Serum from women with preeclampsia partially corrects the abnormal in vitro prostacyclin secretion of preeclamptic villous cytotrophoblasts but not that of prostaglandin E2 or endothelin-1

OBJECTIVE: This study was conducted (1) to determine in vitro placental villous cytotrophoblast secretion of prostacyclin, prostaglandin E₂, and endothelin-1, (2) to examine the effect of serum from normal and preeclamptic women on secretion of these vasoactive substances, and (3) to determine whether responses to these sera by cytotrophoblasts from preeclamptic pregnancies are different from those of normal pregnancies. STUDY DESIGN: Cytotrophoblasts isolated from human placentas collected at cesarean section from normal and preeclamptic women were incubated for 20 hours in 20% (vol/vol) sera from preeclamptic or gestational age–matched normal pregnant women. Levels of prostacyclin (measured as 6-keto-prostaglandin F_1α), prostaglandin E₂, and endothelin-1 were measured in cytotrophoblast supernatants. RESULTS: In normal pregnancy sera preeclamptic cytotrophoblasts secreted significantly lower amounts of prostacyclin and prostaglandin E₂ but higher amounts of endothelin-1 than did normal cytotrophoblasts. In preeclamptic sera the abnormality of prostacyclin secretion by preeclamptic cytotrophoblasts was partially corrected, but there was no effect on prostaglandin E₂ or endothelin-1 secretion. Preeclamptic sera had no effect on secretion by normal cytotrophoblasts. CONCLUSIONS: The differences between normal and preeclamptic cytotrophoblasts in prostacyclin, PGE₂, and endothelin-1 secretion and in response to preeclamptic serum suggest altered arachidonic acid metabolism in preeclampsia.(Am J Obstet Gynecol 1997;177:1491-5.)     

Alteration of vascularization in preeclamptic placentas measured by three-dimensional power Doppler ultrasound

Abstract

Objective: To evaluate the alteration of vascularization in preeclamptic placentas measured by three-dimensional (3D) power Doppler ultrasound.

Methods: We performed a prospective study of placental vascularization and placental volume in 27 singleton pregnancies complicated by preeclampsia and 41 normal pregnancies from 27 to 39 weeks of gestation. The placental volume was analyzed using the VOCAL imaging analysis program and 3D power histogram was used to calculate the placental vascular indices including vascularization index (VI), flow index (FI) and vascularization flow index (VFI).

Results: Of the 27 preeclamptic pregnancies, 9 were complicated by intrauterine growth restriction and 15 were severe preeclampsia. Furthermore, nine of the preeclamptic pregnancies had abnormal end diastolic flow in the umbilical artery. No significant correlation was noted between the placental vascular indices and gestational age in normal pregnancies. The placental vascular indices including VI, FI and VFI were significantly lower in preeclamptic placentas compared with controls (VI, p?<?0.001; FI, p?=?0.022; VFI, p?<?0.001). Preeclamptic placental volume was also decreased compared with that of the controls (p?=?0.002). After adjustment for confounding factors, significant differences were observed in VI and placental volume. However, no correlation was found between 3D power Doppler vascular indices and umbilical artery flow velocities, and neither intrauterine growth restriction nor the severity of preeclampsia could be predicted by the vascular indices.

Conclusion: VI and placental volume are reduced in preeclamptic placenta. Placental vascular indices using 3D power Doppler ultrasound provide insights of placental vascularization in preeclampsia.     

A piece in the puzzle of intrauterine fetal death: Pathological findings in placentas from term and preterm intrauterine fetal death pregnancies

Objective.?To compare pathological findings of placentas from term and preterm pregnancies complicated by intrauterine fetal death (IUFD).

Study design.?A retrospective cohort study was conducted including deliveries complicated by IUFD. A comparison was made between placentas from term and preterm (<37 weeks' gestation) pregnancies complicated by IUFD. A second analysis was undertaken comparing IUFD placentas delivered before and after 34 weeks' gestation. Uteroplacental insufficiency was defined when one or more of the following pathological features were found: placental infarct, poor vascularity of the chorionic villi, intravascular thrombi and vascular occlusion.

