Disease relevance of Placental Insufficiency

• Hypoxia or hyperoxia in placental insufficiency [1]?
• Thus, pancreatic islets from nutritionally deprived IUGR fetuses caused by chronic placental insufficiency have impaired insulin secretion caused by reduced glucose-stimulated glucose oxidation rates, insulin biosynthesis, and insulin content [2].
• Preeclampsia and other chronic placental insufficiency syndromes are accompanied by prostacyclin deficiency in the mother and in fetomaternal tissues and by an overproduction of thromboxane A2, at least in the placenta [3].
• Lesions of the uteroplacental vasculature may be involved in the pathogenesis of "placental insufficiency" in pregnancies complicated by hypertension, diabetes, systemic lupus erythematosus, and idiopathic fetal growth retardation [4].
• Heritable hypofibrinolysis, mediated by 4G/4G homozygosity for the PAI-1 gene, is an independent significant, potentially reversible risk factor for pregnancy complications, probably acting through thrombotic induction of placental insufficiency [5].

High impact information on Placental Insufficiency

• Maternal decidual IGFBP-1 excess is also associated with impaired fetal growth in midgestation independent of fetal genotype, indicating placental insufficiency [6].
• Decrease prostacyclin production: a characteristic of chronic placental insufficiency syndromes [7].
• It contributes to placental glucose homeostasis and may be a therapeutic target in diseases ranging from placental insufficiency to diabetes in pregnancy [8].
• We determined in vivo and in vitro pancreatic islet insulin secretion and glucose metabolism in fetuses with intrauterine growth restriction (IUGR) caused by chronic placental insufficiency to identify functional deficits in the fetal pancreas that might be caused by nutrient restriction [2].
• The relationship between transplacental O2 diffusion and placental expression of PlGF, VEGF and their receptors in a placental insufficiency model of fetal growth restriction [9].

Chemical compound and disease context of Placental Insufficiency

• In experimental fetal growth restriction, induced by placental insufficiency, the morphology and number of dopaminergic amacrine cells as identified by tyrosine hydroxylase staining were examined [10].
• The increased EFL that occurred after exposure to TCDD might reflect a toxic response initially mediated via endocrine imbalance, leading to placental insufficiency, compromised embryonic circulation, and subsequent EFL [11].
• Therefore, we have used umbilicoplacental embolization to mimic chronic placental insufficiency during late gestation in sheep, to investigate the expression of the steroidogenic enzymes p450scc, 5alpha-reductase type I (5alphaRI), 5alpha-reductase type II (5alphaRII), and allopregnanolone (AP) content in the fetal brain [12].
• Three hundred sixty-two pregnant patients at risk for placental insufficiency were evaluated with the oxytocin challenge test (OCT) and urinary estriol determinations [13].
• Angiotensin sensitivity predicts aspirin benefit in placental insufficiency [14].

Anatomical context of Placental Insufficiency

• Disruption of the Mash2 gene leads to early intrauterine death caused by placental insufficiency with an absent spongiotrophoblast and an underdeveloped chorion [15].
• Moreover, the amniotic fluid levels of the three peptides were evaluated in 20 other pregnant women affected by different pathologic conditions (Cooley's disease, gestosis, diabetes, placental insufficiency, etc.). A silicic acid extraction procedure was performed on the samples [16].
• CONCLUSION: The analysis of velocity waveforms from inferior vena cava and middle cerebral artery can be used to predict acid-base status in growth retarded fetuses secondary to placental insufficiency [17].
• Infants born to the women with placental insufficiency had significantly lower mean FT4 (p = 0.001), TSH (p = 0.002) and rT3 values (p = 0.025) in cord blood, and higher rT3 values on d 5 (p = 0.019) and d 7 (p = 0.025) [18].

Gene context of Placental Insufficiency

• Furthermore, alterations in VEGF, VEGFR-1 and VEGFR-2 mRNA expression, during the period of maximal placental growth, may contribute to the development of placental insufficiency, and ultimately intrauterine growth restriction [19].
• SP-C mRNA tissue levels were not significantly affected by placental insufficiency [20].
• Maternal serum beta-hCG and VEGF concentrations did not correlate except in women with placental insufficiency [21].
• On the contrary, there was no difference in either the TNF-alpha level [1.4 pg/mL (0-4.9)] or the rate of detectable TNF-alpha[57.1% (8/14)] between women with IUGR without placental insufficiency and women in the control group [22].
• These data suggest that, in some patients with recurrent fetal loss, hereditary and acquired APC resistance are potential causes of vascular placental insufficiency [23].

Analytical, diagnostic and therapeutic context of Placental Insufficiency

• HPL and estriol serum levels of placental perfusion as indexes of placental function in EPH gestosis and placental insufficiency [24].

References