Large Placenta Research Articles

Placental weight and excess postpartum haemorrhage: a population study of 308 717 pregnancies

To investigate whether placental weight may be positively associated with the prevalence of excess postpartum haemorrhage because large placentas have large surface areas. Registry-based cross-sectional study. Population study. All singleton deliveries after 21 weeks of gestation in Norway during 1999-2004 (n = 308,717). Data were obtained from the Medical Birth Registry of Norway, which is based on compulsory notification of births by the midwife or doctor in charge of the delivery. Excess postpartum haemorrhage was defined as bleeding of 500 ml or more within 2 hours of delivery. There was a gradual increase in the prevalence of excess postpartum haemorrhage with increasing placental weight (test for trend, P < 0.05). Having a placenta of 1100 g or more was associated with 2.5 times (odds ratio 2.54, 95% CI 2.31-2.79) higher prevalence than having a placenta of 300-499 g, after adjustment for offspring birthweight, parity, caesarean section and placenta-related and delivery-related complications. A large placenta relative to birthweight was also associated with higher prevalence of excess postpartum haemorrhage. The size of the placental surface may explain the positive association of placental weight with the prevalence of postpartum haemorrhage. In pregnancies with a large placenta relative to offspring birthweight, other factors that enhance bleeding may also play a role.

Developmental adaptations to increased fetal nutrient demand in mouse genetic models of Igf2-mediated overgrowth.

The healthy development of the fetus depends on an optimal balance between fetal genetic drive for growth and the maternal ability to provide nutrients through the placenta. Nothing is known about fetal-placental signaling in response to increased fetal demand in the situation of overgrowth. Here, we examined this question using the H19(Δ13) mouse model, shown previously to result in elevated levels of Igf2. Fetal and placental weights in H19(Δ13) were increased by 23% and 45%, respectively, at E19, when compared with wild-type mice. Unexpectedly, we found that disproportionately large H19(Δ13) placentas transport 20-35% less (per gram placenta) glucose and system A amino acids and have similar reductions in passive permeability, despite a significantly greater surface area for nutrient exchange and theoretical diffusion capacity compared with wild-type mice. Expression of key transporter genes Slc2a3 and Slc38a4 was reduced by ∼20%. Decreasing the overgrowth of the H19(Δ13) placenta by genetically reducing levels of Igf2P0 resulted in up-regulation of system A activity and maintenance of fetal overgrowth. Our results provide direct evidence that large placentas can modify their nutrient transfer capacity to regulate fetal nutrient acquisition. Our findings are indicative of fetal-placental signaling mechanisms that limit total demand for maternal nutrients.

Functional full-term placentas formed from parthenogenetic embryos using serial nuclear transfer

Mammalian parthenogenetic embryos invariably die in mid-gestation from imprinted gene defects and placental hypoplasia. Based on chimera experiments, trophoblastic proliferation is supposed to be inhibited in the absence of a male genome. Here, we show that parthenogenetic mouse embryonic cell nuclei can be reprogrammed by serial rounds of nuclear transfer without using any genetic modification. The durations of survival in uteri of cloned foetuses derived from green fluorescent protein (GFP)-labelled parthenogenetic cell nuclei were extended with repeated nuclear transfers. After five repeats, live cloned foetuses were obtained up to day 14.5 of gestation; however, they did not survive longer even when we repeated nuclear transfer up to nine times. All foetuses showed intestinal herniation and possessed well-expanded large placentas. When embryonic stem (ES) cells derived from fertilised embryos were aggregated with the cloned embryos, full-term offspring with large placentas were obtained from the chimeric embryos. Those placentas were derived from parthenogenetic cell nuclei, judging from GFP expression. The patterns of imprinted gene expression and methylation status were similar to their parthenogenetic origin, except for Peg10, which showed the same level as in the normal placenta. These results suggest that there is a limitation for foetal development in the ability to reprogramme imprinted genes by repeated rounds of nuclear transfer. However, the placentas of parthenogenetic embryos can escape epigenetic regulation when developed using nuclear transfer techniques and can support foetal development to full gestation.

