Identification of newborns with Fetal Growth Restriction (FGR) in weight and/or length based on constitutional growth potential

2006 ◽  
Vol 165 (10) ◽  
pp. 717-725 ◽  
Author(s):  
Nicole Mamelle ◽  
Magali Boniol ◽  
Olivier Rivière ◽  
Marie O. Joly ◽  
Georges Mellier ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Growth Potential

INTRAUTERINE GROWTH RETARDATION - A REVIEW ARTICLE

2018 ◽  
pp. 184-195
Author(s):  
Minh Son Pham ◽  
Vu Quoc Huy Nguyen ◽  
Dinh Vinh Tran
Keyword(s):  
Fetal Growth ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Growth Potential ◽  
National Guidelines ◽  
Intrauterine Growth ◽  
No Gold Standard

Small for gestational age (SGA) and fetal growth restriction (FGR) is difficult to define exactly. In this pregnancy condition, the fetus does not reach its biological growth potential as a consequence of impaired placental function, which may be because of a variety of factors. Fetuses with FGR are at risk for perinatal morbidity and mortality, and poor long-term health outcomes, such as impaired neurological and cognitive development, and cardiovascular and endocrine diseases in adulthood. At present no gold standard for the diagnosis of SGA/FGR exists. The first aim of this review is to: summarize areas of consensus and controversy between recently published national guidelines on small for gestational age or fetal growth restriction; highlight any recent evidence that should be incorporated into existing guidelines. Another aim to summary a number of interventions which are being developed or coming through to clinical trial in an attempt to improve fetal growth in placental insufficiency. Key words: fetal growth restriction (FGR), Small for gestational age (SGA)

Definition of Fetal Growth Restriction According to Constitutional Growth Potential

Neonatology ◽  
2001 ◽  
Vol 80 (4) ◽  
pp. 277-285 ◽  
Author(s):  
N. Mamelle ◽  
V. Cochet ◽  
O. Claris
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Growth Potential ◽  
Definition Of

Fetal growth restriction: unresolved issues of risk stratification, early diagnosis, and obstetric management

2021 ◽  
Vol 20 (5) ◽  
pp. 76-86
Author(s):  
N.M. Podzolkova ◽  
◽  
Yu.V. Denisova ◽  
M.Yu. Skvortsova ◽  
T.V. Denisova ◽  
...  
Keyword(s):  
Early Diagnosis ◽  
Risk Stratification ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Diagnostic Methods ◽  
Growth Potential ◽  
Increased Risk ◽  
Obstetric Management ◽  
Language Literature

Fetal growth restriction (FGR) refers to pregnancy complications associated with an increased risk of perinatal morbidity and mortality and is defined in the Russian-language literature as the fetal size and weight retardation in relation to the norm for a given gestational age, and in the English-language literature – as the inability of the fetus to realize its genetically determined growth potential. FGR is the cause of 43% of stillbirths of unspecified etiology, and some cases remain undiagnosed even in high-risk populations due to the lack of universal diagnostic standards for this pathology. The review presents a critical analysis of the existing definitions of FGR, the latest data on risk factors, an assessment of diagnostic methods for its early and late forms, the prospects of using biomarkers and instrumental methods of examination in predicting adverse perinatal outcomes, and an algorithm for the management of pregnancy complicated by FGR. For a more complete coverage of the literature and deeper understanding of the nosology, attention is focused on FGR that is not accompanied by preeclampsia and other hypertensive disorders, which occur in about 30% of cases. Key words: placental insufficiency, fetometry, percentile, pulsatility index, fetal growth restriction For citation: Podzolkova N.M., Denisova Yu.V., Skvortsova M.Yu., Denisova T.V., Shovgenova D.S. Fetal growth restriction: unresolved issues of risk stratification, early diagnosis, and obstetric management. Vopr. ginekol. akus. perinatol. (Gynecology, Obstetrics and Perinatology). 2021; 20(5): 76–86. (In Russian). DOI: 10.20953/1726-1678-2021-5-76-86

scholarly journals Phosphorylation of Yes-associated protein impairs trophoblast invasion and migration: implications for the pathogenesis of fetal growth restriction†

