title: Fetal biochemistry in growth retardation.
abstract: A substantial proportion of fetuses with severe early onset growth retardation are chromosomally abnormal and in these cases detailed ultrasound scanning will often demonstrate the presence of fetal anatomical defects. Chromosomally normal SGA fetuses with no biochemical abnormalities are likely to be normal small fetuses and seem to develop normally. SGA fetuses with evidence of impaired placental perfusion such as altered fetal cardiovascular dynamics and disturbances in biochemical, haematological, metabolic and endocrine status are at increased of neurodevelopmental delay. Although incomplete, the data collected so far suggest the biochemical changes may be caused by reduced placental transfer of nutrients (e.g. oxygen, glucose and essential amino-acids) and subsequent reduced fetal metabolism leading to high levels of substrates (e.g. triglycerides and non-essential amino-acids) and low levels of tissue products (e.g. thyroid hormone, insulin, platelets and white cells).
authors.affiliation: Harris-Birthright Research Centre for Fetal Medicine, Kings' College Hospital, London, UK.
authors.forename: P W
authors.initials: PW
authors.lastname: Soothill
authors.forename: R A
authors.initials: RA
authors.lastname: Ajayi
authors.forename: K N
authors.initials: KN
authors.lastname: Nicolaides
mesh_terms: D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007621:Karyotyping; D011247:Pregnancy; D011256:Pregnancy Outcome / Q000235:genetics