Different Periods of Periconceptional Undernutrition Have Different Effects on Growth, Metabolic and Endocrine Status in Fetal Sheep

Periconceptional undernutrition alters fetal growth and development. However, there are no data on separate effects of undernutrition before and after conception and few on underlying mechanisms. We determined the effects of mild periconceptional undernutrition on late gestation fetal growth, glucose-insulin axis, and maternal and fetal hypothalamic-pituitary-adrenal axes. Ewes were undernourished for 60 d before conception, 30 d after, or both, compared with well-nourished controls. Undernutrition before conception resulted in smaller, slower-growing fetuses with relatively larger placentae. Ewes that gained weight before, but lost weight after mating, or vice versa, had the smallest fetuses. Fetuses of ewes undernourished only before conception grew more slowly following instrumentation, and fetuses in both preconception undernutrition groups slowed their growth with a maternal fast. The fetal glucose-insulin axes and maternal and fetal hypothalamic-pituitary-adrenal axis were not different among groups. Maternal undernutrition at different periods around conception has different effects on fetal growth trajectory that are not reflected in size in late gestation. Preconceptional undernutrition alone alters fetal growth responses to late gestation stressors, suggesting that maternal nutrition is important at both times, and that fetal effects are neither due solely to substrate limitation, nor to excess fetal glucocorticoid exposure at the time of undernutrition.

Placental Weight Relative to Birth Weight and Long-term Cardiovascular Mortality: Findings From a Cohort of 31,307 Men and Women

Birth weight is inversely associated with risk of adult cardiovascular disease, and evidence exists that fetal adaptation to challenges in the intrauterine environment may adversely affect long-term cardiovascular health. The placenta is in a key position to mediate such effects because adequate placental function is necessary for delivery of nutrients, oxygen, and hormones to the fetus. This prospective population study based on data from the hospital birth charts of 31,307 Norwegian men and women born between 1934 and 1959 assessed whether placental weight relative to birth weight was associated with risk of death from cardiovascular disease in adulthood. During 45 years of follow-up, 382 people died from cardiovascular disease (median age, 51.3 years). Results showed that the placenta-to-birth-weight ratio was positively associated with cardiovascular disease mortality; the sex- and cohort-adjusted hazard ratio for the highest versus the lowest third was 1.38 (95% confidence interval: 1.07, 1.77). The authors concluded that a disproportionately large placenta relative to birth weight was associated with increased risk of cardiovascular disease death. This finding suggests that placental function is important in the association of intrauterine factors with cardiovascular disease later in life.

Detection of differentially expressed genes between Erhualian and Large White placentas on day 75 and 90 of gestation

BackgroundPlacental efficiency is strongly associated with litter size, fetal weight and prenatal mortality. Together with its rapid growth during late gestation, the Large White pig breed shows a significant increase in placental size and weight, but this does not occur in the highly prolific Chinese pig breeds. To understand the molecular basis of placental development during late gestation in Chinese indigenous and Western breeds with different placental efficiency, female placental samples were collected from six pregnant Erhualian gilts at gestation day 75 (E75) and day 90 (E90) and from six pregnant Large White gilts at gestation day 75 (L75) and day 90 (L90). Two female placentas from one sow were used to extract RNA and then pooled in equal volumes. Twelve pooled samples were hybridized to the porcine Affymetrix GeneChip.ResultsA total of 226 and 577 transcripts were detected that were differentially expressed between E75 and L75 and between E90 and L90 (p < 0.01, q < 0.2), respectively. Gene Ontology (GO) analysis revealed that these genes belong to the class of genes that participate in angiogenesis and development. Real-time RT-PCR confirmed the differential expression of eight selected genes. Significant differential expression of five genes in the VEGF pathway was also detected between the breeds. A search of chromosomal location revealed that 44 differentially expressed genes located to QTL regions related to reproduction. Differential expression of six candidate imprinted genes was also confirmed. Three of the six genes (PLAGL1, DIRAS3, and SLC38A4) showed monoallelic expression in the porcine placenta.ConclusionOur study detected many genes that showed differential expression between placentas of two divergent breed of pigs, and confirmed the imprinting of three genes. These findings help to elucidate the genetic control of placental efficiency and improve the understanding of placental development.