2020 ◽  
Vol 103 (4) ◽  
pp. 866-879
Author(s):  
Hao Wang ◽  
Ping Xu ◽  
Xiaofang Luo ◽  
Mingyu Hu ◽  
Yamin Liu ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Cell Function ◽  
Hippo Pathway ◽  
Growth Restriction ◽  
Growth Potential ◽  
Biomechanical Analysis ◽  
Trophoblast Invasion ◽  
Invasion And Migration ◽  
And Migration

Abstract Fetal growth restriction (FGR) is a condition in which a newborn fails to achieve his or her prospective hereditary growth potential. This condition is associated with high newborn mortality, second only to that associated with premature birth. FGR is associated with maternal, fetal, and placental abnormalities. Although the placenta is considered to be an important organ for supplying nutrition for fetal growth, research on FGR is limited, and treatment through the placenta remains challenging, as neither proper uterine intervention nor its pathogenesis have been fully elucidated. Yes-associated protein (YAP), as the effector of the Hippo pathway, is widely known to regulate organ growth and cancer development. Therefore, the correlation of the placenta and YAP was investigated to elucidate the pathogenic mechanism of FGR. Placental samples from humans and mice were collected for histological and biomechanical analysis. After investigating the location and role of YAP in the placenta by immunohistochemistry, we observed that YAP and cytokeratin 7 have corresponding locations in human and mouse placentas. Moreover, phosphorylated YAP (p-YAP) was upregulated in FGR and gradually increased as gestational age increased during pregnancy. Cell function experiments and mRNA-Seq demonstrated impaired YAP activity mediated by extracellular signal-regulated kinase inhibition. Established FGR-like mice also recapitulated a number of the features of human FGR. The results of this study may help to elucidate the association of FGR development with YAP and provide an intrauterine target that may be helpful in alleviating placental dysfunction.

INTRAUTERINE GROWTH RETARDATION - A REVIEW ARTICLE

2018 ◽  
Vol 8 (6) ◽  
pp. 184-195
Author(s):  
Son Pham Minh ◽  
Huy Nguyen Vu Quoc ◽  
Vinh Tran Dinh
Keyword(s):  
Fetal Growth ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Growth Potential ◽  
National Guidelines ◽  
Intrauterine Growth ◽  
No Gold Standard

Small for gestational age (SGA) and fetal growth restriction (FGR) is difficult to define exactly. In this pregnancy condition, the fetus does not reach its biological growth potential as a consequence of impaired placental function, which may be because of a variety of factors. Fetuses with FGR are at risk for perinatal morbidity and mortality, and poor long-term health outcomes, such as impaired neurological and cognitive development, and cardiovascular and endocrine diseases in adulthood. At present no gold standard for the diagnosis of SGA/FGR exists. The first aim of this review is to: summarize areas of consensus and controversy between recently published national guidelines on small for gestational age or fetal growth restriction; highlight any recent evidence that should be incorporated into existing guidelines. Another aim to summary a number of interventions which are being developed or coming through to clinical trial in an attempt to improve fetal growth in placental insufficiency. Key words: fetal growth restriction (FGR), Small for gestational age (SGA)

Decorin expression is decreased in human idiopathic fetal growth restriction

2010 ◽  
Vol 22 (6) ◽  
pp. 949 ◽  
Author(s):  
B. C. Swan ◽  
P. Murthi ◽  
G. Rajaraman ◽  
N. A. Pathirage ◽  
J. M. Said ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Dermatan Sulfate ◽  
Growth Restriction ◽  
Growth Potential ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Clinically Significant ◽  
Normal Placenta

Fetal growth restriction (FGR) is a clinically significant pregnancy disorder in which the fetus fails to achieve its full growth potential in utero. Most cases of FGR are idiopathic and are associated with placental thrombosis. Previous studies suggest that proteoglycans, such as decorin, that contain the glycosaminoglycan dermatan sulfate are the principal anticoagulants in the normal placenta. The present study investigated decorin expression in placentas from pregnancies complicated by idiopathic FGR (n = 26) and gestation-matched controls (n = 27). Real-time polymerase chain reaction demonstrated significantly reduced decorin mRNA expression in FGR compared with control (1.52 ± 0.14 v. 2.21 ± 0.22, respectively; P < 0.01). Immunoblotting revealed decreased decorin protein (40 kDa) expression in FGR compared with controls (420.8 ± 39.0 v. 690.1 ± 42.2, respectively; n = 12 in each group; P = 0.0007). Immunohistochemistry demonstrated the presence of immunoreactive decorin protein in the placental villous stroma surrounding the fetal capillaries and a significant decrease in decorin protein presence in FGR compared with control (1.75 ± 0.66 v. 2.98 ± 1.12, respectively; n = 6 in each group; P < 0.01, t-test). This is the first study to demonstrate reduced decorin in idiopathic FGR, indicating a potentially significant role for decorin in the aetiology of placental thrombosis in idiopathic FGR.

