosis did not differ in the third trimester of normal pregnancy and gestosis-complicated pregnancy. Increased expression of Fas, caspase-8, and caspase-3 in placental tissue during normal pregnancy was shown to contribute to the suppression of angiogenesis and growth of placental tissue. No differences were found in the expression of FasL (CD95L), caspase-2, caspase-9, and Mcl-1 by placental cells during normal pregnancy and gestosis-complicated pregnancy. Increased expression of TRAIL by trophoblast cells is a protective mechanism from apoptotic signals of maternal cytotoxic lymphocytes and NK cells during gestosis.     

Heme oxygenases in pregnancy II: HO-2 is downregulated in human pathologic pregnancies

PROBLEM: We previously reported a diminished expression of the heme-degrading enzymes heme oxygenases (HO)-1 and HO-2 in decidua and placenta from mice undergoing Th1-mediated abortion, strongly indicating the protective effect of HO in murine pregnancy maintenance. Here we investigated whether the expression of HO-1 and HO-2 is also reduced at the feto-maternal interface of pathologic human pregnancies. METHOD OF STUDY: Immunohistochemistry was used to detect HOs expression in placental and decidual first-trimester tissue from patients with: spontaneous abortion (n = 14), choriocarcinoma (n = 14), hydatidiform mole (H-mole) (n = 12), compared with normally progressing pregnancies (n = 15). Further, we investigated early third-trimester decidual and placental tissue from patients with pre-eclampsia (n = 13) compared with fetal growth retardation (n = 14) as age-matched controls. RESULTS: In first trimester tissue, we observed a significant reduction of HO-2 expression in invasive trophoblast cells, endothelial cells, and syncytiotrophoblasts in samples from patients with spontaneous abortion compared with normal pregnancy. H-mole samples showed a diminished expression of HO-2 in invasive trophoblast cells and endothelial cells in comparison with NP, whereas choriocarcinoma samples showed no significant differences compared with the control. In third trimester tissue, HO-2 was also reduced in syncytiotrophoblasts and invasive trophoblast cells from pre-eclampsia compared with samples from fetal growth retardation. HO-1 expression was diminished in all pathologies investigated; however, the differences did not reach levels of significance. CONCLUSIONS: Our data indicate that HOs play a crucial role in pregnancy and low expression of HO-2, as observed in pathologic pregnancies, may lead to enhanced levels of free heme at the feto-maternal interface, with subsequent upregulation of adhesion molecules, allowing enhanced inflammatory cells migration to the feto-maternal interface.     

Pregnancy and fetal outcomes in patients with lupus nephritis]

To determine risk factors for pregnancy and fetal outcomes in patients with lupus nephritis during pregnancy and postpartum, 26 patients with 34 pregnancies between 1986 and 2004 were reviewed retrospectively. Of the 34 pregnancies, we observed 23(67.6%) live births at term, 5(14.7%) premature births, 2(5.9%) spontaneous abortions and 4(11.8%) artificial abortions. After exclusion of artificial abortions, live birth rate was 93.3%; it was not significantly difference versus 88.1% in 197 pregnancies without nephritis. But in pregnancies with active nephritis, there were an increased number of pre-term deliveries (57.1% vs. 4.8%). Frequency of flare was analyzed in 30 pregnancies with lupus nephritis by trimester and postpartum. In addition to 7 flares that occurred in the postpartum, 8 flares occurred during pregnancy (3[20%] in the first trimester, 3[20%] in the second trimester, 2[13%] in the third trimester). There was higher rate of flare compared to that 115 lupus patients with 129 pregnancies between 1986 and 2001 (50% vs. 22.5%). Renal flare in 29 pregnancies was 6(20.7%), three flares occurred in the first trimester, 3 in the second trimester. In the analysis of laboratory data of 28 pregnancies at onset of pregnancy, fetal gestational age significantly associate with proteinuria, plasma creatinine level and SLEDAI, fetal birth weight significantly associate with proteinuria and plasma creatinine level. Of the 34 pregnancies, 11 underwent renal biopsy prior to pregnancy, pregnancy and fetal outcomes were poorly in the class IV patients. In conclusion, pregnancy is safe for the majority of mothers if it is planned when lupus nephritis is quiescent.     

The placentas of patients with severe acute respiratory syndrome: a pathophysiological evaluation

AIMS: The pathology of the placentas delivered from pregnant women who had severe acute respiratory syndrome (SARS) in Hong Kong was studied. METHODS: The pathology of the placentas was retrospectively studied in detail and compared with control sets. The clinical data of the women and neonates were also reviewed. RESULTS: A total of seven placentas were studied. The placentas from two women convalescent from SARS in the first trimester were normal. In three placentas delivered in the acute stage of SARS, there were increases in intervillous or subchorionic fibrin which might be related to disturbances in maternal placental blood flow due to the hypoxic respiratory disease. Extensive fetal thrombotic vasculopathy (FTV) with sharply demarcated zones of avascular fibrotic villi was noted in the placentas of two patients convalescent from SARS in the third trimester. Both pregnancies had intrauterine growth retardation, oligohydramnios and newborns small for gestation. The aetiology of the FTV might be related to thrombotic tendency due to SARS or placental hypoxia. CONCLUSIONS: This report highlights placental pathology that was probably the result of pathophysiological alteration of the maternal fetal unit during SARS. Further studies are required to delineate the relationship between severe maternal respiratory disease, placental pathology and pregnancy outcome.     

Maternal Antibodies to Paternal B-Lymphocytes in Normal and Abnormal Pregnancy

ABSTRACT: Sera were obtained prior to conception and during the first trimester of subsequent pregnancies from 22 women over 27 pregnancies; on 15 occasions these pregnancies ended in spontaneous abortion, whereas the remaining 12 achieved live normal babies. In only one pregnancy ending in abortion could antibodies directed to paternal B-lymphocytes determined by the EA rosette inhibition (EAI) assay be detected in the mother's serum, whereas five of the 12 successful pregnancies were associated with such detectable antibodies. Cytotoxic antibodies were also found in all but one of these EAI-positive pregnancies and no antibody activity was present in sera obtained from five primigravidae. These results indicated that normal, but not abnormal, pregnancies were often associated with blocking antibody formation, suggesting that such antibodies may protect the fetus from abortion. However, the failure to detect antibody activity in sera from first trimester primigravidae argues against a central role for blocking antibody, alone, in the maintenance of outbred pregnancy.