Abstract
SGA is often defined as a birth weight and/or length < −2 SDS for gestational age and gender [43]. A frequent cause of SGA is fetal growth restriction (FGR), often associated with perinatal mortality and morbidity and also implicated in a higher risk of cardio-metabolic disease in adulthood. Currently, no tools are available to predict or prevent FGR. Both genetic and environmental factors may affect fetal growth, but the underlying molecular mechanisms are still unclear. Genetic and epigenetic factors account for 30-50% of the variation in birth weight [44]. Chromosomal anomalies account for up to 19% of FGR fetuses, while the rate of submicroscopic duplications/deletions and single-gene disorders in FGR with normal karyotype is not defined [44]. A recent study showed that genomic microarray analysis (CMA) identifies sub-microscopic anomalies in 6.8% of fetuses with early growth restriction after common aneuploidies were excluded [45]. To date, the use of CMA is recommended for a fetus with one or more major malformations identified by ultrasound. Epigenetic mechanisms also explain abnormal fetal growth in conditions such as Silver-Russell and Beckwith-Wiedemann syndrome.
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