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Levels of placenta growth factor in gestational trophoblastic diseases.

OBJECTIVE: The aim of the current study was to investigate levels of placenta growth factor in the tissues and sera of the patients with gestational trophoblastic disease and to determine its usefulness for the treatment of gestational trophoblastic disease. STUDY DESIGN: Placenta growth factor concentrations were measured in the tissue homogenates of 12 normal placentas, 33 complete hydatidiform moles, and 6 gestational choriocarcinomas. Serum placenta growth factor levels were determined in 59 women with normal pregnant course, in 30 women with complete hydatidiform mole, in 36 women with persistent gestational trophoblastic disease, and 100 nonpregnant healthy volunteers. RESULTS: Serum and tissue placenta growth factor levels in the patients with mole tended to be decreased compared with the levels in normal pregnancy; the levels were increased significantly in patients with choriocarcinoma. When serum placenta growth factor levels were >20 pg/mL (normal upper limit in nonpregnant women), placenta growth factor-to-human chorionic gonadotropin ratios were increased significantly in patients with persistent gestational trophoblastic disease. CONCLUSION: Serum placenta growth factor levels are not of any predictive value in patients with hydatidiform mole. However, elevated serum placenta growth factor levels with increased placenta growth factor-to-human chorionic gonadotropin ratios are suggestive of persistent gestational trophoblastic disease.

Choriocarcinoma↗

Obstetric history and the risk of placenta previa.

OBJECTIVE: To evaluate secular trends in the occurrence of placenta previa and whether placenta previa is associated with the outcome of previous pregnancies, cesarean section, and sociodemographic factors. DESIGN: A cohort study based on the Medical Birth Registry of Norway. Placenta previa in the second pregnancy was investigated for associations with outcomes in the first pregnancy and sociodemographic factors. RESULTS: In birth orders 1 and 2 the occurrence of placenta previa was 1.2 and 2.2 per 1,000, respectively, with no secular trend. The occurrence increased with maternal age and was lowest in women aged 20-29 years. The recurrence rate was 23 per 1,000 (adjusted odds ratio (OR) of recurrence=9.7). In women with prior delivery at < or =25 gestational weeks the risk of placenta previa was 6.7 per 1,000 (adjusted OR=3.0). In women with prior placental abruption the risk was 5.8 per 1,000 (OR=2.6). In women with prior perinatal death the risk was 4.4 per 1,000 (adjusted OR= 1.8). No independent relationship emerged with socio-economic factors, previous birthweight, and a history of pregnancy induced hypertension. Cesarean section was associated with subsequent development of placenta previa (adjusted OR= 1.3). CONCLUSIONS: We found no secular trends in the occurrence of placenta previa. Placenta previa is associated with previously described risk factors for placental abruption. The increased risk of placenta previa subsequent to placental abruption supports the theory of a shared etiologic factor. However, placenta previa and placental abruption do not share a common etiology in relation to a history of pregnancy induced hypertension, fetal growth retardation, and socio-economic factors.

Abruptio Placentae↗

Non-enzymatic antioxidative defence mechanisms against reactive oxygen species in bovine-retained and not-retained placenta: vitamin C and glutathione.

Vitamin C and glutathione (GSH) are water-soluble antioxidants which take part in defence mechanisms against reactive oxygen species (ROS). They may also be involved in processes of releasing/retaining bovine fetal membranes. Hence vitamin C, reduced (GSH) and oxidised (GSSG) glutathione levels were determined in retained and not-retained bovine fetal membranes in order to describe the non-enzymatic antioxidative status. Placental samples were collected immediately after spontaneous delivery or during caesarean section before term and at term, and 6 groups were formed as follows: (A) pre-term caesarean section without retained placenta; (B) pre-term caesarean section with retained placenta; (C) term caesarean section without retained placenta; (D) term caesarean section with retained placenta; (E) spontaneous delivery without retained placenta and (F) spontaneous delivery with retained placenta. Homogenates of maternal and fetal placental tissues were prepared, and vitamin C, GSH and GSSG were measured spectrophotometrically. Vitamin C levels were significantly higher in the maternal part than in the fetal part of the placenta in all groups examined. In retained placenta cases the levels were significantly lower than in control cows, except in pre-term groups. GSH concentrations were significantly higher in placentas without retention than with retention. GSSG levels showed the opposite relationship and were significantly higher in samples with retention of fetal membranes than in controls. Further experiments on antioxidative as well as oxidative status in bovine placenta are necessary.

