The value of angiogenetic biomarkers in the detection of early onset fetal growth restriction

•The diagnosis of fetal growth restriction (FGR) due to uteroplacental insufficiency improves perinatal outcome.•Using angiogenic markers to diagnose small for gestational age fetuses can enhance the current diagnostic FGR consensus.•Further studies are needed to integrate angiogenic markers into ul...

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Published in:European journal of obstetrics & gynecology and reproductive biology 2024-08, Vol.299, p.91-95
Main Authors: Giorgione, Veronica, Ramnarine, Stephan, Malik, Amna, Bhide, Amarnath
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Language:English
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Angiogenic markers
Fetal growth restriction
Uteroplacental insufficiency
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description •The diagnosis of fetal growth restriction (FGR) due to uteroplacental insufficiency improves perinatal outcome.•Using angiogenic markers to diagnose small for gestational age fetuses can enhance the current diagnostic FGR consensus.•Further studies are needed to integrate angiogenic markers into ultrasound parameters currently used for FGR diagnosis. The identification of fetal growth restriction (FGR) due to uteroplacental insufficiency is important to improve perinatal outcomes. To distinguish FGR from small for gestational age (SGA), FGR consensus definition is currently based on biometry and/or additional biophysical parameters. This study aims to verify if this definition might be modified by including circulating angiogenic factors. This historical cohort study included singleton pregnancies with SGA fetuses after 20 weeks. All patients underwent detailed ultrasound and measurements of soluble fms-like tyrosine kinase 1 (sFlt-1) and placental growth factor (PlGF) at first assessment. ISUOG criteria for FGR were applied. Total PlGF was calculated using free PlGF, sFlt-1 and a receptor pharmacology model, and multiple of the median (MoM) values for sFlt-1, free PlGF, total PlGF and sFlt-1/PlGF ratio were calculated to adjust for gestational age. 72 pregnancies with SGA were first evaluated at median (IQR) of 28+5 (26+2 –31+3) weeks’ gestation, and 51 fetuses (70.8 %) satisfied the FGR consensus definition. Pregnancies with FGR showed significantly lower levels of free and total PlGF MoM (0.12, 95 % IQR: 0.07–0.36 vs 0.32, 95 % IQR: 0.20–0.53, p = 0.008) and 0.26, 95 % CI: 0.16–0.55 vs 0.43, 95 % IQR: 0.23–0.53, p = 0.028) respectively; and higher sFlt-1 MoM (4.62, 95 % IQR: 1.80–7.30 vs 1.74, 95 % IQR:1.11–3.61, p = 0.014) than pregnancies not classified as FGR. Free and total PlGF MoM correlated significantly with gestational age at delivery (r = 0.776, p 
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The identification of fetal growth restriction (FGR) due to uteroplacental insufficiency is important to improve perinatal outcomes. To distinguish FGR from small for gestational age (SGA), FGR consensus definition is currently based on biometry and/or additional biophysical parameters. This study aims to verify if this definition might be modified by including circulating angiogenic factors. This historical cohort study included singleton pregnancies with SGA fetuses after 20 weeks. All patients underwent detailed ultrasound and measurements of soluble fms-like tyrosine kinase 1 (sFlt-1) and placental growth factor (PlGF) at first assessment. ISUOG criteria for FGR were applied. Total PlGF was calculated using free PlGF, sFlt-1 and a receptor pharmacology model, and multiple of the median (MoM) values for sFlt-1, free PlGF, total PlGF and sFlt-1/PlGF ratio were calculated to adjust for gestational age. 72 pregnancies with SGA were first evaluated at median (IQR) of 28+5 (26+2 –31+3) weeks’ gestation, and 51 fetuses (70.8 %) satisfied the FGR consensus definition. Pregnancies with FGR showed significantly lower levels of free and total PlGF MoM (0.12, 95 % IQR: 0.07–0.36 vs 0.32, 95 % IQR: 0.20–0.53, p = 0.008) and 0.26, 95 % CI: 0.16–0.55 vs 0.43, 95 % IQR: 0.23–0.53, p = 0.028) respectively; and higher sFlt-1 