scholarly journals Thrombophilias and adverse pregnancy outcome – A confounded problem!

2008 ◽  
Vol 99 (01) ◽  
pp. 77-85 ◽  
Author(s):  
Nard G Janssen ◽  
Jakoba J Kalk ◽  
William M Hague ◽  
Gustaaf A Dekker ◽  
Willem J Kist ◽  
...  
Keyword(s):  
Pregnancy Outcome ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Adverse Pregnancy Outcome ◽  
Fetal Loss ◽  
Severity Of Illness ◽  
Growth Restriction ◽  
Abruptio Placentae ◽  
Recurrent Fetal Loss ◽  
Adverse Pregnancy

SummaryIt was the objective of this study to analyse the influence of confounders, such as ethnicity, severity of illness and method of testing, in articles concerning the still moot relationship of thrombophilias to adverse pregnancy outcome (APO). Relevant casecontrol studies were identified using Medline and EMBASE databases between 1966 and 2006. Search terms were recurrent fetal loss, intrauterine fetal death, preeclampsia, HELLP-syndrome, eclampsia, fetal growth restriction, abruptio placentae, combined with maternal thrombophilias. Data was extracted from the articles per subgroup ofAPO regardless of confounder. These subgroups were tested if they fulfilled the heterogeneity testing criterion (I2 > 35%) to weigh the influence of the confounder. Confounders were selected and examined with Mantel- Haenszel method. Increased thrombophilia prevalence was confirmed in most adverse pregnancy outcomes. Ethnicity, genetic testing only and severity of illness were confounders in the various forms of APO. Stronger relationships between factor V Leiden and severity of disease were found in 2nd and 3rd trimester than 1st trimester recurrent fetal loss, in preeclampsia with: blood pressure ≥160/110 mmHg than ≥140/90 mmHg; proteinuria ≥5 grams per day than < 5 grams; onset before than after 28 weeks, in fetal growth restriction <3rd percentile than <5th, than <10th, and in earlier occurrence of abruptio placentae than 3rd trimester. In conclusion, reports on the prevalence of maternal thrombophilias and APO are influenced by various confounders, which are not always appropriately analysed. The differences we have identified reflect the differential impact of these confounders. These data emphasise the importance of more uniform research.

scholarly journals The Role of Placental Homeobox Genes in Human Fetal Growth Restriction

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Padma Murthi ◽  
Gayathri Rajaraman ◽  
Shaun Patrick Brennecke ◽  
Bill Kalionis
Keyword(s):  
Pregnancy Outcome ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Transcriptional Control ◽  
Molecular Mechanisms ◽  
Adverse Pregnancy Outcome ◽  
Growth Restriction ◽  
Placental Development ◽  
Increased Risk ◽  
Adverse Pregnancy

Fetal growth restriction (FGR) is an adverse pregnancy outcome associated with significant perinatal and paediatric morbidity and mortality, and an increased risk of chronic disease later in adult life. One of the key causes of adverse pregnancy outcome is fetal growth restriction (FGR). While a number of maternal, fetal, and environmental factors are known causes of FGR, the majority of FGR cases remain idiopathic. These idiopathic FGR pregnancies are frequently associated with placental insufficiency, possibly as a result of placental maldevelopment. Understanding the molecular mechanisms of abnormal placental development in idiopathic FGR is, therefore, of increasing importance. Here, we review our understanding of transcriptional control of normal placental development and abnormal placental development associated with human idiopathic FGR. We also assess the potential for understanding transcriptional control as a means for revealing new molecular targets for the detection, diagnosis, and clinical management of idiopathic FGR.

Description of a method for inducing fetal growth restriction in the spiny mouse

2017 ◽  
Vol 8 (5) ◽  
pp. 550-555 ◽  
Author(s):  
H. Dickinson ◽  
S. Ellery ◽  
M. Davies-Tuck ◽  
M. Tolcos ◽  
I. Nitsos ◽  
...  
Keyword(s):  
Blood Flow ◽  
Fetal Growth ◽  
Gestational Age ◽  
Fetal Growth Restriction ◽  
Fetal Loss ◽  
Small Animal ◽  
Major Complication ◽  
Growth Restriction ◽  
Spiny Mouse ◽  
Uterine Blood Flow