Results.?During the study period, 849 placentas of IUFD were examined. Gross and microscopic pathological finding were noted. When comparing gross and microscopic findings in term and preterm (<37 weeks) IUFD placentas, higher rates of calcifications, tissue congestion and cellular metaplasia were found in term vs. preterm placentas. Significantly increased rates of poor tissue vascularity, placental vascular occlusion and uteroplacental insufficiency were demonstrated in preterm IUFD placentas. When comparing pathological findings in IUFD placentas delivered before and after 34 weeks' gestation, higher rates of abnormal cord insertion, calcifications, tissue congestion, infarcts and intravascular thrombi as well as poor tissue vascularity and placental vascular occlusion were demonstrated in IUFD placentas delivered before 34 weeks. Regardless of gestational age at the time of IUFD in more than 90% of placentas vascular wall thickening was found. A third of both term and preterm placentas demonstrated histological chorioamionitis.

Conclusions.?A vast majority of IUFD placentas reveal numerous pathological findings that reflect uteroplacental insufficiency and abnormal blood supply. Different characteristics were noted in term and preterm placentas of pregnancies complicated by IUFD. Better definition of causes and associated placental pathological findings of IUFD might aid clinicians in counseling such patients regarding the reason and risk of recurrence in subsequent pregnancies.     

细胞外基质金属蛋白酶诱导因子在绒毛和胎盘组织中的表达

目的 探讨细胞外基质金属蛋白酶诱导因子(EMMPRIN)在绒毛及胎盘组织中的表达以及表达部位。方法 分别取36例妊娠6～9周妇女的早孕绒毛组织、7例因病理指征行中期引产妇女的胎盘组织和11例足月妊娠妇女的胎盘组织,免疫组化方法检测绒毛组织和胎盘组织中EMMPRIN的表达部位变化特点。结果 (1)表达部位：EMMPRIN在早孕绒毛组织、中期和足月妊娠的胎盘组织中均有高度表达。在早孕绒毛组织中的表达部位主要集中在绒毛内细胞滋养细胞、合体滋养细胞及细胞滋养层柱细胞;在中期和足月妊娠的胎盘组织中,主要表达于底蜕膜的绒毛外细胞滋养细胞。(2)表达特点：在早孕绒毛组织中细胞滋养细胞、合体滋养细胞和细胞滋养层柱细胞的。EMMPRIN阳性率随妊娠进展逐渐下降。在妊娠中期的胎盘组织中,细胞滋养细胞、合体滋养细胞和细胞滋养层柱细胞的EMMPRIN阳性率分别为5／7、3／7、5／7;在足月妊娠的胎盘组织中,细胞滋养细胞、合体滋养细胞和细胞滋养层柱细胞的EMMPRIN阳性率分别为73％、18％和82％。在中期和足月妊娠的底蜕膜中的EMMPRIN阳性率较弱,且趋于稳定。而早期妊娠阶段,侵入到底蜕膜的绒毛外细胞滋养细胞中。EMMPRIN阳性表达则随孕周进展逐渐增强。结论 EMMPRIN在妊娠早期与胚胎植入有关,在妊娠的中晚期则可能参与妊娠维持。     

Expression Patterns of Two Serine Protease HtrA1 Forms in Human Placentas Complicated by Preeclampsia with and without Intrauterine Growth Restriction