From preterm birth, placenta and thyroid to the perineum

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Brief hyperglycaemia in the early pregnant rat increases fetal weight at term by stimulating placental growth and affecting placental nutrient transport

In pregnant women with type 1 diabetes, suboptimal glucose control in the first trimester is a strong predictor for giving birth to a large fetus. However, the mechanisms underlying this association are unknown. We hypothesized that transient hyperglycaemia in early pregnancy results in (1) increased placental growth and (2) an up-regulation of placental nutrient transport capacity, which leads to fetal overgrowth at term. In order to test this hypothesis, pregnant rats were given intraperitoneal injections of glucose (2 g kg(-1), resulting in a 50-100% increase in blood glucose level during 90 min) or saline (control) in either early or late gestation using four different protocols: one single injection on gestational day (GD) 10 (n=5), three injections on GD 10 (n=8-9), six injections on GD 10 and 11 (n=9-11) or three injections on GD 19 (n=7-8). Multiple injections were given approximately 4 h apart. Subsequently, animals were studied on GD 21. Three glucose injections in early pregnancy significantly increased placental weight by 10%, whereas fetal weight was found to be increased at term in response to both three (9% increase in fetal weight, P<0.05) and six glucose injections (7%, P=0.05) in early gestation. A single glucose injection on GD 10 or three injections of glucose on GD 19 had no effect on placental or fetal growth. In groups where a change in feto-placental growth was observed, we measured placental system A and glucose transport activity in the awake animals on GD 21 and placental expression of the glucose and amino acid transporters GLUT1, GLUT3, SNAT2 (system A), LAT1 and LAT 2 (system L). Placental system A transport at term was down-regulated by six glucose injections in early pregnancy (by -33%, P<0.05), whereas placental mRNA and protein levels were unchanged. No long-term alterations in maternal metabolic status were detected. In conclusion, we demonstrate that transient hyperglycaemia in early pregnancy is sufficient to increase fetal weight close to term. In contrast, brief hyperglycaemia in late pregnancy did not stimulate fetal growth. Increased fetal growth may be explained by a larger placenta, which would allow for more nutrients to be transferred to the fetus. These data suggest that maternal metabolic control in early pregnancy is an important determinant for feto-placental growth and placental function throughout the remainder of gestation. We speculate that maternal metabolism in early pregnancy represents a key environmental cue to which the placenta responds in order to match fetal growth rate with the available resources of the mother.

Changes in cell cycle and extracellular matrix gene expression during placental development in deer mouse (Peromyscus) hybrids

Crosses between two species of the rodent genus Peromyscus produce defects in both growth and development. The defects are pronounced in the hybrid placentas. Peromyscuys maniculatus (strain BW) females mated to P. polionotus (strain PO) males produce placentas half the size of the parental species, as well as growth-retarded embryos. In contrast, PO females mated to BW males result in defective conceptuses that display embryonic and placental overgrowth. These 'parent-of-origin'-dependent phenotypes are consistent with previous studies that demonstrated altered expression of imprinted genes and genetic linkage of the overgrowth phenotypes to imprinted domains. In the present study, we take a broader approach in assessing perturbations in hybrid placental gene expression through the use of Mus musculus cDNA microarrays. In verifying classes of genes identified in microarray screens differentially regulated during hybrid placental development, we focused on those influencing the cell cycle and extracellular matrix (ECM). Our work suggests that cell cycle regulators at the G(1)/S phase check-point are downregulated in the large hybrid placenta, whereas the small hybrid placenta is more variable. The ECM genes are typically downstream targets of cell cycle regulation and their misregulation is consistent with many of the dysmorphic phenotypes. Thus, these data suggest imbalances in proliferation and differentiation in hybrid placentation.

Evaluación de las estrategias terapéuticas en el síndrome nefrótico congénito tipo finlandés

