scholarly journals Placental Insufficiency and Fetal Growth Restriction

2011 ◽  
Vol 61 (5) ◽  
pp. 505-511 ◽  
Author(s):  
Usha Krishna ◽  
Sarita Bhalerao
2021 ◽  
Vol 74 (2) ◽  
pp. 213-219
Author(s):  
Varvara A. Berezhna ◽  
Tetiana V. Mamontova ◽  
Antonina M. Gromova

The aim: To elucidate the possible involvement of M1 and M2 macrophages in the placentas of women, whose pregnancies were complicated by fetal growth restriction (FGR) and resulted in term births after 37 weeks of gestation and preterm births up to 37 weeks of gestation. Materials and methods: CD68+ and CD163+ macrophages were studied by immunohistochemical method, placental morphology in the placentas of 16 women whose pregnancies were complicated by FGR and resulted in term births at a gestational age after 37 weeks (1-st group, n = 7) or resulted in preterm births at a gestational age up to 37 weeks (2-nd group, n = 9). The control group consisted of 10 placentas of women with physiological pregnancies and births. Results: Women 2-nd group showed significantly low weight of the placenta, a short gestation period at the time of delivery, and a prolonged labor period than women of the control group (p <0.001; p <0.001; p <0.05, respectively). The level of CD68+ and CD163+ macrophages in the placentas of women 2-nd group was significantly higher than in woman 1-st group (p <0.001, p <0.001, respectively). A significant correlation was found between the expression level of CD68+ monocytes in the intervillous space and the weight of a newborn (r = – 0.765; p = 0.016) in women 2-nd group. Conclusions: These studies suggest that in the placentas of women whose pregnancies were complicated by FGR and resulted in preterm births, the increased activation of CD68+ macrophages of the pro-inflammatory pool may be associated with disorders of the vascular and stromal component of the villous chorion with the development of involutive and dystrophic changes. In general, this fact probably determines the progress of chronic placental insufficiency and aggravates the development of fetal growth restriction.


Author(s):  
Ilaria Fantasia ◽  
Sofia Bussolaro ◽  
Tamara Stampalija ◽  
Daniel Rolnik

Background: Pregnancies complicated by placental insufficiency are characterised by increased oxidative stress. It has been suggested that melatonin has antioxidant properties and contributes to the maintenance of placental homeostasis. Objective: To systematically review the available literature about melatonin in pregnancies complicated by placental insufficiency, specifically preeclampsia and fetal growth restriction, exploring three different aspects: 1) maternal melatonin levels; 2) expression and activity of melatonin placental receptors; 3) effects of maternal melatonin administration. Search strategy: PubMed (Medline) and Scopus were searched until December 2020. Selection criteria: Published literature in English language describing the role of melatonin in pregnancies complicated by placental insufficiency, with a specific focus on preeclampsia and fetal growth restriction. Data collection and analysis: Identified studies were screened and assessed independently by two authors. Data were extracted and compiled in a qualitative evidence synthesis. Main results: Pregnancies complicated by placental insufficiency show a significant reduction in maternal systemic serum melatonin levels and a significant reduction in the expression of placental melatonin receptors. Melatonin administration in pregnancy seems safe and may reduce oxidative stress. Conclusion: The circadian pattern of melatonin secretion seems to be altered in pregnancies complicated by placental insufficiency. This is reflected by lower production of melatonin, with consequent lower systemic and placental concentrations, and lower expression of melatonin receptors, thus reducing the local release of the indole and its autocrine function. Funding: None Keywords: Melatonin, Preeclampsia, Fetal growth restriction, Placental insufficiency, Review.


2019 ◽  
Vol 39 (9) ◽  
pp. 1196-1203
Author(s):  
Claire Blythe ◽  
Rita E. Zapata Vazquez ◽  
Maria S. Cabrera ◽  
Sandra Zekic Tomas ◽  
Dilly OC Anumba ◽  
...  

2021 ◽  
Vol 22 (8) ◽  
pp. 4186
Author(s):  
Anna Kajdy ◽  
Jan Modzelewski ◽  
Aneta Cymbaluk-Płoska ◽  
Ewa Kwiatkowska ◽  
Magdalena Bednarek-Jędrzejek ◽  
...  

Abnormally accelerated, premature placental senescence plays a crucial role in the genesis of pregnancy pathologies. Abnormal growth in the third trimester can present as small for gestational age fetuses or fetal growth restriction. One differs from the other by the presence of signs of placental insufficiency and the risk of stillbirth. The majority of stillbirths occur in normally grown fetuses and are classified as “unexplained”, which often leads to conclusions that they were unpreventable. The main characteristic of aging is a gradual decline in the function of cells, tissues, and organs. These changes result in the accumulation of senescent cells in mitotic tissues. These cells begin the aging process that disrupts tissues’ normal functions by affecting neighboring cells, degrading the extracellular matrix, and reducing tissues’ regeneration capacity. Different degrees of abnormal placentation result in the severity of fetal growth restriction and its sequelae, including fetal death. This review aims to present the current knowledge and identify future research directions to understand better placental aging in late fetal growth restriction and unexplained stillbirth. We hypothesized that the final diagnosis of placental insufficiency can be made only using markers of placental senescence.


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