Intrauterine or fetal growth restriction (IUGR) is a major complication of pregnancy and leads to significant perinatal morbidities and mortality. Typically, induction of IUGR in animals involves the complete occlusion or ablation of vessels to the uterus or placenta, acutely impairing blood flow and fetal growth, usually with high fetal loss. We aimed to produce a model of reduced fetal growth in the spiny mouse with minimal fetal loss. At 27 days gestational age (term is 38–39 days), a piece of silastic tubing was placed around the left uterine artery to prevent the further increase of uterine blood flow with advancing gestation to induce IUGR (occluded). Controls were generated from sham surgeries without placement of the tubing. Dams were humanely euthanized at 37 days gestational age and all fetuses and placentas were weighed and collected. Of the 17 dams that underwent surgery, 15 carried their pregnancies to 37 days gestational age and 95% of fetuses survived to this time. The difference in fetal body weight between occluded and control was ~21% for fetuses in the left uterus side: there were no differences for fetuses in the right uterus side. Offspring from the occluded group had significantly lower brain, liver, lung, kidney and carcass weights compared with shams. Preventing the gestation-related increase of uterine blood flow induced significant growth restriction in the fetal spiny mouse, with minimal fetal loss. This technique could be readily adapted for other small animal.

scholarly journals Effect of Endogenic and Exogenic Oxidative Stress Triggers on Adverse Pregnancy Outcomes: Preeclampsia, Fetal Growth Restriction, Gestational Diabetes Mellitus and Preterm Birth

2021 ◽  
Vol 22 (18) ◽  
pp. 10122
Author(s):  
Eun Hui Joo ◽  
Young Ran Kim ◽  
Nari Kim ◽  
Jae Eun Jung ◽  
Seon Ha Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Preterm Birth ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Fetal Growth ◽  
Pregnancy Outcomes ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Adverse Pregnancy

Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) in cells and tissues and the ability of a biological system to detoxify them. During a normal pregnancy, oxidative stress increases the normal systemic inflammatory response and is usually well-controlled by the balanced body mechanism of the detoxification of anti-oxidative products. However, pregnancy is also a condition in which this adaptation and balance can be easily disrupted. Excessive ROS is detrimental and associated with many pregnancy complications, such as preeclampsia (PE), fetal growth restriction (FGR), gestational diabetes mellitus (GDM), and preterm birth (PTB), by damaging placentation. The placenta is a tissue rich in mitochondria that produces the majority of ROS, so it is important to maintain normal placental function and properly develop its vascular network to ensure a safe and healthy pregnancy. Antioxidants may ameliorate these diseases, and related research is progressing. This review aimed to determine the association between oxidative stress and adverse pregnancy outcomes, especially PE, FGR, GDM, and PTB, and explore how to overcome this oxidative stress in these unfavorable conditions.

scholarly journals Toll-like receptor-4 null mutation causes fetal loss and fetal growth restriction associated with impaired maternal immune tolerance in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hon Y. Chan ◽  
Lachlan M. Moldenhauer ◽  
Holly M. Groome ◽  
John E. Schjenken ◽  
Sarah A. Robertson
Keyword(s):  
Treg Cell ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Fetal Loss ◽  
Treg Cells ◽  
Growth Restriction ◽  
Null Mutation ◽  
Toll Like Receptor ◽  
Wild Type ◽  
Toll Like Receptor 4

AbstractMaternal immune adaptation to accommodate pregnancy depends on sufficient availability of regulatory T (Treg) cells to enable embryo implantation. Toll-like receptor 4 is implicated as a key upstream driver of a controlled inflammatory response, elicited by signals in male partner seminal fluid, to initiate expansion of the maternal Treg cell pool after mating. Here, we report that mice with null mutation in Tlr4 (Tlr4−/−) exhibit impaired reproductive outcomes after allogeneic mating, with reduced pregnancy rate, elevated mid-gestation fetal loss, and fetal growth restriction, compared to Tlr4+/+ wild-type controls. To investigate the effects of TLR4 deficiency on early events of maternal immune adaptation, TLR4-regulated cytokines and immune regulatory microRNAs were measured in the uterus at 8 h post-mating by qPCR, and Treg cells in uterus-draining lymph nodes were evaluated by flow cytometry on day 3.5 post-coitum. Ptgs2 encoding prostaglandin-endoperoxide synthase 2, cytokines Csf2, Il6, Lif, and Tnf, chemokines Ccl2, Cxcl1, Cxcl2, and Cxcl10, and microRNAs miR-155, miR-146a, and miR-223 were induced by mating in wild-type mice, but not, or to a lesser extent, in Tlr4−/− mice. CD4+ T cells were expanded after mating in Tlr4+/+ but not Tlr4−/− mice, with failure to expand peripheral CD25+FOXP3+ NRP1− or thymic CD25+FOXP3+ NRP1+ Treg cell populations, and fewer Treg cells expressed Ki67 proliferation marker and suppressive function marker CTLA4. We conclude that TLR4 is an essential mediator of the inflammation-like response in the pre-implantation uterus that induces generation of Treg cells to support robust pregnancy tolerance and ensure optimal fetal growth and survival.

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