Congenital nephrotic syndrome of the Finnish type (CNFS) is caused by mutations in the nephrin gene. This disease manifests as massive proteinuria, gross peripheral edema, and ascites during the first weeks of life. In the last few years the prognosis has improved due to new treatment strategies: antiproteinuria drugs, intensive nutrition, nephrectomy, dialysis, and renal transplantation. The aim of this study was to determine the impact of these therapeutic measures. We performed a descriptive retrospective epidemiological study of 12 patients diagnosed with CNSF between January 1985 and August 2005. We included patients aged less than 14 years old with massive proteinuria and generalized edema during the neonatal period, a large placenta (> 25 % of birth weight), and normal glomerular filtration rate during the first 6 months of life, in whom other causes of congenital nephrotic syndrome were ruled out. The diagnosis was established after a median period of 17 days (range 6-30). The most commonly used treatments were albumin infusions (91.7 %), angiotensin-converting enzyme inhibitors (66.7 %), and indomethacin (58.3 %). Dialysis was started in 58.3 %, at a median age of 3.76 years (2.81-7.6). The main complication was acute peritonitis (85.7 %). Renal transplantation was performed in 58.3 % of the patients; of these, 71.4 % have normal renal function after a median follow-up of 3.73 years (0.8-6.3). The median plasma albumin level during the pretransplant period was 0.17 g/dL (0.12-0.28). Plasma cholesterol and triglyceride levels decreased significantly after renal transplantation (p = 0.043). Fifty percent of the patients achieved adequate height and weight for their age and gender. Mortality was 33.3 %. Antiproteinuria drugs and intensive nutritional therapy improve clinical control and delay the start of dialysis and renal transplantation, increasing the probability of success.

The worldwide burden of postpartum haemorrhage: Policy development where inaction is lethal

Most maternal deaths occur to women who are not attended by trained health professionals. Postpartum hemorrhage is the single most common cause of maternal death. The delivery of large haemochorial placenta in our species predisposes to heavy bleeding and can be dealt with only by using effective uterotonics. The 1987 Safe Motherhood Initiative has failed to reduce maternal mortality significantly, and shortages of trained personnel will not be remedied in the foreseeable future. Bold new policies are imperative and need to be derived from an appropriate evidence base. It is suggested that these should include the low-cost shock garments in primary health facilities and making misoprostol easily accessible in both the public and private sector.

Aerobic exercise for women during pregnancy

Physiological responses of the fetus (especially increase in heart rate) to single, brief bouts of maternal exercise have been documented frequently. Many pregnant women wish to engage in aerobic exercise during pregnancy but are concerned about possible adverse effects on the outcome of pregnancy. The objective of this review was to assess the effects of advising healthy pregnant women to engage in regular aerobic exercise (at least two to three times per week), or to increase or reduce the intensity, duration, or frequency of such exercise, on physical fitness, the course of labour and delivery, and the outcome of pregnancy. We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (June 2005), MEDLINE (1966 to 2005 January Week 1), EMBASE (1980 to 2005 January Week 1), Conference Papers Index (earliest to 2005 January Week 1), contacted researchers in the field and searched reference lists of retrieved articles. Acceptably controlled trials of prescribed exercise programs in healthy pregnant women. Both review authors independently assessed trial quality and extracted data. Study authors were contacted for additional information. Eleven trials involving 472 women were included. The trials were small and not of high methodologic quality. Five trials reported significant improvement in physical fitness in the exercise group, although inconsistencies in summary statistics and measures used to assess fitness prevented quantitative pooling of results. Seven trials reported on pregnancy outcomes. A pooled increased risk of preterm birth (relative risk 1.82, 95% confidence interval (CI) 0.35 to 9.57) with exercise, albeit statistically nonsignificant, does not cohere with the absence of effect on mean gestational age (weighted mean difference +0.3, 95% CI -0.2 to +0.9 weeks), while the results bearing on growth of the fetus are inconsistent. One small trial reported that physically fit women who increased the duration of exercise bouts in early pregnancy and then reduced that duration in later pregnancy gave birth to larger infants with larger placentas. Regular aerobic exercise during pregnancy appears to improve (or maintain) physical fitness. Available data are insufficient to infer important risks or benefits for the mother or infant. Larger and better trials are needed before confident recommendations can be made about the benefits and risk of aerobic exercise in pregnancy.

