Maternal medicine: Morphometric placental villous and vascular abnormalities in early- and late-onset pre-eclampsia with and without fetal growth restriction

Department of Surgical Research, NPIMR, Northwick Park Hospital, Harrow, UK.
BJOG An International Journal of Obstetrics & Gynaecology (Impact Factor: 3.45). 06/2006; 113(5):580-9. DOI: 10.1111/j.1471-0528.2006.00882.x
Source: PubMed


To evaluate placental morphology in pregnancies complicated by early- and late-onset pre-eclampsia (PET) with and without fetal growth restriction (FGR) using stereological techniques.
A total of 69 pregnant women were studied. Twenty women had pregnancies complicated by PET, 17 by FGR and 16 by both PET and FUR; the remaining 16 were from gestational-age-matched controls. Each group was further classified into early onset (<34 weeks) and late onsets (>34 weeks) based on gestational ages.
NPIMR at Northwick Park and St Marks Hospital.
placentae from pregnant women.
Formalin-fixed, wax-embedded sections stained with anti-CD34 antibodies and counterstained with haematoxylin.
Volumes, surface areas, lengths, diameters and shape factors of the villous tissues and fetal vasculature in the intermediate and terminal villi of all the groups studied.
Terminal villi volume and surface area were compromised in early-onset PET cases, late-onset PET had no impact on peripheral villi or vasculature features. The morphology of the vascular and villous subcomponents in the intermediate and terminal villi was significantly influenced by late-onset FGR, whereas early-onset FGR caused a reduction in placental weight. Length estimates were not influenced by PET, FGR or age of onset. Intermediate arteriole shape factor was significantly reduced in late-onset FGR.
Isolated early-onset PET was associated with abnormal placental morphology, but placentas from late-onset PET were morphologically similar to placentas from gestational-age-matched controls, confirming the existence of two subsets of this condition and supporting the hypothesis that late-onset PET is a maternal disorder and not a placental disease.

