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PubMed2003

[Morphometric indices of the altered feto-placental flow through the blood-placental barrier in pregnant women with hypertension].

OBJECTIVES: In a pregnancy complicated with hypertension, blood flow analysis in the artery allows us to foresee threat to the fetus. Abnormal blood flow in umbilical artery makes it possible to discover vascular changes in the placenta which can endanger the life of the fetus. DESIGN IN THIS STUDY: I tried to find possible correlations between quality indices of blood flow in the foetal umbilical artery evaluated in Doppler USG in pregnancies complicated with hypertension and parameters of low molecular exchange. MATERIAL AND METHODS: 53 pregnancies complicated with hypertension were selected for evaluation. On basis of the result of umbilical artery flow, patients were divided into two groups: first group of 35 patients with normal values of foeto-placental flow, the second--18 patients with abnormal results of foeto-placental flow out of whom 2 were diagnosed with absence of end-diastolic blood flow. The number of epithelial plates, the number of epithelial plates in 1 mm2 and number of vessels in terminal villi were counted. The area, perimeter and diameters of terminal villi, length, thickness and area of thin epithelial plate, area of the blood vessel were estimated. RESULTS: The morphometric analysis indicates that the quality of the foeto-placental blood flow in pregnant women with hypertension results in parameters of the filtration area in terminal villi. In cases of complicated foeto-placental blood flow, thicker blood-placental barrier i.e. epithelial plate was found. CONCLUSIONS: The results of our study indicate that the quality of feto-placental flow in pregnant women with hypertension results in parameters of the filtration area in terminal villi. In cases of complicated feto-placental blood flow a thicker blood-placental barrier i.e. epithelial plate was found.

Adult↗
PubMed1994

[Color Doppler of the utero placental territory and its relationship with the placental localization: normal and elevated resistance groups].

Forty two pregnancies of gestational age between 20 and 40 weeks were studied, 26 with normal uterine artery resistance; Group A, and 16 with elevated UA resistance; Group B. Three categories of placental location were established: Type I; central, Type II; partially lateralized including uterine midline, Type III; completely lateralized not including uterine midline. A Diasonic doppler duplex color equipment was used to assess the systole/diastole ratio (s/d ratio). Five different pints of the uteroplacental vascular territory were evaluated in each patient; right and left bottom uterine artery (cervico ithsmical union), right and left top UA (laterally outstanding point of the uterine wall), and inter villous space. The results were analyzed with Statview (Macintosh) statistics software. Placental Type II, prevailed on Group A, Type III prevailed on Group B, Types II and III were predominantly located on the right side of the uterus. S/D ratio was higher in Group B than in Group A in all five sites. S/D rel was higher on left side than on right side measurements. On Group B, left placental side patients had significantly higher s/d rel on non placental uterine artery than right placental side patients. When one altered uterine Doppler flow value is found, all the uteroplacental vascular territory show a high resistance patterns. The lateral placental location patterns tend to express higher resistance values. Right lateral placental locations have even higher resistance values than left ones. The placental location classification is suggested as a screening method for detecting the group of patients in risk of having altered values of Uterine Doppler Flow Velocimetry.

Blood Flow Velocity↗
PubMed1987

Restriction of placental size in sheep enhances efficiency of placental transfer of antipyrine, 3-O-methyl-D-glucose but not of urea.

When placental growth is restricted, fetal growth is reduced but the fetal to placental weight ratio increases, suggesting that the efficiency of placental transfer may have increased. Therefore, placental transfer of antipyrine, 3-O-methyl-D-glucose and urea was measured in control pregnant sheep and in sheep with restricted placental growth (pre-pregnancy excision of endometrial caruncles). Clearance of each decreased with placental weight but clearance of antipyrine and of 3-O-methyl-D-glucose per kg of placenta increased as placental weight decreased. The small placenta exhibited increased efficiency of flow-determined transfer of antipyrine and of facilitated-diffusion transfer of glucose but not of passive transfer of the hydrophilic substance, urea. These compensatory changes should help to maintain oxygen and glucose to the fetus when the growth of the placenta has been limited by reduction of the number of placental attachment sites.

3-O-Methylglucose↗
PubMed2006

Placental expression of secreted frizzled related protein-4 in the rat and the impact of glucocorticoid-induced fetal and placental growth restriction.

