The human umbilical cord forms a connection between the placenta and the foetus. It is composed of two arteries and one vein surrounded by 
                  Wharton's jelly. Pre-eclampsia is accompanied by extensive remodeling of extracellular matrix of umbilical cord. Matrix metalloproteinases (MMPs) are engaged in degradation of extracellular matrix proteins and activation/inactivation of certain cytokines and enzymes. These enzymes will probably play a central role in the release of matrix-embedded cytokines and growth factors. MMP-2 (gelatinase A) is the main collagenolytic enzyme of both umbilical artery and vein. Other metalloproteinases are present in several times lower amounts. Reduced activity of collagen-degrading enzymes may be a factor, which enhances the accumulation of collagen and some other proteins in the pre-eclamptic umbilical cord tissues. It seems to be possible that similar alterations occur in other fetal blood vessels. It may result in an increase in peripheral  resistance as well as an increase in the blood pressure in the fetal vascular system. Some observations suggest that the raised pressure may persist after birth. Pre-eclampsia may be a factor that evokes an initiation of hypertension in utero and its amplification through childhood and adulthood.

Lech Romanowicz

Zofia Galewska

Extracellular Matrix Remodeling of the Umbilical Cord in Pre-eclampsia as a Risk Factor for Fetal Hypertension

Magnesium deficiency in pregnancy frequently occurs because of inadequate or low intake of magnesium. Magnesium deficiency during pregnancy can induce not only maternal and fetal nutritional problems, but also consequences that might last in offspring throughout life. Many epidemiological studies have disclosed that small for gestational age (SGA) is associated with an increased risk of insulin resistance in adult life. We reported that intracellular magnesium of cord blood platelets is lower in SGA groups than that in appropriate for gestational age groups, suggesting that intrauterine magnesium deficiency may result in SGA. Taken together, intrauterine magnesium deficiency in the fetus may lead to or at least program insulin resistance after birth. In this review, we propose that intrauterine magnesium deficiency may induce metabolic syndrome in later life. We discuss the potential contribution of aberrant magnesium regulation to SGA and to the pathogenesis of metabolic syndrome.

Junji Takaya

Kazunari Kaneko

Small for Gestational Age and Magnesium in Cord Blood Platelets: Intrauterine Magnesium Deficiency May Induce Metabolic Syndrome in Later Life

Cerebral palsy is a major neonatal handicap with unknown aetiology. There is evidence that prenatal brain injury is the leading cause of CP. Severe placental pathology accounts for a high percentage of cases. Several factors predispose to prenatal brain damage but when and how they act is unclear. The aim of this paper was to determine if hypoxia during pregnancy leads to damage in fetal brain and to evaluate the localization of this injury. An animal model of chronic hypoxia produced by chronic administration of a nitric oxide synthase inhibitor (L-NAME) was used to evaluate apoptotic activity in fetal  brains and to localize the most sensitive areas. L-NAME reproduces a preeclamptic-like condition with increased blood pressure, proteinuria, growth restriction and intrauterine mortality. Apoptotic activity was increased in L-NAME brains and the most sensitive areas were the subventricular and pallidum zone. These results may explain the clinical features of CP. Further studies are needed.

Bego&#241;a Pellicer

Sonia Herraiz

Antonio Leal

Carlos Sim&#243;n

Antonio Pellicer

Prenatal Brain Damage in Preeclamptic Animal Model Induced by Gestational Nitric Oxide Synthase Inhibition

Glomerular VEGF expression is critical for the maintenance and function of an intact filtration barrier. Alterations in glomerular VEGF bioavailability result in endothelial as well as in podocyte damage. Renal involvement in preeclampsia includes proteinuria, podocyturia, elevated blood pressure, edema, glomerular capillary endotheliosis, and thrombotic microangiopathy. At least the renal signs, symptoms, and other evidence can sufficiently be explained by reduced VEGF levels. The aim of this paper was to summarize our pathophysiological understanding of the renal involvement of preeclampsia and point out similarities to the renal side effects of VEGF-ablation therapy.

Janina Müller-Deile

Mario Schiffer

Renal Involvement in Preeclampsia: Similarities to VEGF Ablation Therapy

<i>Objective</i>. Small for gestational age (SGA) is associated with increased neonatal morbidity and mortality. At present, evidence on whether these pregnancies should be managed expectantly or by induction is lacking. To get insight in current policy we analysed data of the National Dutch Perinatal Registry (PRN). 
<i>Methods</i>. We used data of all nulliparae between 2000 and 2005 with a singleton in cephalic presentation beyond 36+0 weeks, with a birth weight below the 10th percentile. We analysed two groups of pregnancies: (I) with isolated SGA and (II) with both SGA and hypertensive disorders. Onset of labour was related to route of delivery and neonatal outcome.
<i>Results</i>. Induction was associated with a higher risk of emergency caesarean section (CS), without improvement in neonatal outcome. For women with isolated SGA the relative risk of emergency CS after induction was 2.3 (95% Confidence Interval [CI] 2.1 to 2.5) and for women with both SGA and hypertensive disorders the relative risk was 2.7 (95% CI 2.3 to 3.1).
<i>Conclusion</i>. Induction in pregnancies complicated by SGA at term is associated with a higher risk of instrumental deliveries without improvement of neonatal outcome. Prospective studies are needed to determine the best strategy in suspected IUGR at term.