Placental Traits in Pen-fed Goats and Goats Kept on Rangeland

Mallado, M., Olivares, L., Diaz, H. and Villarreal, J.A. 2006. Placental traits in pen-fed goats and goats kept on rangeland. J. Appl. Anim. Res., 29: 133–136. To determine if rearing conditions (pen vs. extensive grazing) alters placental development, mixed-breed goats were kept either under intensive (n=31) or extensive (n=40) condition in a desert rangeland. Does kept under pen conditions had higher (P<0.01) serum glucose, urea, cholesterol, total proteins and phosphorus values than grazing goats. There was no effect of rearing conditions on kid birth weight, but placentas from nutrient-restricted mothers were 56% heavier (P<0.01) at parturition than pen-fed does. Placentas from the grazing goats had less placentomes and feto-maternal contact area compared to pen-fed goats. Body condition score was significantly correlated with placental weight (r= −0.69) and placenta to birth weight ratio (r= 0.74). These results showed that live weight of offspring born from nutrient-restricted mothers was not compromised, but chronic nutrient deprivation resulted in larger placentas with fewer placentomes.

Large Offspring or Large Placenta Syndrome? Morphometric Analysis of Late Gestation Bovine Placentomes from Somatic Nuclear Transfer Pregnancies Complicated by Hydrallantois

Somatic nuclear transfer (NT) in cattle is often complicated by fetal oversize (i.e., large offspring syndrome), hydrallantois, and placentomegaly in late gestation. The aims of this work were to obtain data on the placentome structure in NT-recipient cows with hydrallantois (NTH) and to relate these with fetal and placental weights to better understand the abnormalities observed in NTH pregnancies during the third trimester. Pregnant cows were slaughtered between Gestation Days 180 and 280. The fetuses were weighed, and the placentomes were numbered and weighed. Placentomes were examined by histologic and stereological techniques. Macroscopic data showed that placental overgrowth preceded fetal overgrowth, and the ratio of the fetal to the total placentome weight in the NTH group was lower than that in controls after Gestation Day 220. This suggests that placental overgrowth is due to placental default rather than due to fetal overgrowth, as shown also by stereological analysis showing primary deregulation of the growth of cotyledonary tissues. Observed alterations, such as thinning of the maternal epithelium within placentomes and increased trophoblastic surface, could be secondary adaptations. Thus, placental growth deregulations would be due to modifications of the expression of placental factors. Various examples of placental deficiency were observed, suggesting that some fetal abnormalities observed in NTH calves, such as enlarged heart, enlarged umbilical cord, and abdominal ascites, are consequences of placental dysfunction. Therefore, the condition described by the term "large offspring syndrome" might better be described by "large placenta syndrome," because this syndrome affects an average of 50% of late-gestation NT pregnancies. No conclusion can be drawn from this work on apparently normal pregnancies.

Placental ischaemia is a consequence rather than a cause of pre-eclampsia

The aetiology or pre-eclampsia remains unknown, but it is widely accepted that the disorder is placental in origin. Failed trophoblast invasion of the maternal spiral arteries is accepted to be a central pathogenetic mechanism. However, the concept of failed trophoblast invasion is based on an assumption rather than direct scientific observation and there are other likely explanations for this phenomenon. The criteria for disease causation, such as the Bradford-Hill criteria are central to the ascertainment of causal relationships in modern medicine and these criteria are used here to assess the relationship between the placenta and pre-eclampsia. There is a strong association between pre-eclampsia and small (rather than large) placentas and an appropriate dose-response relationship does not exist. Failed trophoblast invasion of the spiral arteries is not specific to pre-eclampsia and occurs in other pregnancy complications and in up to 40% of biopsies from normal pregnancies and the relationship between placental ischaemia and pre-eclampsia is very inconsistent. A placental cause for pre-eclampsia is not consistent with the pathogenesis of other pregnancy complications like gestational diabetes mellitus. If pre-eclampsia was a disease of trophoblast origin, the risk of the disease should be determined by trophoblast rather than maternal factors. However, evidence from assisted reproduction shows that the risk of a woman developing pre-eclampsia is almost entirely dependent on maternal factors and independent of the embryo from which the placenta develops. There is currently no plausible proven mechanism by which the placenta causes pre-eclampsia. The syndrome typically gets worse, and can arise de-novo after the placenta has been removed, calling into question the role of the placenta in its causation. Uterine artery ligation in humans, unlike in animal experiments, is not associated with an increased incidence of pre-eclampsia, calling into question the role of poor utero-placental perfusion in the cause of the disease in humans. The signals that initiate maternal adaptive responses during pregnancy come from or through the placenta into the maternal milieu but as is the case with gestational diabetes mellitus, are not necessarily the cause of maternal disease. Pre-eclampsia causes renal, hepatic, myocardial, cerebral and adrenal ischaemia--that is ischaemia in all highly vascular organs. Placental ischaemia, like ischaemia in all other organs, is a consequence rather than a causal factor in the development of the syndrome and this has profound consequences for research strategies.