Wnt genes regulate a diverse range of developmental processes, including placental formation. Activation of the WNT pathway results in translocation of beta-catenin (CTNNB1) into the nucleus and the subsequent activation of transcription factors that promote proliferation. The secreted frizzled related proteins (SFRPs) are thought to inhibit WNT signaling by binding to the WNT ligand or its frizzled receptor. In this study, we compared the expression patterns of one of these secreted molecules, SFRP4, in the two morphologically and functionally distinct regions of the rat placenta during the last third of pregnancy. In addition, we assessed whether placental SFRP4 expression is altered in a model of glucocorticoid-induced placental growth restriction. Temporal analyses of the rat placenta by quantitative RT-PCR, in situ hybridization, and immunohistochemistry during the final third of pregnancy demonstrated elevated levels of Sfrp4 mRNA and SFRP4 protein near term, specifically in trophoblast cells of the basal zone. This increase in expression of SFRP4 in basal zone trophoblasts was associated with a reduction in CTNNB1 nuclear translocation, consistent with inhibition of the WNT pathway. Maternal dexamethasone treatment (1 microg/ml of drinking water, Days 13-22), which has previously been shown to reduce placental growth, further increased the expression of Sfrp4 mRNA in both the basal and labyrinth zones of the placenta at Day 22. Collectively, these data demonstrate that increased expression of SFRP4 is associated with reduced growth of placental regions in normal pregnancy and after glucocorticoid-induced growth retardation. These observations, together with associated changes in CTNNB1 localization, support the hypothesis that increased placental expression of SFRP4 inhibits the WNT pathway and thereby influences placental growth via effects on cell fate signaling.

Animals↗
PubMed1991

Effects of nifedipine on normotensive rat placental blood flow, placental weight and fetal weight.

Recently, nifedipine (Ca antagonist) has been used for the treatment of preeclampsia. In this study, we investigated the effects of nifedipine on the normotensive Wistar Kyoto rat's placental blood flow, fetal weight and placental weight. We measured the rat's placental blood flow using clearance of hydrogen gas generated by electrolysis. The placental blood flow, placental and fetal weights of nifedipine-treated rats (5, 10 and 25 mg/kg) were significantly (p less than 0.05) reduced compared with normal pregnant rats. These data suggest that nifedipine might have some reducing effects on placental blood flow, fetal weight and placental weight.

Animals↗
PubMed2006

Glucocorticoids prevent the normal increase in placental vascular endothelial growth factor expression and placental vascularity during late pregnancy in the rat.

Increased glucocorticoid exposure reduces fetal growth and predisposes to an increased risk of disease in later life. In addition to direct effects on fetal growth, glucocorticoids also compromise fetal growth indirectly via detrimental effects on placental growth and function. The current study investigated the effects of dexamethasone-induced intrauterine growth restriction on placental vascular development and expression of the endothelial cell-specific mitogen, vascular endothelial growth factor (VEGF). Separate analyses were conducted for the three main VEGF isoforms (VEGF120, VEGF164, and VEGF188) in the two functionally and morphologically distinct regions of the rat placenta, the basal and labyrinth zones. Quantitative PCR and immunohistochemical analysis demonstrated that expression of VEGF was markedly up-regulated specifically in the rapidly growing labyrinth zone over the final third of normal pregnancy. Unbiased stereological analyses showed an associated increase in the volume and surface area of maternal and fetal blood spaces, including vascular remodeling of the fetal capillary network near term. In contrast, dexamethasone-induced fetal and placental growth restriction reduced expression of the Vegf120 and Vegf188 isoforms and prevented normal labyrinthine vascular development near term. Most notably, dexamethasone impaired the normal increase in fetal vessel density over the final third of pregnancy, with no effect on the density of maternal blood spaces. Overall, this study quantifies the labyrinth zone-specific increases in placental VEGF expression and vascular development during normal pregnancy, and shows that these increases are prevented by maternal dexamethasone treatment. Our data suggest that glucocorticoid-induced restriction of fetal and placental growth is mediated, in part, via inhibition of placental VEGF expression and an associated reduction in placental vascularization.

Animals↗
PubMed1990

Transplantable rat choriocarcinoma cells express placental lactogen: identification of placental lactogen-I immunoreactive protein and messenger ribonucleic acid.