Preeclampsia (PE) and intrauterine growth restriction (IUGR) are pregnancy-specific disorders that have in common abnormal placental implantation, a marked proliferation of villous cytotrophoblastic cells and focal necrosis of the syncytiotrophoblast. Several studies show an ischemic placenta with a high-resistance vasculature, which cannot deliver an adequate blood supply to the feto-placental unit. The cause of PE is a matter of debate, but recently studies in mice suggest that the primary feto-placental lesions are sufficient to initiate the disease.HtrA1, a member of the family of HtrA proteins, is a secreted multidomain protein with serine protease activity. It is expressed in first and third trimester of gestation. In specimens from the first trimester of gestation, immunostaining for HtrA1 is generally found in both layers of villous trophoblast, syncytiotrophoblast and cytotrophoblast. Cytoplasm of extravillous trophoblast and extracellular matrix of cell islands and cell columns are labeled for HtrA1. Specimens from third trimester of gestation show a more intense positivity for HtrA1 in the syncytiotrophoblast than in cytotrophoblast. The extravillous trophoblast and the decidual cells, is positive for HtrA1. The purpose of this study is to investigate the expression pattern of HtrA1 in placentas from PE without IUGR (maternal PE) and with IUGR (fetal PE) by quantitative western blotting and immunohistochemistry. By quantitative western blotting analysis we observed a significant upregulation of ～30 kDa HtrA1 form in PE. Differently, we detected a significant total HtrA1 down-regulation in PE–IUGR. Moreover, immunostaining for HtrA1 was positive in the villous trophoblast, in the syncytial knots and irregularly in the fetal vessel walls in PE placentas while immunostaining for HtrA1was present particularly in the syncytial knots in PE–IUGR placentas. In conclusion, we suggest that the ～30 kDa HtrA1 form can be correlated to maternal PE while that the significant down-regulation of total HtrA1 can be correlated to placental PE. These HtrA1 alterations could be considered as possible markers to discriminate placental PE from maternal PE.     

Matrix metalloproteinases and their inhibitors in gestational trophoblastic diseases and normal placenta.

OBJECTIVE: Our purpose was to investigate the expression of matrix metalloproteinases (MMPs) in gestational trophoblastic diseases and normal first-trimester placenta. METHODS: Paraffin sections of 16 partial moles, 25 complete moles, 10 gestational choriocarcinomas, and 11 normal first-trimester placentas were studied immunohistochemically for expression of MMP-1, MMP-2, MMP-3, MMP-9, MMP-13, and tissue inhibitor of metalloproteinase-1 (TIMP-1). RESULTS: Nine (90.0%) of the choriocarcinoma cases showed strong intensity of staining for MMP-1. Choriocarcinoma exhibited significantly stronger staining for MMP-1 than syncytiotrophoblast in normal placenta (P < 0.01), partial mole (P < 0.01), and complete mole (P < 0.01). Choriocarcinoma also showed significantly stronger staining for MMP-1 than the extravillous trophoblast in placenta (P < 0.05). MMP-2 was expressed only in syncytio- and extravillous trophoblasts in normal placenta, partial mole, and complete mole. Choriocarcinoma and the extravillous trophoblast in partial mole and complete mole had significantly stronger staining for MMP-2 than the extravillous trophoblast in placenta (P < 0.05, P < 0.01, P < 0.01, respectively). Choriocarcinoma also exhibited significantly stronger staining for MMP-2 than syncytiotrophoblasts in placenta (P < 0.01), partial mole (P = 0.05), and complete mole (P < 0.01). The expression of MMP-3, MMP-9, and MMP-13 was similar in all four tissues with the predominance of syncytiotrophoblast for MMP-3 and MMP-13 and cytotrophoblast for MMP-9. While 8 (73.0%) placentas, 14 (87.5%) partial moles, and 19 (76.0%) complete moles showed strong immunoreactivity for TIMP-1 in syncytiotrophoblasts, no strong staining was found in choriocarcinomas (P < 0.01, P < 0.01, P < 0.01, respectively). CONCLUSION: The extravillous trophoblast of first-trimester placenta has significantly less expression of MMP-1 than choriocarcinoma and significantly less expression of MMP-2 than choriocarcinoma and extravillous trophoblast of partial and complete mole. The expression of TIMP-1 was significantly less in choriocarcinoma than the syncytiotrophoblast of normal placenta, partial mole, and complete mole. MMPs and their inhibitors may play a role in the pathogenesis of gestational trophoblastic diseases.     