Elevated Circulating Insulin-Like Growth Factor Binding Protein-1 Is Sufficient to Cause Fetal Growth Restriction

IGF binding protein-1 (IGFBP-1) inhibits the mitogenic actions of the IGFs. Circulating IGFBP-1 is elevated in newborns and experimental animals with fetal growth restriction (FGR). To establish a causal relationship between high circulating IGFBP-1 and FGR, we have generated transgenic mice using the mouse alpha-fetoprotein gene promoter to target overexpression of human IGFBP-1 (hIGFBP-1) in the fetal liver. These transgenic mice (AFP-BP1) expressed hIGFBP-1 mainly in the fetal hepatocytes, starting at embryonic d 14.5 (E14.5), with lower levels in the gut. The expression peaked at 1 wk postnatally (plasma concentration, 474 +/- 34 ng/ml). At birth, AFP-BP1 pups were 18% smaller [weighed 1.34 +/- 0.02 g compared with 1.62 +/- 0.04 g for wild type (WT); P < 0.05], and they did not demonstrate any postnatal catch-up growth. The placentas of the AFP-BP1 mice were larger than WT from E16.5 onwards (150 +/- 12 for AFP-BP1 vs. 100 +/- 5 mg for WT at E16.5; P < 0.05). Thus, this model of FGR is associated with a larger placenta, but without postnatal catch-up growth. Overall, these data clearly demonstrate that high concentrations of circulating IGFBP-1 are sufficient to cause FGR.

Periconceptional nutrition and the relationship between maternal body weight changes in the periconceptional period and feto‐placental growth in the sheep

Recent studies in the sheep have shown that maternal undernutrition during the periconceptional period, when the nutrient demands of the embryo are minimal, can alter the subsequent development of the metabolic, endocrine and cardiovascular systems and that these effects may, in part, depend on embryo number. We have tested the hypotheses that there are relationships between maternal weight or body condition at the time of conception and feto-placental growth during the first 55 days of pregnancy, and that periconceptional undernutrition has a differential effect on these relationships in singleton and twin pregnancies. We have investigated the effect of periconceptional undernutrition in the ewe (control n= 24, restricted at 70% of control feed allowance, PCUN n= 21) from 45 days prior to mating until 7 days after mating on placental and fetal weight and on placental histology in singleton and twin pregnancies at 53-56 days' gestation, i.e. during the period of maximal placental growth. In control, but not PCUN ewes carrying singleton pregnancies, there were direct relationships between maternal weight gain during the periconceptional period and uteroplacental weights at 53-56 days' gestation. There were direct relationships, however, between placental and fetal weights in both control and PCUN singleton pregnancies. In contrast to the singletons, in control twin pregnancies, there was no effect of maternal weight gain in the periconceptional period on any measure of uteroplacental growth, and there was also no relationship between placental and fetal weight. This lack of a relationship may be related to the increased uteroplacental weight and mean placentome weight in the twin pregnancies (control singletons: 2.45 +/- 0.18 g; control twins: 4.10 +/- 0.62 g). In the PCUN group, however, a greater weight loss between the start of the feeding regime and post mortem at approximately day 55, was associated with a larger placenta and fetus, and the direct relationship between placental and fetal mass was restored. In summary, the present study has demonstrated that there are important relationships between maternal weight gain during the periconceptional period and feto-placental growth during the first 56 days of pregnancy, and that periconceptional undernutrition has a differential effect on these relationships in singleton and twin pregnancies. In singleton pregnancies, periconceptional undernutrition disrupts the relationship between maternal weight gain during the periconceptional period and uteroplacental growth, and in twin pregnancies periconceptional undernutrition results in the emergence of an inverse relationship between maternal weight gain during early pregnancy and uteroplacental growth and a dependence of fetal growth on placental growth. These changes highlight the importance of the periconceptional environment in setting the placental and fetal growth trajectories, and have implications for the programmed development of the metabolic, cardiovascular and endocrine systems of the fetus and adult.