scholarly journals eNOS knockout mouse as a model of fetal growth restriction with an impaired uterine artery function and placental transport phenotype

2012 ◽  
Vol 303 (1) ◽  
pp. R86-R93 ◽  
Author(s):  
Laura C. Kusinski ◽  
Joanna L. Stanley ◽  
Mark R. Dilworth ◽  
Cassandra J. Hirt ◽  
Irene J. Andersson ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Vascular Function ◽  
Uterine Artery ◽  
Nutrient Transport ◽  
Growth Restriction ◽  
Growth Potential ◽  
Abdominal Circumference ◽  
Maternal Undernutrition ◽  
Endothelial Nitric Oxide

Fetal growth restriction (FGR) is the inability of a fetus to reach its genetically predetermined growth potential. In the absence of a genetic anomaly or maternal undernutrition, FGR is attributable to “placental insufficiency”: inappropriate maternal/fetal blood flow, reduced nutrient transport or morphological abnormalities of the placenta (e.g., altered barrier thickness). It is not known whether these diverse factors act singly, or in combination, having additive effects that may lead to greater FGR severity. We suggest that multiplicity of such dysfunction might underlie the diverse FGR phenotypes seen in humans. Pregnant endothelial nitric oxide synthase knockout (eNOS−/−) dams exhibit dysregulated vascular adaptations to pregnancy, and eNOS−/− fetuses of such dams display FGR. We investigated the hypothesis that both altered vascular function and placental nutrient transport contribute to the FGR phenotype. eNOS−/− dams were hypertensive prior to and during pregnancy and at embryonic day (E) 18.5 were proteinuric. Isolated uterine artery constriction was significantly increased, and endothelium-dependent relaxation significantly reduced, compared with wild-type (WT) mice. eNOS−/− fetal weight and abdominal circumference were significantly reduced compared with WT. Unidirectional maternofetal 14C-methylaminoisobutyric acid (MeAIB) clearance and sodium-dependent 14C-MeAIB uptake into mouse placental vesicles were both significantly lower in eNOS−/− fetuses, indicating diminished placental nutrient transport. eNOS−/− mouse placentas demonstrated increased hypoxia at E17.5, with elevated superoxide compared with WT. We propose that aberrant uterine artery reactivity in eNOS−/− mice promotes placental hypoxia with free radical formation, reducing placental nutrient transport capacity and fetal growth. We further postulate that this mouse model demonstrates “uteroplacental hypoxia,” providing a new framework for understanding the etiology of FGR in human pregnancy.

scholarly journals Analysis of fetal growth restriction in pregnancy in subjects attending in an obstetric clinic of a tertiary care teaching hospital

2018 ◽  
Vol 7 (3) ◽  
pp. 973
Author(s):  
Ashish Seal ◽  
Arup Dasgupta ◽  
Mousumi Sengupta ◽  
Rinini Dastider ◽  
Sukanta Sen
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Intrauterine Growth Restriction ◽  
Tertiary Care ◽  
Growth Restriction ◽  
Growth Potential ◽  
Crown Rump Length ◽  
Mortality And Morbidity ◽  
Intrauterine Growth ◽  
In Pregnancy

Background: Intrauterine growth restriction (IUGR) is defined as fetal growth less than the normal growth potential of a specific infant because of genetic or environmental factors. Fetal growth restriction or intrauterine growth restriction is one of the leading causes of perinatal mortality and morbidity in newborns. Fetal growth restriction is a complex multifactorial condition resulting from several fetal and maternal disorders. Objective of present study was to find out incidence of IUGR and assessment and evaluation of different important changes in IUGR.Methods: Women who attended the Obstetric OPD in their 1st trimester of pregnancy and those who were thought would be able to visit the antenatal clinic for their fortnightly check-up regularly were screened for intrauterine foetal growth retardation. Women with irregular and uncertain menstrual history and where the 1st trimester USG foetal crown rump length did not corroborate with the menstrual gestational age were excluded from this study.Results: Incidence of IUGR was 18.2% and 84% were found to be asymmetrical. IUGR was found to be double among primigravids and women above 30 years. It had been observed that IUGR was associated with certain conditions like short stature (52%), pregnancy induced hypertension (24%) and anaemia (12%).Conclusions: Thus, early USG screening along with robust screening for maternal BMI, nutritional status, and anaemia can assist the obstetric team in providing early diagnosis, prompt intervention, and better outcome in pregnancy with fetal growth restriction.