Animals↗

[Localization of the placenta by means of nuclear medical methods].

Accurate localization of the placenta in the cavity of the uterus is indicated prior to transabdominal amniocentesis and in cases where hemorrhages occur during pregnancy. Several nucleo-medical techniques are available for this purpose. Earlier a so-called placentography was performed, a method later replaced by placental scintigraphy. Today the gamma scintillation camera is ideal for localizing the seat of the placenta. In case of a normally embedded placenta, the profile view makes it possible to determine whether the placenta is attached to the anterior or posterior wall. In case of an anterior wall placenta it is possible with a radioactively labelled marker to draw the outline of the placenta on the abdomen of the patient so that the examiner is certain to puncture in an area that does not contain the placenta. Diagnosis of placenta praevia is assured in all cases by use of the gamma scintillation camera. Short-term introduction of an emitter into the posterior fornix vaginae makes it possible to determine the position of the internal orifice of the cervix uteri. If the caudal part of the placenta extends up to this mark, a placenta praevia is likely and all obstetrical precautions indicated have to be taken.

Female↗

[The study on mechanism of abruptio placentae caused by chorioamnionitis].

The cause of abruptio placentae has not been elucidated yet. Although preeclampsia is frequently associated with abruptio placentae, the rate of abruptio placentae caused by preeclampsia has decreased recently. Many current reports have indicated that chorioamnionitis is an important cause of abruptio placentae. To clarify the relationship between chorioamnionitis and abruptio placentae, we performed immunostaining for fibronectin, fibronectin receptor and granulocyte elastase of placenta with or without abruptio placentae. In cases of abruptio placentae caused by chorioamnionitis, granulocyte elastase was stained strongly and fibronectin receptor was stained weakly in decidual cells, especially in the parts of granulocyte elastase invased. In III stage chorioamnionitis without abruptio placentae, granulocyte elastase was stained moderately and the intensity of fibronectin receptor did not decrease. There was no difference between fibronectin staining in all cases. When purified granulocyte elastase was added to the cultured decidual cells, the staining intensity of fibronectin receptor became weak in those cells. These results suggest that marked imbalance between neutrophil invasion and an inhibitor, such as alpha 1 antitrypsin, initiates granulocyte elastase release and promotes the reduction of the fibronectin receptor in decidual cells resulting in weakening of the adherence of decidual cells. This may be one of the mechanisms of abruptio placentae caused by chorioamnionitis.

Abruptio Placentae↗

Diesel exhaust affects immunological action in the placentas of mice.

We investigated the effect of diesel exhaust (DE) on pregnancy and fetal development in mice at day 14 postcoitum (pc) with a special focus on the placenta. The number of absorbed fetuses increased in groups exposed to DE, and congestion was observed in histological sections of placentas. During placental absorption expression of CYP1A1 mRNA decreased to undetectable levels, whereas expression of TNF alpha mRNA increased approximately twofold over that of the control. Levels of CYP1A1 mRNA in normal placentas from DE-exposed mice were unchanged. mRNA levels of inflammatory cytokines IL-2, IL-5, IL-12 alpha, IL-12 beta, and GM-CSF increased in placentas exposed to DE (0.3 and 3.0 mg diesel exhaust particles (DEP)/m3). Expression of IL-5 mRNA was markedly increased in DE-exposed placentas, although levels were barely detectable in control placentas. IL-6 mRNA expression was increased approximately 10-fold in placentas exposed to DE (3.0 mg DEP/m3). It has been reported that expression of mRNA encoding proteins involved in immune function in the placenta is increased during fetal absorption in mice. In the present study, expression of such mRNA by the placenta was increased by DE exposure. Because it is believed that expression of mRNA in the placenta also affects fetal development, DE may promote fetal absorption. These findings suggest that in mice exposure to DE affects fetal absorption and placental function by modifying expression of immune-related genes during early gestation and expression of endocrine-related genes during late gestation.