MoM (4.62, 95 % IQR: 1.80–7.30 vs 1.74, 95 % IQR:1.11–3.61, p = 0.014) than pregnancies not classified as FGR. Free and total PlGF MoM correlated significantly with gestational age at delivery (r = 0.776, p &lt; 0.001 and r = 0.707, p &lt; 0.001, respectively). sFlt-1 MoM and sFlt-1/PlGF ratio MoM also correlated with gestational age at delivery (r = -0.681, p &lt; 0.001 and r = -0.823, p &lt; 0.001). Six cases identified as FGR at first ultrasound were not confirmed at birth showing significantly higher levels of free PlGF MoM (0.77, 95 % IQR: 0.27–3.07 vs 0.17, 95 % IQR: 0.08–0.43, p = 0.022). These findings show that total as well as free PlGF levels are lower in pregnancies affected with placental growth restriction. Angiogenic biomarkers might improve the differentiation between placental growth restriction and constitutional smallness. 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Total PlGF was calculated using free PlGF, sFlt-1 and a receptor pharmacology model, and multiple of the median (MoM) values for sFlt-1, free PlGF, total PlGF and sFlt-1/PlGF ratio were calculated to adjust for gestational age. 72 pregnancies with SGA were first evaluated at median (IQR) of 28+5 (26+2 –31+3) weeks’ gestation, and 51 fetuses (70.8 %) satisfied the FGR consensus definition. Pregnancies with FGR showed significantly lower levels of free and total PlGF MoM (0.12, 95 % IQR: 0.07–0.36 vs 0.32, 95 % IQR: 0.20–0.53, p = 0.008) and 0.26, 95 % CI: 0.16–0.55 vs 0.43, 95 % IQR: 0.23–0.53, p = 0.028) respectively; and higher sFlt-1 MoM (4.62, 95 % IQR: 1.80–7.30 vs 1.74, 95 % IQR:1.11–3.61, p = 0.014) than pregnancies not classified as FGR. 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The identification of fetal growth restriction (FGR) due to uteroplacental insufficiency is important to improve perinatal outcomes. To distinguish FGR from small for gestational age (SGA), FGR consensus definition is currently based on biometry and/or additional biophysical parameters. This study aims to verify if this definition might be modified by including circulating angiogenic factors. This historical cohort study included singleton pregnancies with SGA fetuses after 20 weeks. All patients underwent detailed ultrasound and measurements of soluble fms-like tyrosine kinase 1 (sFlt-1) and placental growth factor (PlGF) at first assessment. ISUOG criteria for FGR were applied. Total PlGF was calculated using free PlGF, sFlt-1 and a receptor pharmacology model, and multiple of the median (MoM) values for sFlt-1, free PlGF, total PlGF and sFlt-1/PlGF ratio were calculated to adjust for gestational age. 72 pregnancies with SGA were first evaluated at median (IQR) of 28+5 (26+2 –31+3) weeks’ gestation, and 51 fetuses (70.8 %) satisfied the FGR consensus definition. Pregnancies with FGR showed significantly lower levels of free and total PlGF MoM (0.12, 95 % IQR: 0.07–0.36 vs 0.32, 95 % IQR: 0.20–0.53, p = 0.008) and 0.26, 95 % CI: 0.16–0.55 vs 0.43, 95 % IQR: 0.23–0.53, p = 0.028) respectively; and higher sFlt-1 MoM (4.62, 95 % IQR: 1.80–7.30 vs 1.74, 95 % IQR:1.11–3.61, p = 0.014) than pregnancies not classified as FGR. Free and total PlGF MoM correlated significantly with gestational age at delivery (r = 0.776, p &lt; 0.001 and r = 0.707, p &lt; 0.001, respectively). sFlt-1 MoM and sFlt-1/PlGF ratio MoM also correlated with gestational age at delivery (r = -0.681, p &lt; 0.001 and r = -0.823, p &lt; 0.001). Six cases identified as FGR at first ultrasound were not confirmed at birth showing significantly higher levels of free PlGF MoM (0.77, 95 % IQR: 0.27–3.07 vs 0.17, 95 % IQR: 0.08–0.43, p = 0.022). These findings show that total as well as free PlGF levels are lower in pregnancies affected with placental growth restriction. Angiogenic biomarkers might improve the differentiation between placental growth restriction and constitutional smallness. 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subjects Angiogenic markers
Fetal growth restriction
Uteroplacental insufficiency
title The value of angiogenetic biomarkers in the detection of early onset fetal growth restriction
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