Expression of Human Leukocyte Antigen-G during Normal Placentation and in Preeclamptic Pregnancies

Objectives. This study was undertaken to investigate the expression pattern of human leukocyte antigen-G (HLA-G) during normal placentation and determine whether altered expression of HLA-G is associated with severe preeclampsia. Methods. We investigated HLA-G protein levels in first (n = 27), second (n = 7), and third trimester placentas (n = 10) from normal pregnancies, and determined HLA-G levels in term placentas from normal (n = 15) and severe preeclamptic pregnancies (n = 14) using real-time RT-PCR and western blot analysis. Results. In normal placentas, HLA-G protein expression reached a peak level at gestational weeks 6 and 7, then gradually decreased from week 8 to third trimester (p < 0.05). In preeclamptic placentas, both HLA-G mRNA and protein levels were decreased significantly in comparison with normal term placentas (p < 0.05). Conclusion. HLA-G may contribute to placentation during early and mid-term pregnancy, and participate in maintaining gestation during term pregnancy. The reduced level of HLA-G may be associated with pathogenesis of preeclampsia.     

Trophoblast expression of EGFR (epidermal growth factor receptor) in the preeclampsia placenta

Placental pathology in preeclampsia and retarded fetuses is associated with changes of the pattern of expression of EGFR. The purpose of this study was to investigate the expression of epidermal growth factor receptor in trophoblast populations of preeclampsia and retarded fetuses in comparison with normal controls. Tissue microarray with paraffin sections containing a general of 90 placental specimens including 30 preeclamptic cases, 30 retarded fetuses and 30 normal pregnancies (controls) were studied immunohistochemically for epidermal growth factor receptor in the syncytiotrophoblast and villous cytotrophoblast. Epidermal growth factor receptor levels were estimated semiquantitatively. The percentage of strong/intermediate immunoreactivity of epidermal growth factor receptor in the syncytiotrophoblast was significantly higher in normal placental cases (98%) than in pathological conditions (P = .03), although strong/intermediate immunoreactivity in the syncytiotrophoblast was significantly lower in pathologic cases (35%) than controls (P < .001). No correlation (P > 0.01) was found between the trophoblast expression of EGFR and the weight of the newborn fetuses. Epidermal growth factor receptor expression in the villous and extravillous cytotrophoblastic cells were significantly different between controls and preeclamptic cases (P > .05). CONCLUSION: The development of pathologic pregnancies is possibly related to the differential expression of epidermal growth factor receptor in the syncytiotrophoblast.     

Elastic fibres in the human placenta

Recent studies described the presence of elastic fibres within stem villi of human term placenta. This particular study focuses on changes of the elastic fibre system in placental villous tree from placentas of different gestational ages. The presence of elastic fibres was researched by light and electron microscopy in first-, second-trimester and term human placentas. Light microscopic analysis revealed elastic fibres in the stroma of main stem villi and in large vessels present in the chorionic plate of term placentas. Transmission electron microscopy revealed a wide variation in microfibrillar component deposition in placentas from all the gestational ages studied. Although minimal amount of the microfibrillar component was observed only in some main stem villi of second-trimester placentas, abundant microfibrillar material was present in all types of placental villi in placental sections from term pregnancies. The amorphous component was only occasionally identified in sections from the chorionic plate of second trimester placentas. In ultra-thin sections from placental tissues from the 37th to the 42nd weeks of gestation, we can observe the amorphous component of the elastic fibres. Bundles of microfibrils with scanty participation of the amorphous component of the elastic fibres can be observed in stem villi. In mature intermediate villi, cells and their processes with distinct plasma membranes were seen close to some bundles of microfibrillar component, at times with small spots of the amorphous component. This study shows that elastic fibres of the villous stroma, are mainly composed of the microfibrillar component, while the amorphous component appears more frequently in advanced stages of villous differentiation of term placentas.     

