scholarly journals Diagnosis and Management of Fetal Growth Restriction

2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
Jacqueline E. A. K. Bamfo ◽  
Anthony O. Odibo
Keyword(s):  
Metabolic Syndrome ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Clinical Management ◽  
Later Life ◽  
Growth Restriction ◽  
Surveillance Program ◽  
Mortality And Morbidity ◽  
Diagnosis And Management ◽  
Biophysical Profile

Fetal growth restriction (FGR) remains a leading contributor to perinatal mortality and morbidity and metabolic syndrome in later life. Recent advances in ultrasound and Doppler have elucidated several mechanisms in the evolution of the disease. However, consistent classification and characterization regarding the severity of FGR is lacking. There is no cure, and management is reliant on a structured antenatal surveillance program with timely intervention. Hitherto, the time to deliver is an enigma. In this paper, the challenges in the diagnosis and management of FGR are discussed. The biophysical profile, Doppler, biochemical and molecular technologies that may refine management are reviewed. Finally, a model pathway for the clinical management of pregnancies complicated by FGR is presented.

scholarly journals Placenta-specific Slc38a2/SNAT2 knockdown causes fetal growth restriction in mice.

2021 ◽  
Author(s):  
Owen Vaughan ◽  
Katarzyna Maksym ◽  
Elena Silva ◽  
Kenneth Barentsen ◽  
Russel V Anthony ◽  
...  
Keyword(s):  
Amino Acid ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Late Onset ◽  
Specific Treatment ◽  
Later Life ◽  
Growth Restriction ◽  
Amino Acid Transport System ◽  
Mortality And Morbidity ◽  
Appropriate For Gestational Age

Fetal growth restriction (FGR) is a complication of pregnancy that reduces birth weight, markedly increases infant mortality and morbidity and is associated with later-life cardiometabolic disease.  No specific treatment is available for FGR. Placentas of human FGR infants have low abundance of sodium-coupled neutral amino acid transporter 2 (Slc38a2/SNAT2), which supplies the fetus with amino acids required for growth. We determined the mechanistic role of placental Slc38a2/SNAT2 deficiency in the development of restricted fetal growth, hypothesizing that placenta-specific Slc38a2 knockdown causes fetal growth restriction in mice. Using lentiviral transduction of blastocysts with a small hairpin RNA, we achieved 59% knockdown of placental Slc38a2, without altering fetal Slc38a2 expression. Placenta-specific Slc38a2 knockdown reduced near-term fetal and placental weight, fetal viability, trophoblast plasma membrane SNAT2 protein abundance, and both absolute and weight-specific placental uptake of the amino acid transport System A tracer, 14C-methylaminoisobutyric acid. We also measured human placental SLC38A2 gene expression in a well-defined term clinical cohort and found that SLC38A2 expression was decreased in late-onset, but not early-onset FGR, compared to appropriate for gestational age control placentas. The results demonstrate that low placental Slc38a2/SNAT2 causes fetal growth restriction and could be a target for clinical therapies for late-onset FGR.

scholarly journals Polish Society of Gynecologists and Obstetricians Recommendations on diagnosis and management of fetal growth restriction

2020 ◽  
Vol 91 (10) ◽  
pp. 634-643
Author(s):  
Sebastian Kwiatkowski ◽  
Andrzej Torbe ◽  
Dariusz Borowski ◽  
Grzegorz Breborowicz ◽  
Krzysztof Czajkowski ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Diagnosis And Management ◽  
Polish Society

scholarly journals Early‐onset fetal growth restriction: A systematic review on mortality and morbidity

2019 ◽  
Vol 99 (2) ◽  
pp. 153-166 ◽  
Author(s):  
Anouk Pels ◽  
Irene M. Beune ◽  
Aleid G. van Wassenaer‐Leemhuis ◽  
Jacqueline Limpens ◽  
Wessel Ganzevoort
Keyword(s):  
Systematic Review ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Early Onset ◽  
Growth Restriction ◽  
Mortality And Morbidity
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