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Available from: Michael Egbor, Nov 21, 2014
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    • "While the numbers in these groups were small the trend suggests this may be indicative of a more severe form of the disease [23] [25] associated with restricted uteroplacental blood flow [26]. Abnormal placental morphology including significantly reduced intervillous space and terminal villi volume [24] may play a role in the long term deficit of motor development seen in offspring with preeclampsia. Future research comparing the impact of early and late onset preeclampsia on motor development and the role of reduced placental function will require a larger sample size to support these findings. "
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    ABSTRACT: Hypertension in pregnancy and preeclampsia have been linked to poor outcomes in cognitive, mental and psychomotor development; however, few longitudinal studies have researched their effect on offspring motor development, particularly in late childhood and adolescence. The purpose of this study was to determine if maternal hypertensive diseases during pregnancy are a risk factor for compromised motor development at 10, 14, and 17years. Longitudinal cohort study using data from the Western Australian Pregnancy Cohort Study (Raine). Offspring (n=2868) were classified by their maternal blood pressure profiles during pregnancy: normotension (n=2133), hypertension (n=626) and preeclampsia (n=109). Offspring motor development, at 10, 14, and 17years was measured by the Neuromuscular Developmental Index (NDI) of the McCarron Assessment of Motor Development (MAND). Linear mixed models were used to compare outcomes between pregnancy groups. Offspring from pregnancies complicated by preeclampsia had poorer motor outcomes at all ages than offspring from either normotensive mothers (p⩽0.001) or those with hypertension (p=0.002). Hypertensive diseases during pregnancy, in particular preeclampsia, have long term and possibly permanent consequences for motor development of offspring. Copyright © 2014 International Society for the Study of Hypertension in Pregnancy. Published by Elsevier B.V. All rights reserved.
    Pregnancy Hypertension 07/2014; 4(3). DOI:10.1016/j.preghy.2014.04.003
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    • "FGR affects 4–7% of live births in developed countries and contributes significantly to prematurity, perinatal morbidity, and mortality (Wang et al., 2007). Investigations using random block sampling and stereological studies reported reductions in the number, surface area, and volume of terminal villi in FGR-affected placentae, compared with placentae from uncomplicated pregnancies (Biagiotti et al., 1999; Egbor et al., 2006; Biswas et al., 2008; Vedmedovska et al., 2011; Almasry et al., 2012; Almasry and Elfayomy, 2012). Additionally, villous vessels exhibited fewer branches, and a majority of the vessels were slender and uncoiled (Teasdale, 1984; Teasdale and Jean-Jacques, 1988; Jackson et al., 1995; Chen et al., 2002; Mayhew, 2003; Tomas et al., 2010). "
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    ABSTRACT: Homeobox genes are essential for both the development of the blood and lymphatic vascular systems, as well as for their maintenance in the adult. Homeobox genes comprise an important family of transcription factors, which are characterized by a well conserved DNA binding motif; the homeodomain. The specificity of the homeodomain allows the transcription factor to bind to the promoter regions of batteries of target genes and thereby regulates their expression. Target genes identified for homeodomain proteins have been shown to control fundamental cell processes such as proliferation, differentiation, and apoptosis. We and others have reported that homeobox genes are expressed in the placental vasculature, but our knowledge of their downstream target genes is limited. This review highlights the importance of studying the cellular and molecular mechanisms by which homeobox genes and their downstream targets may regulate important vascular cellular processes such as proliferation, migration, and endothelial tube formation, which are essential for placental vasculogenesis and angiogenesis. A better understanding of the molecular targets of homeobox genes may lead to new therapies for aberrant angiogenesis associated with clinically important pregnancy pathologies, including fetal growth restriction and preeclampsia.
    Frontiers in Pharmacology 06/2014; 5:133. DOI:10.3389/fphar.2014.00133 · 3.80 Impact Factor
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    • "Preeclampsia with an early onset (before 34 gestational weeks) is especially harmful to the fetus, due to a strong association with intrauterine growth restriction and preterm birth [4]. Early onset preeclampsia is believed to have a stronger association with placental dysfunction and thus be more dependent on underlying abnormal placentation, while late onset preeclampsia is thought to be a mainly maternal disease with a weaker association with placental dysfunction [6] [7]. "
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    ABSTRACT: Introduction Preeclampsia affects about 3% of pregnancies and the placenta is believed to play a major role in its pathophysiology. Lately, the role of the placenta has been hypothesised to be more pronounced in preeclampsia of early (<34 weeks) rather than late (> 34 weeks) onset. 31P Magnetic Resonance Spectroscopy (MRS) enables non-invasive, in vivo studies of placental metabolism. Our aim was to study placental energy and membrane metabolism in women with normal pregnancies and those with early and late onset preeclampsia. Methods The study population included fourteen women with preeclampsia (five with early onset and nine with late onset preeclampsia) and sixteen women with normal pregnancy (seven with early and nine with late pregnancy). All women underwent a 31P-MRS examination of the placenta. Results The phosphodiester (PDE) spectral intensity fraction of the total 31P signal and the phosphodiester/phosphomonoester (PDE/PME) spectral intensity ratio was higher in early onset preeclampsia than in early normal pregnancy (p=0.03 and p=0.02). In normal pregnancy the PDE spectral intensity fraction and the PDE/PME spectral intensity ratio increased with increasing gestational age (p=0.006 and p=0.001). Discussion Since PDE and PME are related to cell membrane degradation and formation, respectively, our findings indicate increased cell degradation and maybe also decreased cell proliferation in early onset preeclampsia compared to early normal pregnancy, and with increasing gestational age in normal pregnancy. Conclusions Our findings could be explained by increased apoptosis due to ischemia in early onset preeclampsia and also increased apoptosis with increasing gestational age in normal pregnancy.
    Placenta 05/2014; 35(5). DOI:10.1016/j.placenta.2014.02.005 · 2.71 Impact Factor
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