Aberrations of early trophoblast differentiation predispose to pregnancy failure: lessons from the anti-phospholipid syndrome

OBJECTIVES: The epithelium of the human placenta comprises an inner cytotrophoblast (CT) which proliferates and fuses with the outer differentiated syncytiotrophoblast (ST). Turnover has been studied focussing on second and third trimester placentas but with a paucity of data describing the normal first trimester trophoblast. The aim of this study was to compare the nuclear CT:ST ratio in normal and pathological pregnancy and thus establish the relationship between cytotrophoblast and syncytiotrophoblast nuclear number during early gestation. METHODS: Archival first trimester material from placentas from healthy pregnancy and recurrent miscarriage (anti-phospholipid syndrome) was stained with H&E, cytokeratin-7 and Mib-1. The area of trophoblast as a fraction of total villous area was calculated and the number of sectioned cytotrophoblast and syncytiotrophoblast nuclei as well as the number of proliferating cytotrophoblast was evaluated. RESULTS: Normal features of trophoblast development during the first trimester (rise in trophoblast area, increase in number of syncytiotrophoblast nuclei, increase in number of proliferating cytotrophoblast, decrease in the nuclear CT:ST ratio) are absent/reversed in tissues from recurrent miscarriage (decreasing trophoblast area, constant number of syncytiotrophoblast nuclei, decreasing number of proliferating trophoblast, constant nuclear CT:ST ratio). CONCLUSIONS: Proliferation of cytotrophoblast in early gestation provides a pool of trophoblast stem cells critical for ongoing placental development. Premature cytotrophoblast differentiation in favour of syncytial fusion results in deficiencies of cytotrophoblast and rarification of villous trophoblast. Abnormal trophoblast differentiation in early gestation may be due to a premature onset of maternal perfusion of the placenta and may be a likely antecedent for conditions associated with failure of placentation such as recurrent miscarriage.     

A novel change in cytologic localization of human chorionic gonadotropin and human placental lactogen in first-trimester placenta in the course of gestation.

Cytologic localization of human chorionic gonadotropin and human placental lactogen in developing human early placenta was analyzed by avidin-biotin immunoperoxidase techniques with an affinity-purified polyclonal antibody to beta-human chorionic gonadotropin carboxyl terminal peptide and a polyclonal antibody to human placental lactogen. In 4- to 5-week placentas human chorionic gonadotropin and human placental lactogen were found to be primarily localized to cytotrophoblasts, whereas in 6- to 12-week placentas these substances were exclusively localized to syncytiotrophoblast. We previously reported that a similar change in cytologic localization of epidermal growth factor and its receptor from cytotrophoblasts to syncytiotrophoblast in first-trimester placenta appeared between 5 and 6 weeks of gestation. Because epidermal growth factor was demonstrated to stimulate human chorionic gonadotropin and human placental lactogen production by early placental tissues, their simultaneous expression, as well as epidermal growth factor and its receptor in the cytotrophoblast of 4- to 5-week placenta and in the syncytiotrophoblast of 6- to 12-week placenta, implies that human chorionic gonadotropin and human placental lactogen production by first-trimester placenta may be regulated in an autocrine manner, wherein epidermal growth factor may serve as the signal. These findings suggest that in very early placenta, before 6 weeks of gestation, no sequential expression of human chorionic gonadotropin and human placental lactogen closely linked to syncytia formation may exist and that both can be expressed in the cytotrophoblast or undifferentiated stem cell of villous trophoblast in very early placenta.     

Placental expression of insulin-like growth factor-I,fibroblast growth factor-basic,and neural cell adhesion molecule in preeclampsia

Objective. To investigate placental expression of insulin-like growth factor-I (IGF-I), fibroblast growth factor-basic (FGF-b), and neural cell adhesion molecule (N-CAM) in preeclampsia.

Study design. An immunohistochemical analysis using IGF-I, FGF-b, and N-CAM antibodies was conducted on 4% paraformaldehyde-fixed placental tissues of preeclamptic patients (N = 14) and normotensive pregnant subjects (N = 10). Immunostaining patterns of chorionic villi and amniochorionic membranes were assessed.

Results. Significantly increased FGF-b and N-CAM immunoreactivities in cytotrophoblasts and increased FGF-b immunoreactivity in capillary endothelium of chorionic villi of preeclamptic subjects were noted. Significantly increased FGF-b and decreased N-CAM immunoreactivities in extravillous trophoblasts and decidual cells of amniochorionic membranes obtained from preeclamptic subjects were demonstrated. Additionally, a significantly increased IGF-I immunoreactivity was shown in decidual cells of preeclamptic cases.