K. E. Boers

J. A. M. van der Post

Ben W. J. Mol

J. M. M. van Lith

S. A. Scherjon

Labour and Neonatal Outcome in Small for Gestational Age Babies Delivered Beyond 36+0 Weeks: A Retrospective Cohort Study

Currently, only two preeclampsia susceptibility genes (<i>ACVR2A</i>, <i>STOX1</i>) have been identified within confirmed regions with significant genome-wide linkage, although many genetic screens in multiple populations have been performed. In this paper, we focus on the <i>STOX1</i> gene. The epigenetic status of this gene is discussed explaining the maternal transmission of the <i>STOX1</i> susceptibility allele observed in preeclamptic families. The known upstream regulation and downstream effector genes of the transcription factor STOX1 are described. Finally, we propose a model in which we combine the cell type-specific and allele-specific effects of STOX1. This includes intrinsic effects (differential CpG island methylation) and extrinsic effects (regulation of effector genes).

Marie van Dijk

Cees B. M. Oudejans

STOX1: Key Player in Trophoblast Dysfunction Underlying Early Onset Preeclampsia with Growth Retardation

<i  >Objective</i>. The purpose of this study was to elucidate the impact of the clinical presentation on perinatal outcome in placental abruption. 
<i  >Study Design</i>. A retrospective study was performed in 97 placental abruptions.  Placental abruptions were classified according to clinical presentation: pregnancy-induced hypertension (HT, <svg style="vertical-align:-0.10033pt;width:42.912498px;" id="M1" height="10.8125" version="1.1" viewBox="0 0 42.912498 10.8125" width="42.912498"  xmlns="http://www.w3.org/2000/svg">
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</svg>), threatened premature labor and/or premature rupture of membranes (TPL/ROM, <svg style="vertical-align:-0.17555pt;width:42.912498px;" id="M2" height="11.1" version="1.1" viewBox="0 0 42.912498 11.1" width="42.912498"  xmlns="http://www.w3.org/2000/svg">
	<g transform="matrix(1.25,0,0,-1.25,0,11.1)">
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</svg>), clinically low risk (LR, <svg style="vertical-align:-0.10033pt;width:42.912498px;" id="M3" height="10.8125" version="1.1" viewBox="0 0 42.912498 10.8125" width="42.912498"  xmlns="http://www.w3.org/2000/svg">
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</svg>), and others (<svg style="vertical-align:-0.17555pt;width:42.912498px;" id="M4" height="10.9125" version="1.1" viewBox="0 0 42.912498 10.9125" width="42.912498"  xmlns="http://www.w3.org/2000/svg">
	<g transform="matrix(1.25,0,0,-1.25,0,10.9125)">
		<g transform="translate(72,-63.27)">
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</svg>).  Perinatal outcomes were compared among the HT, TPL/ROM, and LR groups. 
<i  >Results</i>. The HT had significantly higher incidence of IUGR, IFUD, and low fibrinogen. The TPL/ROM had less severe disease.  However, the LR had significantly higher incidence of IUFD, low UA pH &#x3c; 7.1, low Apgar score of &#x3c;7 at 5&#x2009;min, and low fibrinogen. <i  >Conclusion</i>. Disease severity in placental abruption is likely to depend on the clinical presentation.

Seishi Furukawa

Hiroshi Sameshima

Tsuyomu Ikenoue

Masanao Ohashi

Yoshio Nagai

Is the Perinatal Outcome of Placental Abruption Modified by Clinical Presentation?

About this journal

<p><em>Journal of Pregnancy</em> publishes original research articles, review articles, and clinical studies related to all aspects of pregnancy and childbirth. Topics include biomedical aspects of pregnancy labour, maternal health and breastfeeding.</p>


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<p>Chief Editor, Dr. Ozgu-Erdinc, has been an active practitioner for over 30 years. Her research is focused on gestational diabetes mellitus screening, diagnosis and management including being actively involved in clinical research for new and novel ways to improve outcomes for mothers and babies.</p>


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Journal of Pregnancy - Table of contents 2011

title

Journal of Pregnancy publishes original research articles, review articles, and clinical studies related to all aspects of pregnancy and childbirth. Topics include biomedical aspects of pregnancy labour, maternal health and breastfeeding.

Journal of Pregnancy