Early onset fetal growth restriction (FGR) may be due to impaired placentation, environmental or toxic exposure, congenital infections or genetic abnormalities. Remarkable research, mainly based on retrospective series, has been published on the diverse genetic causes. Those have become more and more relevant with the improvement in the accuracy of the analysis techniques and the rising of breakthrough genomewide methods such as the whole genome sequencing. However, no publication has presented an integrated view of management of those fetuses with an early and severe affection. In this review, we explored to which extent genetic syndromes can cause FGR fetuses without structural defects. The most common chromosomal abnormalities (Triploidies and Trisomy 18), submicroscopic chromosomal anomalies (22q11.2 microduplication syndrome) and single gene disorders (often associated with mild ultrasound findings) related to early and severe FGR had been analysed. Finally, we addressed the impact of epigenetic marks on fetal growth, a matter of growing importance. At the end of this review, we should be able to provide an adequate counseling to parents in terms of diagnosis, prognosis and management of those pregnancies.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/pd.5635 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Comparative anatomy of the subclavius muscle and clavicle: a histological study using human, swine and mouse fetuses.
Folia Morphol (Warsz)
January 2025
Department of Histology and Developmental Biology, Tokyo Dental College, Tokyo, Japan.
Background: Some mammals including the swine carry a fibrous vestigial clavicle, but a subclavius muscle (SBM) extends between the first rib and the supraspinatus muscle surface fascia. We aimed to examine development of the SBM and clavicle for finding a specific factor to provide the curious morphology.
Materials And Methods: Histological sections of early- and midterm fetuses of the swine, human and mouse were observed and compared at the almost same morphological stage.
Chronic nicotine exposure induces molecular and transcriptomic endophenotypes associated with mood and anxiety disorders in a cerebral organoid neurodevelopmental model.
Front Pharmacol
December 2024
Addiction Research Group, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
Introduction: Prenatal nicotine exposure (PNE) from maternal smoking disrupts regulatory processes vital to fetal development. These changes result in long-term behavioral impairments, including mood and anxiety disorders, that manifest later in life. However, the relationship underlying PNE, and the underpinnings of mood and anxiety molecular and transcriptomic phenotypes remains elusive.
View Article and Find Full Text PDFBackground Fetal growth restriction (FGR) is a leading risk factor for stillbirth, yet the diagnosis of FGR confers considerable prognostic uncertainty, as most infants with FGR do not experience any morbidity. Our objective was to use data from a large, deeply phenotyped observational obstetric cohort to develop a probabilistic graphical model (PGM), a type of "explainable artificial intelligence (AI)", as a potential framework to better understand how interrelated variables contribute to perinatal morbidity risk in FGR. Methods Using data from 9,558 pregnancies delivered at ≥ 20 weeks with available outcome data, we derived and validated a PGM using randomly selected sub-cohorts of 80% (n = 7645) and 20% (n = 1,912), respectively, to discriminate cases of FGR resulting in composite perinatal morbidity from those that did not.
View Article and Find Full Text PDFWhile most pregnancies are affected by nausea and vomiting, hyperemesis gravidarum (HG) is at the severe end of the clinical spectrum and is associated with dehydration, undernutrition, and adverse maternal, fetal, and child outcomes. Herein we performed a multi-ancestry genome-wide association study (GWAS) of severe nausea and vomiting of pregnancy of 10,974 cases and 461,461 controls across European, Asian, African, and Latino ancestries. We identified ten significantly associated loci, of which six were novel ( , , , , , and and confirmed previous genome-wide significant associations with risk genes , , , and .
View Article and Find Full Text PDFElevated levels of exogenous prolactin promote inflammation at the maternal-fetal interface via the JAK2/STAT5B signaling axis.
Front Immunol
December 2024
Department of Microbiology, Biochemistry, and Immunology, Morehouse School of Medicine, Atlanta, GA, United States.
The placenta is a unique organ with various immunological and endocrinological roles that modulate maternal and fetal physiology to promote maternal-fetal tolerance, pregnancy maintenance, and parturition at term. During pregnancy, the hormone prolactin (PRL) is constitutively secreted by the placenta and is necessary for implantation, progesterone support, fetal development, and overall immune modulation. While PRL is essential for pregnancy, studies suggest that elevated levels of serum PRL (hyperprolactinemia) are associated with adverse pregnancy outcomes, including miscarriage, preterm birth, and preeclampsia.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!