Conclusion. Investigation of the regional distribution of IGF-I, FGF-b, and N-CAM at the maternal–fetal interface establishes a better understanding of cell-specific altered growth processes, which may be associated with the pathogenesis of preeclampsia.     

Expression and cellular localisation of chloride intracellular channel 3 in human placenta and fetal membranes

Chloride channels regulate the movement of a major cellular anion and are involved in fundamental processes that are critical for cell viability. Regulation of intracellular chloride is achieved by multiple classes of channel proteins. One class of putative channels are the chloride intracellular channel (CLIC) family. Evidence suggests that several CLICs are expressed in human placenta, although their roles in this tissue are not certain. Northern blot analysis has shown that CLIC3 is highly expressed in placenta relative to other human tissues; however, its cellular distribution is not known. This study used microarray expression profiling to clarify which CLICs are expressed in human placenta and RT-PCR, Western blot and immunohistochemistry to determine the expression pattern of CLIC3 in human placenta and fetal membranes. Placentas and fetal membranes were obtained from term pregnancies after delivery and placental tissue was obtained from first trimester following either chorionic villous sampling or elective pregnancy termination. Trophoblast cells were isolated from first trimester and term placentas and placental endothelial cells were isolated from term placentas. Microarray expression profiling identified high expression of mRNA for CLICs 1, 3 and 4 in the isolated first trimester and term trophoblast cells. High mRNA expression in the isolated endothelial cells was also found for CLICs 1 and 4, but not CLIC3. Low expression was found for CLIC5 in all three types of isolated cells. RT-PCR confirmed that CLIC3 mRNA was expressed in trophoblast cells at both gestational ages, but was not present in endothelial cells. CLIC3 mRNA was also identified in whole placental extracts at both gestational ages and in term amnion and choriodecidua. Immunohistochemistry using a chicken anti-human CLIC3 antibody localised strong CLIC3-specific staining to the syncytiotrophoblast and villous cytotrophoblast cells in both first trimester and term placentas, and weaker staining in extravillous trophoblast cells in first trimester. In fetal membranes at term strong CLIC3-specific staining was localised to chorionic trophoblast cells, with weaker staining in amniotic epithelial and decidual cells. It was previously shown that chloride uptake was increased into cells that had been transfected with CLIC3. CLIC3 may facilitate chloride ion movement and the regulation of cellular processes associated with the movement of chloride in the placental and fetal membrane cells in which it is expressed.     

Placental growth hormone is increased in the maternal and fetal serum of patients with preeclampsia

Objectives. Placental growth hormone (PGH) is a pregnancy-specific protein produced by syncytiotrophoblast and extravillous cytotrophoblast. No other cells have been reported to synthesize PGH Maternal. PGH Serum concentration increases with advancing gestational age, while quickly decreasing after delivery of the placenta. The biological properties of PGH include somatogenic, lactogenic, and lipolytic functions. The purpose of this study was to determine whether the maternal serum concentrations of PGH change in women with preeclampsia (PE), women with PE who deliver a small for gestational age neonate (PE + SGA), and those with SGA alone.

Study design. This cross-sectional study included maternal serum from normal pregnant women (n = 61), patients with severe PE (n = 48), PE + SGA (n = 30), and SGA alone (n = 41). Fetal cord blood from uncomplicated pregnancies (n = 16) and PE (n = 16) was also analyzed. PGH concentrations were measured by ELISA. Non-parametric statistics were used for analysis.