Animals↗

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.

Female↗

Assessment of asbestos burden in the placenta and tissue digests of stillborn infants in South Texas.

The primary aim of this prospective study was to examine the tissues and placentas of autopsied stillborn infants for presence of asbestos fibers. Asbestos burden of lung, liver, skeletal muscle, and placenta digests of 82 stillborn infants was determined using standard bleach digestion technique. The digests were examined by electron microscopy, and the types of fibers determined using energy dispersive x-ray analysis and selected area diffraction analysis. Digests of 45 placentas collected from deliveries of liveborn healthy infants were processed and examined similarly as controls. Asbestos fibers were detected in 50% of the fetal digests and 23% of the placental digests of stillborn infants. Of the fibers present, 88% were chrysotile, 10% were tremolite, and 2% were actinolite and anthophyllite. Fibers measured 0.5-16.73 microgram in length (mean 1.55 microgram), and 0.03-0.8 microgram in width (mean 0.098 microgram). Lungs were most frequently positive for fibers (50%), followed by muscle (37%), placenta (23%), and liver (23%). Mean fiber counts were highest in the liver (58,736 f/g), followed by placenta (52,894 f/g), lungs (39,341 f/g), and skeletal muscle (31,733 f/g). Digests of 15% of the control placentas also showed asbestos fibers, although in very small numbers. The mean fiber count of the stillborn placentas (52,894 f/g) was significantly higher than the mean fiber count of the control placentas (mean 19 f/g) (p = 0.001). A highly significant association was found between fiber presence in stillborns and a maternal history of previous abortions (p = 0.007). A significant association was also found between fiber presence and placental diseases (p = 0.041). An association was suggested between working mothers and fiber presence (p = 0.19), although it did not reach statistical significance. The study documents the presence of small and thin asbestos fibers in stillborn fetal tissues and placenta. Significantly higher number of fibers were found in stillborn tissues compared to controls (liveborn placenta). The absence of a maternal history of asbestos-related occupations suggests that the fibers may have been acquired through environmental exposure.

Adult↗

Effect of maternal hypokalaemia on unidirectional maternofetal and net potassium fluxes across the placenta of the anaesthetized rat.

Potassium (K+) fluxes across the placenta of rats, at 21 days gestation, fed a low K+ diet or a control diet were studied. The rats on the low K+ diet had a significantly (P less than 0.001) lower arterial plasma K+ concentration compared to those on the control diet (1.95 +/- 0.12 and 2.93 +/- 0.06 mmol/l respectively; mean +/- s.e., n = 17). Fetal umbilical arterial plasma K+ concentration was unaltered in maternal hypokalaemia and was significantly (P less than 0.001) higher than that of maternal plasma (4.58 +/- 0.15 and 4.66 +/- 0.12 mmol/l in low K+ and control groups respectively). Net K+ flux across the placentas (as measured by fetal accretion between days 20 and 21 of gestation) of hypokalaemic mothers (0.106 +/- 0.02 mumol/min/g placenta, n = 6) was not different to that in controls (0.104 +/- 0.01 mumol/min/g placenta, n = 8). Unidirectional maternofetal flux (Jmf) across the placentas, measured as the accumulation of 42K in the fetuses after injection of the radioisotope into maternal blood, was also not significantly different between the hypokalaemic and control mothers (0.5 +/- 0.08 mumol/min/g placenta, n = 8 versus 0.63 +/- 0.06 mumol/min/g placenta, n = 7, respectively). However, measurement of Jmf by perfusion of the placentas through their fetal circulations yielded a higher value than the accumulation method and in this analysis was significantly (P less than 0.02) lower in the low K+ than in the control group (0.75 +/- 0.10 mumol/min/g placenta, n = 11, and 1.27 +/- 0.14 mumol/min/g placenta, n = 9, respectively). These results show that net placental K+ fluxes are unaltered during maternal hypokalaemia but suggest that unidirectional maternofetal fluxes may be reduced.

