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A New Approach for Classifying Fetal Growth Restriction.

ABSTRACT:

Background

Fetal growth restriction is commonly defined using small for gestational age (SGA) birth (birthweight < 10th percentile) as a proxy, but this approach is problematic because most SGA infants are small but healthy. In this proof-of-concept study, we sought to develop a new approach for identifying fetal growth restriction at birth that combines information on multiple, imperfect measures of fetal growth restriction in a probabilistic manner.

Methods

We combined information on birthweight, placental weight, placental malperfusion lesions, maternal disease, and fetal acidemia using latent profile analysis to classify fetal growth in births at the Royal Victoria Hospital in Montreal, Canada, 2001-2009. We examined the clinical characteristics and health outcomes of infants classified as growth-restricted and nongrowth-restricted by our model, and among the subgroup of growth-restricted infants who had a birthweight ≥10th percentile (i.e., would have been missed by the conventional SGA proxy).

Results

Among 26,077 births, 345 (1.3%) were classified as growth-restricted by our latent profile model. Growth-restricted infants were more likely than nongrowth-restricted infants to have an Apgar score <7 (10% vs. 2%), have hypoglycemia at birth (17% vs. 3%), require neonatal intensive care unit admission (59% vs. 6%), die in the perinatal period (3.8% vs. 0.2%), and require an emergency cesarean delivery (42% vs. 15%). Risks remained elevated in growth-restricted infants who were not SGA, suggesting our model identified at-risk infants not detected using the SGA proxy.

Conclusions

Latent profile analysis is a promising strategy for classifying growth restriction at birth in fetal growth restriction research.

SUBMITTER: Hutcheon JA

PROVIDER: S-EPMC8478298 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Fetal growth restriction (FGR) occurs when the fetus does not reach its genetically programmed intrauterine potential for growth and affects ~5‑10% of pregnancies. This condition is one of the leading causes of perinatal mortality and morbidity associated with obstetric and neonatal complications. Placental dysfunction in FGR causes an impairment in the transfer of nutrients and oxygen from the mother to the developing fetus. Maternal adaptations to placental insufficiency may also play a role in the pathophysiology of FGR. The present study aimed to compare the proteome of the placentas of 18 women with the physiological course of pregnancy and eutrophic fetus [estimated fetal weight (EFW) >10th percentile; control group] and 18 women with late FGR (EFW <10th percentile) diagnosed after 32 weeks of pregnancy, according to the Delphi consensus (study group). The U. Mann‑Whitney test was used to compare two independent groups. The R. Spearman correlation coefficient significance test was used to assess the existence of a relationship between the analyzed measurable parameters. P<0.05 was considered to indicate a statistically significant difference. The tests showed the presence of 356 different proteins which were responsible for the regulation of gene transcription control, inhibiting the activity of proteolytic enzymes, regulation of trophoblast proliferation and angiogenesis and inflammatory response. In the FGR placental proteome, other detected proteins were mostly involved in response to oxidative stress, cellular oxidation and detoxication, apoptosis, hemostatic and catabolic processes, energy transduction protein interactions, cell proliferation, differentiation and intracellular signaling. The present study used chromatographic mass‑spectrometry to compare the placental proteome profiles in pregnancies complicated by late‑onset FGR and normal pregnancy. Comparative analysis of proteomes from normal and FGR placentas showed significant differences. Further research is needed to clarify maternal and fetal adaptations to FGR.