Results. (1) Women with severe PE had a median serum concentration of PGH higher than normal pregnant women (PE: median 23,076 pg/mL (3473–94 256) vs. normal pregnancy: median 12 157 pg/mL (2617–34 016); p < 0.05), pregnant women who delivered an SGA neonate (SGA: median 10 206 pg/mL (1816–34 705); p < 0.05), as well as pregnant patients with PE and SGA (PE + SGA: median 11 027 pg/mL (1232–61 702); p < 0.05). (2) No significant differences were observed in the median maternal serum concentration of PGH among pregnant women with PE and SGA, SGA alone, and normal pregnancy (p > 0.05). (3) Compared to those of the control group, the median umbilical serum concentration of PGH was significantly higher in newborns of preeclamptic women (PE: median 356.1 pg/mL (72.6–20 946), normal pregnancy: median 128.5 pg/mL (21.6–255.9); p < 0.01). (4) PGH was detected in all samples of cord blood.

Conclusions. (1) PE is associated with higher median concentrations of PGH in both the maternal and fetal circulation compared to normal pregnancy. (2) Patients with PE + SGA had lower maternal serum concentrations of PGH than preeclamptic patients without SGA. (3) Contrary to previous findings, PGH was detectable in the fetal circulation. The observations reported herein are novel and suggest that PGH may play a role in the mechanisms of disease in preeclampsia and fetal growth restriction.     

Fas and FasL expression in placentas complicated with intrauterine growth retardation with and without preeclampsia

Objective: To compare the level of Fas and FasL immunohistochemical expression in villous trophoblast (VT), extravillous trophoblast (EVT) cells, decidual cells (DC), endothelial cells (EC) of villous blood vessels and spiral arteries between the study groups of intrauterine growth retardation (IUGR) placentas with and without preeclampsia (PE).

Methods: The study included 17 placentas from pregnancies complicated by IUGR?+?PE and 17 placentas from pregnancies complicated by idiopathic IUGR (I-IUGR). Seventeen placentas from normal pregnancies served as a control group. CD31 was used to detect endothelial cells (EC). Immunohistochemical expression of Fas and FasL was assessed in all examined parts of placenta using the semi-quantitative HSCORE method.

Results: FasL expression was significantly higher in all examined parts of placenta in I-IUGR as compared to IUGR?+?PE and control group. Placentas with IUGR?+?PE had the significantly lowest expression of FasL in VT and EC of villi vessels. Expression of Fas did not differ significantly between the study groups.

Conclusion: Different expression of FasL in placentas from I-IUGR and IUGR?+?PE suggests that FasL probably has a different role in the etiology of these two syndromes.     

The assessment of placental volume and mean gray value in preeclamptic placentas by using three-dimensional ultrasonography

Objectives: We aimed to evaluate the placental volume and placental mean gray value in preeclampsia and healthy placentas by using three-dimensional (3D) ultrasonography and Virtual Organ Computer-aided AnaLysis (VOCAL).

Methods: This case–control prospective study consisted of 27 singleton pregnancies complicated by preeclampsia and 54 healthy singleton pregnancies matched for gestational age, maternal age and parity. Placental volume and placental volumetric mean gray values were evaluated. The placental volume (cm³) was analyzed using the VOCAL imaging program, and 3D histogram was used to calculate the volumetric mean gray value (%).

Results: Preeclamptic and control group consisted of 27 (mean age: 28.90?±?5.95 years, mean gestation: 32.0?±?4.55 weeks) and 54 (mean age: 29.48?±?5.78 years, mean gestation: 32.61?±?4.23 weeks) singleton pregnancies, respectively. Placental volume was significantly smaller in preeclampsia (250.62?±?91.69 versus 370.98?±?167.82?cm³; p?=?0.001). Volumetric mean gray value of the placenta was significantly higher in preeclampsia (38.24?±?8.41 versus 33.50?±?8.90%; p?=?0.043). Placental volume was significantly correlated with the estimated fetal weight (r?=?0.319; p?=?0.003). There was negative significant relation between placental volume and umbilical artery pulsatility index, resistance index and systolic/diastolic ratio (r?=?–0.244, p?=?0.024; r?=?–0.283, p?=?0.005; r?=?–0.241, p?=?0.024, respectively).

Conclusions: Placental volume diminishes significantly in preeclampsia, whereas volumetric mean gray values increases. This may reflect the early alterations in preeclamptic placentas, which may help to understand the pathophysiology better.