scholarly journals Maternal exposure to bisphenol A induces fetal growth restriction via upregulating the expression of estrogen receptors.

Chemosphere ◽  
2021 ◽  
pp. 132244
Author(s):  
Yuming Cao ◽  
Zhenlie Chen ◽  
Ming Zhang ◽  
Lei Shi ◽  
Songling Qin ◽  
...  
2013 ◽  
Vol 10 (12) ◽  
pp. 7001-7014 ◽  
Author(s):  
Igor Burstyn ◽  
Jonathan Martin ◽  
Sanjay Beesoon ◽  
Fiona Bamforth ◽  
Qiaozhi Li ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2426
Author(s):  
Nikolaos Vrachnis ◽  
Nikolaos Loukas ◽  
Dionysios Vrachnis ◽  
Nikolaos Antonakopoulos ◽  
Dimitrios Zygouris ◽  
...  

Bisphenol A (BPA), a ubiquitous endocrine-disrupting chemical (EDC), is increasingly hypothesized to be a factor contributing to changes in fetal growth velocity. BPA exposure may be environmental, occupational, and/or dietary, with canned foods and plastic bottles contributing significantly. Our systematic review aims to evaluate the current literature and to investigate the role of BPA in abnormal fetal growth patterns. A search was conducted in the PubMed and Cochrane databases. A total of 25 articles met the eligibility criteria and were included in this systematic review. Eleven of them failed to show a clear relationship between BPA and abnormal fetal growth. The majority of the remaining studies (9/14) found an inverse association of BPA with indicators of fetal growth, whereas three studies suggested increased fetal growth, and two studies produced contradictory findings. Of note, both of the studies that collected a sample (amniotic fluid) directly reflecting BPA concentration in the fetus during the first half of pregnancy revealed an inverse association with birth weight. In conclusion, there is mounting evidence that combined exposure to BPA from dietary and non-dietary sources during pregnancy may contribute to abnormal fetal growth; a tendency towards fetal growth restriction was shown, especially when exposure occurs during the first half.


Author(s):  
Yakubova D.I.

Objective of the study: Comprehensive assessment of risk factors, the implementation of which leads to FGR with early and late manifestation. To evaluate the results of the first prenatal screening: PAPP-A, B-hCG, made at 11-13 weeks. Materials and Methods: A retrospective study included 110 pregnant women. There were 48 pregnant women with early manifestation of fetal growth restriction, 62 pregnant women with late manifestation among them. Results of the study: The risk factors for the formation of the FGR are established. Statistically significant differences in the indicators between groups were not established in the analyses of structures of extragenital pathology. According to I prenatal screening, there were no statistical differences in levels (PAPP-A, b-hCG) in the early and late form of FGR.


2018 ◽  
pp. 184-195
Author(s):  
Minh Son Pham ◽  
Vu Quoc Huy Nguyen ◽  
Dinh Vinh Tran

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)


Author(s):  
I.V. Komarova, A.A. Nikiforenko, A.V. Fedunyak

Literature reports of placental mosaicism, including trisomy 22, were analyzed. The chance of correlation of placental aneuploidy with fetus aneuploidy, also the probability of complications in pregnancy and fetal growth restriction and postnatal patients growth in the cases of confined placental mosaicism, were demonstrated. The case of prenatal diagnosis of confined placental mosaicism of trisomy 22 with favorable outcome is presented. The necessity of cytogenic assay of amniocytes and fetal lymphocytes in the case of placental heteroploidy diagnosis was emphasized.


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