The purpose of this investigation was to evaluate the abilities of a transplantable rat choriocarcinoma (Rcho) to produce placental PRLs. The Rcho tumor was analyzed biochemically and histologically for the expression of placental PRLs. Expression of placental PRL mRNAs was determined by Northern blot and in situ hybridization analyses. Expression of placental PRL proteins was determined by Western blot and immunocytochemical analyses. Histologically, Rcho tumors were characterized by the appearance of giant cell surrounding hemorrhagic regions. Female rats bearing the Rcho tumor beneath their kidney capsule showed extensive mammary gland development. The Rcho tumors expressed placental lactogen-I (PL-I) mRNA and protein, but there was no evidence of placental lactogen-II (PL-II), PRL-like protein-A (PLP-A), or PRL-like protein-B (PLP-B). Rcho PL-I mRNA and proteins migrated as a 1-kilobase species and a 36- to 40-kDa species similar to those expressed by normal rat trophoblast tissues. The cell type responsible for Rcho PL-I production was the giant cell, similar to that observed in normal rat trophoblast tissues. In summary, we have demonstrated the production of PL-I by a transplantable rat choriocarcinoma (Rcho). The Rcho tumor resembles rat trophoblast tissue at early postimplantation stages (days 6-10 of gestation) and may be a useful tool for studying placental PRL expression during trophoblast differentiation.

Animals↗
PubMed1980

[Studies on the clinical significance of the placental implantation site and the change of placental volume by uterine contraction (author's transl)].

Using ultrasonography, the influence of placental implantation site on the fetal position, duration of gestation, duration of labor, etc. was investigated on 321 patients in the 3rd trimester. Moreover, the change of placental volume in connection with the uterine contraction was also studied and the following results were obtained. 1) As for the placental implantation site, it was found on the posterior uterine wall in 139, on the anterior 97, right lateral 55, and on the left lateral in 30. 2) When the placenta was implanted at the uterine cornus, more fetuses were with breech presentation, and when it was found on the lateral site, the fetuses were with the position facing the placenta. 3) In multiparae, the gestational duration was longer when the placenta was implanted on the right side of uterus than on the left or anterior side. (p less than 0.05) 4) Placental implantation site had no relation with labor duration, fetal weight, placental weight, amount of haemorrhage during labor and cord-coiling. 5) During uterine contraction, the placental volume did not change when the pressure was 30 mmHg. During contraction, when the pressure was 50 mmHg, the placental volume became less by 30 cm3 than during interval. During interval, intraplacental blood volume wa 177 cm3.

Birth Weight↗
PubMed2004

Placental hormones and fetal-placental development.

Production of growth promoting substances by the placenta is regulated differently from the way production of similar compounds is regulated by maternal organs in various cases. Gene duplication is one of the mechanisms that facilitated the evolution of placental specific endocrine activity. Cattle, sheep and goats, although evolutionarily related, differ significantly from each other in the way their placental growth hormone (GH) and prolactin (PRL)-like hormones have evolved. Cattle carry one copy of the GH gene and there is no evidence yet for expression of that single GH gene copy in the placenta. On the other hand, the ovine GH gene has been duplicated and both oGH copies are expressed in the placenta during early stages of gestation. Prolactin gene duplication in ruminants resulted in the formation of specific placental-expressed prolactin-related genes including the placental lactogen (PL) gene. In homologous state, ovine PL manifests PRL activity, but antagonizes GH activity. Ovine PL activity which can be mediated by PRL receptors or by hetero-dimerization of GH and PRL receptors, provide a novel regulatory mechanism for somatogenic activity dependent on the coexistence of both GH and PRL receptors in the same cells. Another mechanism for specific placental endocrine activity is silencing of the alleles through genetic imprinting. Disruption of genetic imprinting of placental genes has been proposed as one of the explanations for the loss of cloned fetuses generated by somatic cell nuclear transfer.

Animals↗
PubMed1984

Intrauterine growth of the guinea pig fetal-placental unit throughout pregnancy: regulation by utero-placental blood flow.