scholarly journals Maternal proteomic profiling reveals alterations in lipid metabolism in late-onset fetal growth restriction

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Cristina Paules ◽  
Lina Youssef ◽  
Jezid Miranda ◽  
Francesca Crovetto ◽  
Josep Maria Estanyol ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Protein Interactions ◽  
Fetal Growth Restriction ◽  
Late Onset ◽  
Growth Restriction ◽  
Growth Potential ◽  
P Value ◽  
Biological Processes ◽  
Protein Protein Interactions

AbstractFetal growth restriction defined as the failure to achieve the fetal genetic growth potential is a major cause of perinatal morbidity and mortality. The role of maternal adaptations to placental insufficiency in this disorder is still not fully understood. We aimed to investigate the biological processes and protein–protein interactions involved in late-onset fetal growth restriction in particular. We applied 2D nano LC–MS/MS proteomics analysis on maternal blood samples collected at the time of delivery from 5 singleton pregnancies with late-onset fetal growth restriction and 5 uncomplicated pregnancies. Data were analyzed using R package “limma” and Ingenuity Pathway Analysis. 25 proteins showed significant changes in their relative abundance in late-onset fetal growth restriction (p value < 0.05). Direct protein–protein interactions network demonstrated that Neurogenic locus notch homolog protein 1 (NOTCH1) was the most significant putative upstream regulator of the observed profile. Gene ontology analysis of these proteins revealed the involvement of 14 canonical pathways. The most significant biological processes were efflux of cholesterol, efflux of phospholipids, adhesion of blood cells, fatty acid metabolism and dyslipidemia. Future studies are warranted to validate the potential role of the detected altered proteins as potential therapeutic targets in the late-onset form of fetal growth restriction.

205. Homeobox gene TGIF is increased in human idiopathic fetal growth restriction

2008 ◽  
Vol 20 (9) ◽  
pp. 5
Author(s):  
P. Murthi ◽  
N. Pathirage ◽  
A. Borg ◽  
S. Brennecke ◽  
B. Kalionis
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Homeobox Gene ◽  
Growth Restriction ◽  
Growth Potential ◽  
Mrna Levels ◽  
Developmental Abnormalities ◽  
Clinical Criteria ◽  
Targeted Mutation ◽  
Clinically Significant

Fetal Growth Restriction (FGR) is a clinically significant pregnancy disorder in which the fetus fails to achieve its full growth potential in utero. Recently, we identified a novel homeobox gene TGIF, in the placenta using microarray expression profiling (1). Targeted mutation of tgif in mouse results in placental dysfunction (2). In this study, we have investigated TGIF expression levels in idiopathic FGR. FGR-affected placental samples were collected based on strict clinical criteria to ensure inclusion of cases at the severe end of the spectrum of the disease. TGIF mRNA expression was analysed in placentae obtained from pregnancies complicated by idiopathic FGR and gestation-matched control pregnancies (n = 25 each). Real-time PCR showed a significant increase in TGIF mRNA levels in FGR-affected placentae and gestation-matched controls [1.29 ± 0.06 FGR v. 0.78 ± 0.04 Control, P < 0.001]. western blotting using a TGIF polyclonal antibody revealed significantly increased levels of TGIF protein in term FGR-affected placentae compared with term controls [3970 ± 1101 (n = 10) v. 2323 ± 644 (n = 10), P < 0.05]. The spatial distribution of TGIF protein by immunohistochemistry revealed immunoreactive TGIF protein in residual cytotrophoblast cells, syncytiotrophoblast cells, microvascular endothelial cells and in stromal cells. We conclude that increased expression of homeobox gene TGIF may be a contributing factor to the developmental abnormalities seen in the FGR-affected placentae. (1) Murthi P, Hiden U, Rajaraman G, Kalionis B. Placenta May 29, [Epub ahead of print]. (2) Bartholin L, Melhuish TA et al. Dev Biol. 2008 May 2. [Epub ahead of print].

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