Animals↗

IGFBP1 and Follistatin-like 3 genes are significantly up-regulated in expression profiles of the IUGR placenta.

To date, the clinicopathological features of intrauterine growth restriction (IUGR) are not clearly understood, and no effective therapy has been established for IUGR. This is the first study that uses microarray analysis to identify differentially expressed genes in the IUGR placenta. The expression profiles of a total of 9121 genes were examined by cDNA microarray analysis, using mRNA from an appropriate gestational age (AGA) placenta and an IUGR placenta from discordant dichorionic twins. Up-regulation of the IGFBP1 and Follistatin-like 3 genes was detected in the IUGR placenta, with a balanced differential degree of 20.7+/-1.3 and 13.1+/-2.1, respectively, while the balanced differential degrees of other genes were 2.6 or less. The expressions of the IGFBP1 and Follistatin-like 3 genes in four single IUGR and four AGA placentas were also examined by RT-PCR. Consistent with our data in discordant chorionic twin placentas, three of four IUGR placentas showed up-regulation of the IGFBP1 and all four IUGR placentas showed upregulation of Follistatin-like 3 genes when compared to the AGA placentas. Our results suggest that IGFBP1 and Follistatin-like 3 are highly up-regulated in IUGR in the placenta. IGFBP1 and Follistatin-like 3 are known critical regulators of fetal growth and differentiation. Pathways associated with these genes might be important for the pathogenesis of IUGR.

Female↗

Parturition in gilts: duration of farrowing, birth intervals and placenta expulsion in relation to maternal, piglet and placental traits.

Large White x Meishan F2 crossbred gilts (n = 57) were observed continuously during farrowing while the placentae of their offspring were labeled in order to examine the duration of farrowing and placenta expulsion in relation to maternal-, piglet- and placental traits and the duration of birth interval in relation to birth weight, birth order and placental traits. Independently from each other, litter size, gestation length and offspring directed aggression significantly (P 0.05) affected duration of farrowing. An increase in litter size was associated with an increase of duration of farrowing and an increase in gestation length was associated with a decrease of duration of farrowing. Aggressive gilts took longer to farrow, compared to non-aggressive ones. After taking into account litter size, gestation length and offspring directed aggression, placental thickness (i.e., placental weight corrected for placental surface area) was significantly (P < 0.05) related to duration of farrowing, i.e., litters with on average thicker placentae took longer to farrow. The latter effect is the result of the fact that individual placental thickness significantly (P < 0.01) affected individual birth interval, independent of birth weight. The piglet has to break its own membranes to be able to start its journey through the uterus towards the birth channel. Apparently, a thicker placenta offers more resistance and thus prolongs the process of birth. Independent of placental thickness, birth interval significantly (P < 0.01) decreased with an increase in birth order (first born to last born). The high variation of birth intervals for the last born piglets, caused a slight increase in average birth interval for the latter piglets. Litters with on average more areolae per placenta took significantly (P < 0.001) less time to be born than litters with on average less areolae per placenta (independent of total number of piglets born and other placental traits), while birth intervals within litters were not affected by this trait. Thus, these results are probably due to a gilt trait rather than a piglet trait. Since the number of areolae represent the number of uterine glands present, the gilt trait might be uterine development. Duration of placenta expulsion significantly (P < 0.01) increased with an increase of duration of farrowing. Furthermore, the first placenta was expelled significantly (P < 0.01) earlier relative to last piglet when duration of farrowing was protracted, while there was no relation of the time interval between first placenta and last piglet and the duration of placenta expulsion. In conclusion, the most important finding of this study is that placental thickness rather than birth weight appears to play an important role in the duration of birth intervals and as a result, of duration of parturition in gilts.

