Total and Fetal Cell-Free DNA Analysis in Maternal Blood as Markers of Placental Insufficiency in Intrauterine Growth Restriction

2009 ◽  
Vol 26 (1) ◽  
pp. 24-28 ◽  
Author(s):  
M. Al Nakib ◽  
R. Desbrière ◽  
N. Bonello ◽  
F. Bretelle ◽  
L. Boubli ◽  
...  



2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Dong Wook Kwak ◽  
Shin Young Kim ◽  
Hyun Jin Kim ◽  
Ji Hyae Lim ◽  
Young-Han Kim ◽  
...  


2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Raj Raghupathy ◽  
Majedah Al-Azemi ◽  
Fawaz Azizieh

Intrauterine growth restriction (IUGR) is an important perinatal syndrome that poses several serious short- and long-term effects. We studied cytokine production by maternal peripheral blood lymphocytes stimulated by trophoblast antigens. 36 women with a diagnosis of IUGR and 22 healthy women with normal fetal growth were inducted. Peripheral blood mononuclear cells were stimulated with trophoblast antigens and levels of the proinflammatory cytokines IL-6, IL-8, IL-12, IL-23, IFNγ, and TNFα and the anti-inflammatory cytokines IL-4, IL-10, and IL-13 were measured in culture supernatants by ELISA. IL-8 was produced at higher levels by blood cells of the IUGR group than normal pregnant women, while IL-13 was produced at lower levels. IL-8, IFNγ, and TNFα were higher in IUGR with placental insufficiency than in normal pregnancy. IL-12 levels were higher and IL-10 levels were lower in IUGR with placental insufficiency than in IUGR without placental insufficiency. We suggest that a stronger pro-inflammatory bias exists in IUGR as compared to normal pregnancy and in IUGR with placental insufficiency when compared to IUGR without placental insufficiency. Several ratios of proinflammatory to anti-inflammatory cytokines also support the existence of an inflammatory bias in IUGR.



PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0208508 ◽  
Author(s):  
M. Rohan Fernando ◽  
Chao Jiang ◽  
Gary D. Krzyzanowski ◽  
Tifany Somer-Shely ◽  
Wayne L. Ryan


2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Erich Cosmi ◽  
Tiziana Fanelli ◽  
Silvia Visentin ◽  
Daniele Trevisanuto ◽  
Vincenzo Zanardo

Intrauterine growth restriction is a condition fetus does not reach its growth potential and associated with perinatal mobility and mortality. Intrauterine growth restriction is caused by placental insufficiency, which determines cardiovascular abnormalities in the fetus. This condition, moreover, should prompt intensive antenatal surveillance of the fetus as well as follow-up of infants that had intrauterine growth restriction as short and long-term sequele should be considered.



2018 ◽  
Vol 45 (5) ◽  
pp. 302-311 ◽  
Author(s):  
Elisa Bevilacqua ◽  
Jacques C. Jani ◽  
Alexandra Letourneau ◽  
Silvia F. Duiella ◽  
Pascale Kleinfinger ◽  
...  


2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
D. T. Yates ◽  
A. S. Green ◽  
S. W. Limesand

Placental insufficiency (PI) prevents adequate delivery of nutrients to the developing fetus and creates a chronic state of hypoxemia and hypoglycemia. In response, the malnourished fetus develops a series of stress hormone-mediated metabolic adaptations to preserve glucose for vital tissues at the expense of somatic growth. Catecholamines suppress insulin secretion to promote glucose sparing for insulin-independent tissues (brain, nerves) over insulin-dependent tissues (skeletal muscle, liver, and adipose). Likewise, premature induction of hepatic gluconeogenesis helps maintain fetal glucose and appears to be stimulated by both norepinephrine and glucagon. Reduced glucose oxidation rate in PI fetuses creates a surplus of glycolysis-derived lactate that serves as substrate for hepatic gluconeogenesis. These adrenergically influenced adaptive responses promotein uterosurvival but also cause asymmetric intrauterine growth restriction and small-for-gestational-age infants that are at greater risk for serious metabolic disorders throughout postnatal life, including obesity and type II diabetes.



2014 ◽  
Vol 45 (1) ◽  
pp. 36-41 ◽  
Author(s):  
M. S. Quezada ◽  
M. M. Gil ◽  
C. Francisco ◽  
G. Oròsz ◽  
K. H. Nicolaides


2009 ◽  
Vol 16 (7) ◽  
pp. 701-711 ◽  
Author(s):  
Vasilis Sitras ◽  
Ruth Paulssen ◽  
Jørn Leirvik ◽  
Åse Vårtun ◽  
Ganesh Acharya




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