scholarly journals Clinical and pathogenetic variants of fetal growth restriction with different periods of manifestation

2021 ◽  
pp. 54-65
Author(s):  
I. S. Lipatov ◽  
Yu. V. Tezikov ◽  
M. S. Amosov ◽  
E. M. Zumorina
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Clinical Laboratory ◽  
Growth Parameters ◽  
Human Life ◽  
Clinical Manifestations ◽  
Fetal Brain ◽  
Growth Restriction ◽  
Growth Potential ◽  
Obstetric Management

The article presents data on the clinical and pathogenetic variants of fetal growth restriction (FGR). FGR is one of the typical clinical manifestations of large obstetric syndromes, is associated with a high perinatal morbidity and has a significant impact on the quality and duration of human life. The emphasis is made on the differences in pathogenesis, the features of prediction, diagnosis, obstetric management and the assessment of perinatal outcomes in the early and late phenotype of the FGR. The review includes materials from domestic and foreign scientific literature that found in eLibrary and PubMed on this topic and published for the last 10 years. This article discusses the role of the formation of the embryo(feto)placental system under the influence of existing periconceptional risk factors in the implementation of various phenotypes of FGR. An analysis of the literature shows that the fetal growth potential, which genetically and epigenetically determined, changes during pregnancydepending on maternal, placental and fetal factors, which ultimately determine the final weight-growth parameters of the newborn. The issues of informativeness of clinical, laboratory and instrumental predictors, diagnostic criteria, the choice of rational obstetric management in case of FGR of various periods of manifestation are discussed in this article. Convincing data on the perinatal and long-term consequences of intrauterine growth restriction are presented. The pathogenetic variant of FGR determines the features of the functioning of the immune system, has a significant impact on the programming of metabolic and endocrine processes, the formation of fetal brain structures. Identification of pregnant women at risk for the development of FGR of various periods of manifestation, timely diagnosis, selection of the timing and method of delivery should correspond to the main directions of the "4P-model" of modern medicine and represent an integral predictive, preventive and personalized system of examination and observation based on evidence-based medicine data and the requirements of practical obstetrics and perinatology.

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

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)

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

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.

scholarly journals Quantification of fetal organ sparing in maternal low-protein dietary models

2021 ◽  
Vol 6 ◽  
pp. 218
Author(s):  
Patricia Serpente ◽  
Ying Zhang ◽  
Eva Islimye ◽  
Sarah Hart-Johnson ◽  
Alex P. Gould
Keyword(s):  
Protein Content ◽  
Fetal Growth ◽  
Dietary Protein ◽  
Fetal Growth Restriction ◽  
Fetal Brain ◽  
Growth Restriction ◽  
Maternal Malnutrition ◽  
Fetal Organ ◽  
Low Protein ◽  
Organ Sparing

Background: Maternal malnutrition can lead to fetal growth restriction. This is often associated with organ sparing and long-lasting physiological dysfunctions during adulthood, although the underlying mechanisms are not yet well understood. Methods: Low protein (LP) dietary models in C57BL/6J mice were used to investigate the proximal effects of maternal malnutrition on fetal organ weights and organ sparing at embryonic day 18.5 (E18.5). Results:  Maternal 8% LP diet induced strikingly different degrees of fetal growth restriction in different animal facilities, but adjustment of dietary protein content allowed similar fetal body masses to be obtained. A maternal LP diet that restricted fetal body mass by 40% did not decrease fetal brain mass to the same extent, reflecting positive growth sparing of this organ. Under these conditions, fetal pancreas and liver mass decreased by 60-70%, indicative of negative organ sparing. A series of dietary swaps between LP and standard diets showed that the liver is capable of efficient catch-up growth from as late as E14.5 whereas, after E10.5, the pancreas is not. Conclusions: This study highlights that the reproducibility of LP fetal growth restriction studies between laboratories can be improved by careful calibration of maternal dietary protein content. LP diets that induce 30-40% restriction of prenatal growth provide a good model for fetal organ sparing. For the liver, recovery of growth following protein restriction is efficient throughout fetal development but, for the pancreas, transient LP exposures spanning the progenitor expansion phase lead to an irreversible fetal growth deficit.

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)

scholarly journals OP17.08: Assessment of fetal brain volume by tridimensional ultrasound in fetal growth restriction

2012 ◽  
Vol 40 (S1) ◽  
pp. 107-107
Author(s):  
A. R. Caetano ◽  
A. P. Zamarian ◽  
R. Cavalcante ◽  
D. Soares ◽  
P. M. Nowak ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Brain Volume ◽  
Fetal Brain ◽  
Growth Restriction

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.

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