Aggression↗

Enhancement of mitochondrial oxidative stress and up-regulation of antioxidant protein peroxiredoxin III/SP-22 in the mitochondria of human pre-eclamptic placentae.

A growing body of evidence indicates that the pathogenesis of pre-eclampsia is closely associated with oxidative stress occurring in mitochondria. In the present study, we evaluated the degree of mitochondrial lipid peroxidation by assessing the accumulation of 4-hydroxy-2-nonenal (HNE)-modified proteins and examined the expression of mitochondrial antioxidant protein peroxiredoxin III/SP-22 in normal and pre-eclamptic human placentae. The accumulation of HNE-modified proteins increased to a greater extent in both the mitochondria and cytosol of pre-eclamptic placentae than in those of normal placentae. Moreover, the accumulation of HNE-modified proteins was much more evident in the mitochondria than in the cytosol, indicating that lipid peroxidation occurred mainly in the mitochondria of pre-eclamptic placentae. The mRNA expression of peroxiredoxin III/SP-22 was increased about 2-fold in pre-eclamptic placentae compared to normal placentae. The protein levels of peroxiredoxin III/SP-22 were approximately 4-fold higher in pre-eclamptic placentae than in normal placentae. Immunohistochemistry of placental tissues showed that the levels of peroxiredoxin III/SP-22 protein were increased in the trophoblasts of floating villi, stromal cells of stem villi, and decidual cells in pre-eclamptic placentae. These results indicate that peroxiredoxin III/SP-22 plays a crucial role in the protection of placental function from oxidative stress occurring in mitochondria of pre-eclamptic placentae.

Adult↗

Enhanced protein levels of protein thiol/disulphide oxidoreductases in placentae from pre-eclamptic subjects.

Recent studies have indicated that pre-eclampsia is closely associated with oxidative stress both in maternal circulation and in the placenta. Protein thiol/disulphide oxidoreductases, such as thioredoxin, glutaredoxin, and protein disulphide isomerase have recently been found to eliminate reactive oxygen species (ROS) and regenerate oxidatively damaged proteins. Protein thiol/disulphide oxidoreductases may also play a role in combating pre-eclampsia. In this study, we examined the accumulation of 4-hydroxy-2-nonenal (HNE)-modified proteins, which are markers of lipid peroxidation, in human placentae of normal and pre-eclamptic subjects. We also examined the protein levels of thioredoxin, glutaredoxin, and protein disulphide isomerase in placentae. Immunoblotting and immunohistochemistry showed that HNE-modified proteins accumulated to a greater extent in pre-eclamptic placentae than in normal placentae. In both normal and pre-eclamptic placentae, thioredoxin, glutaredoxin, and protein disulphide isomerase were detected in the trophoblasts of the floating villi. The levels of these proteins were increased approximately 2- to 3-fold in the pre-eclamptic placentae compared to the normal placentae. These results indicated that the pre-eclamptic placentae were exposed to oxidative stress and that the protein thiol/disulphide oxidoreductases were adaptively induced in pre-eclamptic placentae, suggesting possible roles for thioredoxin, glutaredoxin, and protein disulphide isomerase in protecting placental functions against oxidative stress caused by pre-eclampsia.

Adult↗

Localization of messenger ribonucleic acid for adrenomedullin and adrenomedullin receptor in the human placenta in normal pregnancies and pregnancies complicated by oligohydramnios.