The relationships between uterine blood flow (UBF) and growth related changes in guinea pig placental weight, fetal weight, and crown-rump (C-R) length were examined at 5-day intervals throughout pregnancy. Between days 5 and 20 (Day 0 = ovulation) of pregnancy, UBF reached peak levels that were related to increases in total uterine weight as a result of fetal-placental differentiation. Between days 20 and 40 of pregnancy, UBF remained at constant, basal levels while placental weight increased at a rate of approximately 500 mg per 5-day interval. During this time period, fetal weight and C-R length continued to increase, but at a less rapid rate. Between days 40 and 55 of pregnancy, a secondary elevation in UBF was observed that was temporally related to third trimester growth of the fetus (ie, weight and C-R length). Near term (day 65), UBF decreased and placental growth reached a plateau, whereas fetal weight and C-R length continued to increase. In order to determine the direct effects of UBF on regulating fetal-placental growth, mid-gestational (days 35-50) pregnant guinea pigs were subjected to UBF reduction and the growth parameters of the manipulated fetal-placental units were then examined at 2, 3, 4, and 10 days post-alteration and compared to controls. The reduction in UBF at hyperemic pregnancy sites to basal flow levels resulted in an abrupt curtailment of subsequent placental growth noticeable within 48 hr of the vascular reduction. Subsequently, fetal weight and crown-rump length parameters were depressed with respect to controls, but not until 4 and 10 days post-alteration, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Transrectal ultrasonography and plasma progestin profiles identifies feto-placental compromise in mares with experimentally induced placentitis.

Transrectal ultrasonography of the caudal uterus and a progestin profile were evaluated for accuracy in identifying mares with feto-placental compromise in a model of placentitis. Twenty-two pregnant ponies were divided into four groups: (1) control mares (n=5); (2) instrumented controls (n=2); (3) instrumented inoculated mares (n=11); (4) inoculated mares (n=4). Mares in Groups 3 and 4 were inoculated with Streptococcus equi subsp. zooepidemicus. Maternal plasma progestins, vulvar discharge, mammary gland development, combined thickness of the uterus and placenta (CTUP) and placental separation were evaluated weekly before instrumentation, inoculation or Day 320 (Groups 1 and 2) and, thereafter, either daily (first three measurements) or several times weekly (last two measurements). Plasma progestin profiles were plotted to identify pattern characteristics. An abbreviated profile was created, consisting of four progestin samples collected at 48-h intervals, with Sample 1 collected the day before inoculation or on Day 285 in controls. Profiles were considered abnormal if Samples 2, 3, or 4 increased or decreased by more than 50% of Sample 1. A CTUP>1.0 cm or placental separation were considered abnormal. Placentitis was confirmed by histology of fetal membranes. Control mares had normal progestin profiles, transrectal ultrasonographic and clinical examinations. Control foals were born after Day 329; six were viable and one died after dystocia. All inoculated mares developed placentitis and foaled before Day 314. Thirteen of 15 foals were not viable. All inoculated mares had abnormal progestin profiles and 13 of the 15 were identified by the abbreviated progestin profile. Transrectal CTUP was affected by gestational age and increased after inoculation (P<0.05). Nine of 15 inoculated mares had a CTUP>1.0 cm by 5-day post-inoculation. By performing both tests, 20 of 22 mares were correctly identified with respect to pregnancy outcome. However, three inoculated mares exhibited minimal clinical signs and likely would not be examined in a clinical setting. These tests were diagnostic for identifying feto-placental compromise in the mare.

Animals↗
PubMed1998

The investigation of placental relaxation and estimation of placental perfusion using echo-planar magnetic resonance imaging.

Echo-planar imaging (EPI) is a form of magnetic resonance imaging (MRI) which acquires images in milliseconds rather than minutes as with conventional MRI. The images produced using EPI are affected by the physiological environment in which the hydrogen atoms producing the signals are found, a process referred to as relaxation. Also by producing images a matter of milliseconds apart, quantification of perfusion within the tissue being imaged is feasible. The objective of this study was to investigate T1 and T2 relaxation times along with perfusion in placentae from normal pregnancies at different gestations and also to compare these to pregnancies complicated by abnormal placental function. A cross-sectional study of normal and compromised pregnancies from 20 weeks to term and a longitudinal study of normal pregnancy were performed. Placental T1, T2 relaxation times, and perfusion were measured using echo-planar magnetic resonance imaging. Placental T1 and T2 relaxation times decreased in normal pregnancy (P<0.001). Relaxation times in pregnancies associated with placental pathology appeared to be reduced for that gestation although the numbers were too small to allow any statistical validation. No differences in placental perfusion with gestation or between normal and compromised pregnancy were demonstrated using this technique. This is the first demonstration of placental magnetic resonance relaxation and perfusion measurements in normal pregnancy using echo-planar magnetic resonance imaging. In the future it may be possible to identify compromised pregnancies by differences in placental T1 and T2 relaxation times, using this novel non-invasive technique.

