The Australian & New Zealand journal of obstetrics & gynaecology · 2018
Placental growth factor as an indicator of fetal growth restriction in late-onset small-for-gestational age pregnancies.
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Anderson Ngaire, De Laat Monique, Benton Samantha, von Dadelszen Peter, McCowan Lesley
Аннотация
BACKGROUND: At-risk small-for-gestational age (SGA) pregnancies in New Zealand are identified using Doppler ultrasound; fetuses with Doppler abnormalities are considered growth restricted (FGR). Low maternal placental growth factor (PlGF) has also been associated with late-onset FGR.
AIMS: To investigate whether low PlGF at diagnosis of late-onset SGA identifies the same fetuses classified FGR by detailed Doppler studies, and the association between low PlGF and adverse pregnancy outcomes.
METHODS: Among an historical database of normotensive suspected SGA pregnancies (fetal abdominal circumference <10th percentile) ≥32 weeks gestation, the ability of low PlGF (<5th percentile) to identify FGR infants was investigated. 'Initial FGR' was an abnormal umbilical artery resistance index (RI) or estimated fetal weight <3rd customised centile. 'Secondary FGR' was abnormal internal carotid RI, cerebro-placental ratio and/or mean uterine artery RI. Development of hypertensive disease and adverse perinatal outcomes were compared by PlGF status.
RESULTS: Of 136 SGA pregnancies, 56 (41.1%) had initial FGR. Of the remaining, 20 (25.0%) had secondary FGR, 17 (21.3%) low PlGF. The sensitivity of low PlGF identifying secondary FGR was 0.30 (95% CI 0.14-0.50), specificity 0.83 (0.70-0.92), positive predictive value 0.47 (0.23-0.72) and negative predictive value 0.70 (0.57-0.81). Overall, low PlGF occurred in 44/136 (32.4%) pregnancies and was associated with gestational hypertensive disease (63.6% vs 15.2%, P < 0.01), adverse perinatal outcome (34.1% vs 15.2%, P = 0.01) and very low birthweight (customised centile 2.2 vs 6.8, P < 0.01).
CONCLUSIONS: At diagnosis of late-onset SGA, low PlGF was poor at identifying Doppler-defined FGR. Low PlGF identified pregnancies at risk of hypertensive disease, adverse perinatal outcome and very low birthweight.
AIMS: To investigate whether low PlGF at diagnosis of late-onset SGA identifies the same fetuses classified FGR by detailed Doppler studies, and the association between low PlGF and adverse pregnancy outcomes.
METHODS: Among an historical database of normotensive suspected SGA pregnancies (fetal abdominal circumference <10th percentile) ≥32 weeks gestation, the ability of low PlGF (<5th percentile) to identify FGR infants was investigated. 'Initial FGR' was an abnormal umbilical artery resistance index (RI) or estimated fetal weight <3rd customised centile. 'Secondary FGR' was abnormal internal carotid RI, cerebro-placental ratio and/or mean uterine artery RI. Development of hypertensive disease and adverse perinatal outcomes were compared by PlGF status.
RESULTS: Of 136 SGA pregnancies, 56 (41.1%) had initial FGR. Of the remaining, 20 (25.0%) had secondary FGR, 17 (21.3%) low PlGF. The sensitivity of low PlGF identifying secondary FGR was 0.30 (95% CI 0.14-0.50), specificity 0.83 (0.70-0.92), positive predictive value 0.47 (0.23-0.72) and negative predictive value 0.70 (0.57-0.81). Overall, low PlGF occurred in 44/136 (32.4%) pregnancies and was associated with gestational hypertensive disease (63.6% vs 15.2%, P < 0.01), adverse perinatal outcome (34.1% vs 15.2%, P = 0.01) and very low birthweight (customised centile 2.2 vs 6.8, P < 0.01).
CONCLUSIONS: At diagnosis of late-onset SGA, low PlGF was poor at identifying Doppler-defined FGR. Low PlGF identified pregnancies at risk of hypertensive disease, adverse perinatal outcome and very low birthweight.