OBJECTIVE: The purpose of this study was to identify the placental expression of adrenomedullin and adrenomedullin receptor messenger ribonucleic acid and compare them between placentas from pregnancies associated with oligohydramnios as a result of uteroplacental insufficiency and placentas from normal pregnancies. STUDY DESIGN: Total ribonucleic acid was extracted from the amnion, chorion, cotyledon, umbilical vein, and umbilical artery in 5 normal placentas and 3 placentas from pregnancies complicated by oligohydramnios. A cell line known to express messenger ribonucleic acid of adrenomedullin and its receptor was used to optimize the polymerase chain reaction and served as a positive control preparation in all experiments. Semiquantitative reverse transcriptase-polymerase chain reaction results for adrenomedullin and adrenomedullin receptor were compared between tissues as densitometric ratios of adrenomedullin or adrenomedullin receptor messenger ribonucleic acid to beta(2)-microglobulin messenger ribonucleic acid. Results were analyzed with a Kruskal-Wallis 1-way analysis of variance. Immunohistochemical staining with an antibody to human adrenomedullin was used to localize adrenomedullin in all tissue types. RESULTS: Messenger ribonucleic acid sequences for adrenomedullin and adrenomedullin receptor genes were identified in all tested placental tissue components. Within the normal placentas the expressions of adrenomedullin and adrenomedullin receptor messenger ribonucleic acid sequences did not differ statistically between the tissue components. Within placentas from patients with oligohydramnios the expressions of adrenomedullin and adrenomedullin receptor messenger ribonucleic acid did not differ statistically between the tissue components. When normal placentas were compared with placentas from pregnancies complicated by oligohydramnios, however, a 5-fold increase in adrenomedullin messenger ribonucleic acid and a 3-fold increase in adrenomedullin receptor messenger ribonucleic acid were seen in placentas from patients with oligohydramnios. Adrenomedullin immunoreactivity was present in all tissues studied. CONCLUSION: The expression of messenger ribonucleic acid for both adrenomedullin and its receptor in these tissue components implies that placental tissues function in both synthesis and action of adrenomedullin. The increased adrenomedullin messenger ribonucleic acid expression in the umbilical artery and the elevated adrenomedullin receptor messenger ribonucleic acid expression in the cotyledons of placentas from patients with oligohydramnios may represent a local fetoplacental physiologic adaptive response to vascular compromise.

Adrenomedullin↗

Expression of insulin-like growth factor II in human placentas from normal and diabetic pregnancies.

The growth and development of the placenta is critical to fetal growth and development; however, little is known regarding the mechanisms controlling placental growth and development. Human placental membranes are known to possess receptors for insulin-like growth factors I and II (IGF-I and IGF-II) from early gestation, and increasing evidence supports a major role for IGF-I and/or IGF-II in fetal growth and development. Therefore, the IGFs may also play a significant role in regulating placental growth and development. We report here that an adult human liver IGF-II cDNA hybridizes to poly(A)+ RNAs of human placentas from different gestational ages. There are four placental poly(A)+ RNA species that hybridize to IGF-II cDNA, the major one of which is about 6000 bases. The sizes of the hybridized transcripts are the same for placentas of different gestational ages. Furthermore, the IGF-II sequences expressed in the human placenta were quantitated by dot blot hybridization. The second trimester placenta expresses more IGF-II mRNA sequences than placenta of first trimester and term. Interestingly, the term placentas from diabetic pregnancies also express more of these sequences than those from normal pregnancies. These results suggest that there are developmental changes in the expression of the IGF-II gene in the placenta and that IGF-II may promote placental growth by way of an autocrine and/or paracrine mechanism. Moreover, fetuses developing in diabetic pregnancies receive a large influx of glucose, which in turn may stimulate the expression of IGF-II sequences in placenta, resulting in higher utilization of glucose and overgrowth of placenta. This may explain the macrosomia and high incidence of malformations and stillbirths known to result from pregnancies in diabetics.

Female↗

Etiology and risk factors for placenta previa: an overview and meta-analysis of observational studies.