Adult↗
PubMed2001

Women with a history of placental abruption: when in a subsequent pregnancy should special surveillance for a recurrent placental abruption be initiated?

BACKGROUND: It is common to admit to hospital or start intensive ambulatory antenatal care of pregnant women with a previous placental abruption using the gestational age of the previous placental abruption as a starting point. In some instances, close surveillance may be commenced much earlier. There is no consensus when in a subsequent pregnancy such measures should be initiated. OBJECTIVE: The analyses aimed at the prevention of complicated (preterm, small for gestational age, or perinatal death) recurrent placental abruptions, assessing at which time in a subsequent pregnancy special surveillance should start in order to anticipate and prevent a recurrence. DESIGN: A cohort study based on the Medical Birth Registry of Norway. Calculation of gestational age specific risks of placental abruption in a second pregnancy and estimation of when to initiate surveillance in order to reduce an increased risk of recurrent placental abruption to the initial level of initial abruption in the second pregnancy. RESULTS: In women with a complicated (preterm, small for gestational age, or perinatal death) first delivery, the risks of an initial and recurrent complicated placental abruption in the second pregnancy were 7/1000 and 33/1000, respectively (relative risk 4.9). To reduce the recurrence risk in a second pregnancy to 7/1000, special surveillance six weeks prior to the gestational age of the initial abruption would be necessary. In women with an uncomplicated first delivery, the risks in the second pregnancy of an initial and recurrent complicated abruption were 3 and 19/1000, respectively (relative risk 7.1). To reduce the recurrence risk to 3/1000, surveillance at least 12 weeks prior would be necessary. CONCLUSION: The increased recurrence rate would necessitate increased awareness in terms of special surveillance in the second pregnancy. In pregnancies at risk of a recurrent placental abruption, monitoring up to three months before the gestational age of the initial abruption is necessary.

Abruptio Placentae↗
PubMed2003

Placental tumor necrosis factor alpha but not gamma interferon is associated with placental malaria and low birth weight in Malawian women.

Malaria in pregnancy predisposes to maternal anemia and low birth weight (LBW). We examined the possible roles of the cytokines tumor necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma) in these adverse outcomes. We measured cytokine concentrations in placental, peripheral, and cord blood plasma in relation to malaria parasitemia and placental monocyte accumulation in 276 Malawian women. Maternal hemoglobin concentration, human immunodeficiency virus status, and infant birth weight were determined. Concentrations of TNF-alpha in placental blood were correlated with densities of Plasmodium falciparum-infected erythrocytes (P < 0.0001) and of intervillous monocyte infiltrates (P < 0.0001) on placental histology. Peripheral blood TNF-alpha concentrations were relatively low and were weakly associated with malaria. TNF-alpha concentrations were higher in placental blood, where they were strongly associated with malaria. Placental plasma TNF-alpha levels were higher in women who had LBW babies (P = 0.0027), women with febrile symptoms (P < 0.0001), and teenage mothers (P = 0.04) than in other women. The presence of TNF-alpha in cord blood was not associated with malaria infection. IFN-gamma levels were infrequently elevated, and elevated IFN-gamma levels were not associated with poor pregnancy outcomes. Placental production of TNF-alpha, but not of IFN-gamma, may be implicated in impaired fetal growth in Malawian women.

AIDS-Related Opportunistic Infections↗
PubMed1977

Measurement of placental blood flow in the pig and its relation to placental and fetal weight.

In 12 pregnant sows (Sus scrofa domestica), containing 144 live fetuses, placental blood flow was measured by the indicator fractionation technique using radioactive microspheres. In 8 of these litters, which contained 96 live fetuses, placental blood flow as obtained in absolute units. Significant positive correlations were observed between placental blood flow and placental weight, between placental blood flow and fetal weight, and between placental weight and fetal weight. It is clear that the runt, by comparison with his littermates, has a low birthweight in association with a small placenta and a low placental blood flow.

Animals↗
PubMed1991

Effects of ketanserin--a serotonin receptor antagonist--on placental blood flow, placental weight and fetal weight of spontaneously hypertensive rats and normal Wistar Kyoto rats.