Biometría placentaria en la predicción de complicaciones de la gestación

The relationship between placental biometry and different complications of pregnancy has been established. However, these measures are complex, time consuming, and they are not a part of U/S examination routine. The objective was to assess the value of placental biometry in the early identification of those pregnancies that will develop pre-eclampsia or fetal growth retardation. A prospective study of an unselected population of 319 in the 20th gestational week was made, measuring the thickness, diameter and area of a placental section. As bibliographical references are scarce, our placental biometric charts are provided. Although there was a tendency to find smaller placentas with these complications (a smaller diameter and section area), the differences were not significant, and the difference was only significant in the in the lowest area in the fetal growth retardation group (p = 0.001; 95% CI, 1.049-3.213). In those cases associated to serious pre-eclampsia and fetal growth retardation under the 5th percentile, the placenta tends to be thicker at 20 weeks, with a lower diameter and section area. However, we could not make any conclusions as the number of cases was too low (4). Uterine artery Doppler is a better predictor. Detailed placentary biometry cannot be incorporated into daily practice, however the measurement of placental thickness has been proposed by some authors as routine, because a large placenta is related to greater perinatal morbidity and mortality.

Preweaning piglet mortality in relation to placental efficiency1

The relationship between placental efficiency (PLEFF, i.e., the ratio of birth weight [BWB] to placental weight [PLW]) and neonatal pig vitality as measured by the probability of preweaning death of live born piglets was examined for 1,036 live born piglets of 118 litters. The data were first analyzed to establish whether the relationships between PLEFF, PLW, and BWB were affected by parity (first vs. higher). Furthermore, the data collected were used to establish whether PLEFF is a better predictor of the risk of neonatal pig mortality before weaning than BWB and PLW. The relationships of BWB to PLW and PLEFF to PLW differed (P <0.01 and P <0.05, respectively) between piglets from gilts and sows. This difference appeared to be due mainly to an additional population of piglets with very large placentas in sows that were not present in gilts. Despite being significant, the courses of the relationships were essentially similar for piglets in gilts and in sows. For the curvilinear relationship of BWB to PLW, up to a certain threshold value, an increase of PLW resulted in an increase in BWB, and thereafter BWB did not change. A consequence of this is that PLEFF at relatively high PLW does not give the same information as PLEFF at relatively low PLW. For the second-order relationship of PLEFF to BWB, PLEFF increased with an increase in BWB, until BWB = 1,657 g, and decreased thereafter. The PLEFF decreased linearly with PLW. A change in PLW had a much larger impact on the value of PLEFF than a change in BWB. Although BWB and PLW were negatively associated with the chance of dying before weaning (P <0.001 and P <0.01, respectively), only PLEFF tended to be negatively associated with the chance of dying only before weaning (P = 0.08). Its underlying trait, BWB, played a greater role on the effect of PLEFF on the chance of preweaning death than PLW. In conclusion, PLEFF in swine is a complicated trait that should be treated with care. It is merely a mathematical derivative of BWB and PLW, whereby the extent to which BWB depends on PLW depends on the value of PLW. Placental functioning and fetal growth capacity, however, also have their effects on the value of BWB. It is concluded that, of the three traits (BWB, PLW, and PLEFF), the best predictor for the chance of preweaning mortality, which also happens to be easiest to measure, remains BWB.

Association between severe nausea and vomiting in pregnancy and lower rate of preterm births.

Nausea and vomiting in pregnancy has been associated with some reduction in miscarriage in other studies. However the relationship between nausea and vomiting during pregnancy and preterm birth/low birthweight in newborns is inconsistent; therefore the objective of the study was to clarify this possible association. The population-based large control (without any defects) data set of the Hungarian Case-Control Surveillance System of Congenital Abnormalities was evaluated. Of 38,151 controls, 3869 (10.1%) had medically recorded and treated nausea and vomiting during pregnancy. The proportion of mothers who later delivered girls was higher in this group. Mothers with nausea and vomiting in pregnancy had a somewhat (0.3 week) longer gestational age and a lower proportion of preterm births (6.4% vs. 9.5%). This finding may be connected with the favourable hormonal milieu (larger placenta, higher level of chorionic gonadotrophin and oestrogens) of pregnant women with nausea and vomiting.