OBJECTIVE: Several clinical and epidemiologic studies have reported disparate data on the prevalence rate as well as risk factors associated with placenta previa--a major cause of third-trimester bleeding. We performed a systematic literature review and identified 58 studies on placenta previa published between 1966 and 2000. STUDY DESIGN: Each study was reviewed independently by the two authors and was scored (on the basis of established criteria) on method of diagnosis of placenta previa and on quality of study design. We extracted data on the prevalence rate of placenta previa, as well as associations with various risk factors from each study. A meta-analysis was then performed to determine the extent to which different risk factors predispose women to placenta previa. RESULTS: Our results showed that the overall prevalence rate of placenta previa was 4.0 per 1000 births, with the rate being higher among cohort studies (4.6 per 1000 births), USA-based studies (4.5 per 1000 births) and hospital-based studies (4.4 per 1000 births) than among case-control studies (3.5 per 1000 births), foreign-based studies (3.7 per 1000 births) and population-based studies (3.7 per 1000 births), respectively. Advancing maternal age, multiparity, previous Cesarean delivery and abortion, smoking and cocaine use during pregnancy, and male fetuses all conferred increased risk for placenta previa. Strong heterogeneity in the associations between risk factors and placenta previa were noted by study design, accuracy in the diagnosis of placenta previa and population-based versus hospital-based studies. CONCLUSION: Future etiological studies on placenta previa must, at the very least, adjust for potentially confounding effects of maternal age, parity, prior Cesarean delivery and abortions.

Epidemiologic Studies↗

Immunocytochemical localization of endothelin-1 in human placenta from normal and preeclamptic pregnancies.

OBJECTIVE: The aim of this study was to examine the distribution of endothelin-1 (ET-1) in the human placenta at different gestational ages and to determine whether differences in ET-1 immunoreactivity occurred in preeclamptic compared with uncomplicated pregnancies. METHODS: Localization of ET-1 was investigated by the immunoperoxidase technique in first-trimester, second-trimester, and term human placentas from normal pregnancies and in placentas from preeclamptic pregnancies. RESULTS: In normal placentas from all gestational ages studied, endothelin-1 immunoreactivity (ET-1 IR) was specifically detected in the endothelium of the fetal vessels and in the syncytiotrophoblast. ET-1 IR was also expressed by the villous cytotrophoblast of first- and second-trimester normal placentas. The extravillous cytotrophoblast of the basal and chorionic plates also exhibited ET-1 IR, but with varying degrees of intensity. In preeclamptic placentas, the expression of ET-1 IR was uneven with a negative staining in all placentas from pregnancies between the 29th and 32nd weeks of gestation. The expression of ET-1 IR was most intense in some syncytiotrophoblast tissue in the terminal villi after the 33rd week of gestation. In placentas from preeclamptic pregnancies between the 35th and the 36th weeks of gestation, strong ET-1 IR expression was evident in the endothelium of fetal vessels and in the syncytiotrophoblast. Regardless of gestational age, ET-1 IR was also observed in the extravillous cytotrophoblast of the basal and chorionic plates of preeclamptic placentas. CONCLUSION: This study demonstrates that ET-1 IR is widely distributed in the human placenta and provides further evidence to support the concept that ET-1 plays an important role as a modulator of vascular tone in the uteroplacental and fetoplacental units and may participate in the pathogenesis of preeclampsia.

Endothelin-1↗

Immunocytochemical staining patterns of placentas associated with hydrops fetalis.

This study examined the morphology and immunocytochemical staining patterns of distribution of beta-human chorionic gonadotropin (beta-HCG), human placental lactogen (HPL), placental alkaline phosphatase (PLAP), and pregnancy-specific beta-1 glycoprotein (SP1) in 13 third-trimester placentas associated with hydrops fetalis and six normal control placentas matched for gestational age (+/- 2 weeks). Seven placentas were hydropic (540-1,080 g) and demonstrated histologic immaturity with large edematous chorionic villi showing few blood vessels, most of which contained immature hematopoietic elements. These placentas showed consistently increased staining for beta-HCG and decreased staining for PLAP when compared with control placentas, a pattern reminiscent of less mature placentas. HPL and SP1 staining were similar to those of controls. Six placentas were either sclerotic (four) or histologically unremarkable (two), and these did not differ in their immunocytochemical staining properties from control placentas. We conclude that third-trimester hydropic placentas, in addition to showing histologic immaturity, exhibit an immunocytochemical staining pattern associated with first-trimester placentas.

Chorionic Gonadotropin↗