Recently, ketanserin (serotonin receptor antagonist) has been reported to be beneficial in the treatment of preeclampsia. In this study, we investigated the effects of ketanserin on the placental blood flow, fetal weight and placental weight in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). We measured the rats' placental blood flow by monitoring the clearance of hydrogen gas generated by electrolysis. In ketanserin (12, 24, 48 mg/kg)-treated SHR, systolic blood pressure was significantly decreased. The placental blood flow was significantly (p less than 0.05) reduced compared to that before treatment in WKY and SHR. The fetal weight decreased dose dependently in WKY, while in SHR it did not decrease significantly. The placental weight of ketanserin-treated rats decreased compared to that before treatment. These data suggest that ketanserin might have some reducing effects on placental blood flow, fetal weight and placental weight proportional to the dose.

Animals↗
PubMed1985

In vitro degradation of angiotensin II (A-II) by human placental subcellular fractions, pregnancy sera and purified placental aminopeptidases.

The degradation of angiotensin II (Asp1-Arg2-Val3-Tyr4-Ile5-His6-Pro7-Phe8: A-II) by human placental particulate and soluble fractions, pregnant and non-pregnant sera, and highly purified placental enzymes such as placental leucine aminopeptidase P-LAP (microsomal), retroplacental serum P-LAP (soluble), aminopeptidase A and post-proline endopeptidase, was studied by measuring liberated amino acids by high performance liquid chromatography. Placental particulate and soluble fractions degraded A-II almost completely into single amino acids. The purified P-LAP (microsomal) actively liberated five amino acids from the N-terminal. The placental particulate fraction containing P-LAP (microsomal) also actively liberated these amino acids. The purified aminopeptidase A liberated Asp1 very actively as expected. When the ratio of the velocity of liberation of each amino acid to P-LAP activity measured with leu-p-nitroanilide as a substrate was calculated, placental soluble fraction liberated Asp1 very actively, but the liberation rate of Asp1 with the purified P-LAP (soluble) was very low. Therefore it seems that the enzyme in the placental soluble fraction and pregnancy serum responsible for the Asp1 liberation is not P-LAP (soluble), but aminopeptidase A. The mixture of purified P-LAP (soluble) and aminopeptidase A showed higher liberation rate of Arg2 and Val3 than that with purified aminopeptidase A alone, demonstrating that once the N-terminal Asp1 was liberated, the P-LAP (soluble) attacks the shorter peptide (angiotension III) very actively. It was concluded that P-LAP (microsomal) together with aminopeptidase A seem to contribute greatly to the degradation of A-II in pregnant women.

Amino Acids↗
PubMed2002

Pregnancy-associated and placental proteins in the placental tissue of normal pregnant women and patients with pre-eclampsia at term.

OBJECTIVE: Pre-eclampsia is a placental disease of unknown cause. Maternal circulating concentrations of a number of protein markers are altered (mainly increased) in pre-eclampsia in comparison with controls of matched gestational age. Inhibin A and activin A were found to be elevated even before the onset of the disease. The aim of this study was to compare the levels of inhibin A, activin A: follistatin ratio, leptin, pregnancy-associated plasma protein-A (PAPP-A), human placental lactogen (HPL), placenta growth factor (PLGF) and pregnancy-specific beta1-glycoprotein (SP1) in placental extracts of normal pregnant women and pre-eclampsia patients at term. METHODS: Placental tissue from normal pregnancies (n=14) and patients with pre-eclampsia (n=13) were collected at term (> or =37 weeks of gestation) and stored at -80 degrees C. The frozen tissue pieces were homogenised and the above-mentioned proteins were measured by specific enzyme-linked immunosorbent assays. RESULTS: Placental contents of inhibin A and PAPP-A were significantly higher (P<0.05) in pre-eclampsia placental extracts compared with the controls. Activin A:follistatin ratio was higher (23) in pre-eclampsia extracts than in the controls (15). Leptin, PLGF, SP1 and HPL levels were not altered in the term pre-eclampsia placenta. Inhibin A and PAPP-A contents were increased in the placental extracts of pre-eclampsia patients. CONCLUSION: Our data suggest that the placenta, possibly by a compensatory mechanism, is at least in part responsible for the altered serum levels observed in pre-eclampsia.

Adult↗