The autopsy and placental histopathological examination results following fetal deaths were analyzed retrospectively in an attempt to explain the stillbirths that occurred from 1996 to 2010 at the Department of Obstetrics and Gynecology, University of Szeged. One hundred and forty fetal deaths were recorded in that period, i.e. a rate of 4.69 stillbirths per 1000 deliveries. The postmortem examination provided the exact cause of the fetal death in 57.9% of the cases. The most common causes were a placental insufficiency (46.9%) and an umbilical cord complication (25.9%). In the first half of the third trimester, a placental insufficiency predominated as the cause of stillbirth, whereas mainly umbilical cord complications occurred around term. In spite of the availability of the autopsy and histopathological examination results, the proportion of unexplained stillbirths in our sample was relatively high. A considerable proportion of stillbirth cases could probably be prevented by more effective screening of a placental insufficiency.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.3109/15513815.2013.850132 | DOI Listing |
J Biol Chem
December 2024
Department of Biological Sciences, University of Memphis, Memphis, TN 38152, USA. Electronic address:
Mitogen-activated protein kinase kinase kinase 4 (MAP3K4) promotes fetal and placental growth and development, with MAP3K4 kinase inactivation resulting in placental insufficiency and fetal growth restriction. MAP3K4 promotes key signaling pathways including JNK, p38, and PI3K/Akt, leading to activation of CREB-binding protein. MAP3K4 kinase inactivation results in loss of these pathways and gain of histone deacetylase 6 (HDAC6) expression and activity.
View Article and Find Full Text PDFReprod Sci
December 2024
Department of Physiology and Aging, College of Medicine, University of Florida, Gainesville, FL, USA.
Fetal growth restriction (FGR) affects between 5-10% of all live births. Placental insufficiency is a leading cause of FGR, resulting in reduced nutrient and oxygen delivery to the fetus. Currently, there are no effective in utero treatment options for FGR, or placental insufficiency.
View Article and Find Full Text PDFClin Epigenetics
December 2024
Center for Medical Genetics, Ghent University Hospital, Ghent, Belgium.
Background: Aberrant embryo implantation and suboptimal placentation can lead to (severe) complications such as preeclampsia and fetal growth restriction later in pregnancy. Current identification of high-risk pregnancies relies on a combination of risk factors, biomarkers, and ultrasound examinations, a relatively inaccurate approach. Previously, aberrant DNA methylation due to placental hypoxia has been identified as a potential marker of placental insufficiency and, hence, potential (future) pregnancy complications.
View Article and Find Full Text PDFAm J Obstet Gynecol
December 2024
department of Obstetrics and Gynaecology, University Medical Center Utrecht, Lundlaan 6, 3584 EA, Utrecht, and department of Obstetrics and Gynaecology, Erasmus Medical Center, Rotterdam, the Netherlands. Electronic address:
Background: Early-onset fetal growth restriction as consequence of placental insufficiency frequently requires iatrogenic, preterm birth. Administration of antenatal corticosteroids reduces risks of neonatal morbidity and mortality following preterm birth and is most beneficial if the neonate is delivered within two weeks following treatment. International guidelines on fetal growth restriction pregnancies do not provide directives regarding the timing of antenatal corticosteroids, resulting in practice variation.
View Article and Find Full Text PDFStem Cell Rev Rep
December 2024
The Department of Obstetrics, Gynaecology and Newborn Health/Mercy Hospital for Women, University of Melbourne, 163 Studley Road, Heidelberg, Victoria, 3084, Australia.
Leucine-rich repeat-containing G protein-coupled receptors 5/4 (LGR5/LGR4) are critical stem cell markers in epithelial tissues including intestine. They agonise wingless-related integration site (WNT) signalling. Until now, LGR5/LGR4 were uncharacterised in placenta, where analogous functions may exist.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!