The problem with using the birthweight:placental weight ratio as a measure of placental efficiency

Christians, Julian K.; Grynspan, David; Greenwood, Susan; Dilworth, Mark

doi:10.1016/j.placenta.2018.06.311

Cited by 27 publications

(28 citation statements)

References 24 publications

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“…A low fetal/placental weight score was an additional independent predictor of early FGR, suggesting that placental efficiency (placental nutrient transport per unit of placental weight) was significantly reduced in this category compared with late fetal growth failure. 18 In the univariate analysis, the score given to represent the number and severity of lesions suggestive of fetal vascular malperfusion was higher among FGR pregnancies (both normotensive and hypertensive) than controls; however, the fetal obstructive pattern was similar between early and late FGR. These findings are consistent with previous data on small-for-gestational-age pregnancies, suggesting that maternal but not fetal vascular malperfusion lesions are more common among early-onset FGR than late-onset FGR.…”

Section: Discussionmentioning

confidence: 93%

“…In our study, increased rates of early infarcts suggesting placental ischemia, distal villous hypoplasia suggesting a reactive proliferating pattern to hypoxia, acute atherosis and persistent endovascular trophoblasts indicating defective remodeling of spiral arteries and decidual arteriopathy were independently correlated with early rather than late FGR. A low fetal/placental weight score was an additional independent predictor of early FGR, suggesting that placental efficiency (placental nutrient transport per unit of placental weight) was significantly reduced in this category compared with late fetal growth failure …”

Section: Discussionmentioning

confidence: 99%

“…Placental area was calculated by assuming an elliptical surface (largest diameter × smallest diameter × π/4). To evaluate placental efficiency (grams of the fetus produced per gram of placenta) we used both fetal/placental weight ratio and a fetal/placental weight score obtained by standardized residuals from linear regression of fetal weight on placental weight …”

Section: Methodsmentioning

confidence: 99%

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Pathologic placental lesions in early and late fetal growth restriction

Spinillo

Gardella

Adamo

et al. 2019

Acta Obstet Gynecol Scand

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Introduction The purpose of the study was to evaluate the differences in individual histopathologic placental lesions in pregnancies complicated by early‐onset (<32 weeks at diagnosis) and late‐onset (≥32 weeks at diagnosis) fetal growth restriction (FGR). Material and methods A cohort study of 440 singleton pregnancies complicated by FGR, diagnosed according to standard ultrasonographic criteria, followed up and delivered at the same institution between 2010 and 2016. Placental lesions were classified according to the Amsterdam Placental Workshop Consensus Criteria. Pathologic examination of placentas from 113 healthy singleton term pregnancies served as controls. Binary and multinomial logistic regression models were used to evaluate the independent association of placental lesions with the type of FGR. Results In our cohort the prevalences of early and late FGR were 37.3% (164/440) and 62.7% (276/440), respectively. The overall rates of preeclampsia (69/164 vs 59/276, P < 0.01) and absent/reversed umbilical artery pulsatility indices (61/164 vs 14/276, P < 0.001) were higher among early FGR than late FGR. Placental characteristics from early and late FGR pregnancies differed mainly in regard to maternal vascular malperfusion scores rather than fetal scores, with preeclampsia found to be a cofactor modulating the rates and severity of associated lesions. In the binary logistic analysis, recent infarcts (OR 2.44, 95% CI 1.2‐5), distal villous hypoplasia (OR 1.8, 95% CI 1.0‐3.2), atherosis (OR 2.71, 95% CI 1.35‐5.47), persistent endovascular trophoblasts (OR 1.67, 95% CI 1.03‐2.7), and a reduced fetal/placental weight score (OR 0.27, 95% CI 0.2‐0.38) were independently associated with an increased likelihood of early FGR compared with late FGR. The sensitivity, specificity, and area under the curve of the model were 60% (95% CI 51.2‐66.2), 89.1% (95% CI 84.9‐92.3), and 0.81 (95% CI 0.77‐0.85), respectively, suggesting a fair to good predictive value. Conclusions Individual placental lesions suggestive of increased rates of ischemia, defective remodeling of spiral arteries, peripheral hypoxia interfering with villus development, and reduced placental efficiency were significantly more common in early FGR than late FGR.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Pathologic placental lesions in early and late fetal growth restriction

Spinillo

Gardella

Adamo

et al. 2019

Acta Obstet Gynecol Scand

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“…Recent literature argues that the FPW is not truly a measure of placental efficiency with histological parameters proving more important. 20 It is likely that due to the low incidence of severe placental disease within our low-risk study population that there are not enough cases of severe preeclampsia to demonstrate a difference in aspirin use on placental histopathology and that future studies should separate early-and late-onset placental disease cases in analysis. Study strengths include that data originate from an RCT with a robust methodology.…”

Section: Discussionmentioning

confidence: 94%

Evaluation of the Effect of Low-Dose Aspirin on Biochemical and Biophysical Biomarkers for Placental Disease in Low-Risk Pregnancy: Secondary Analysis of a Multicenter RCT

et al. 2019

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Objective To assess the effect of aspirin use in low-risk pregnancy on: (1) pregnancy-associated plasma protein-A (PAPP-A) and placental-like growth factor (PLGF); (2) urinary albumin-to-creatinine ratio (ACR) and blood pressure; (3) fetal growth parameters; and (4) placental histopathology. Study Design This secondary analysis from the T rial of low-dose aspirin with an E arly S creening T est for preeclampsia and growth restriction randomized controlled trial was based on low-risk nulliparous women randomized at 11 weeks to (1) aspirin 75 mg; (2) no aspirin; and (3) aspirin based on the preeclampsia Fetal Medicine Foundation screening test. At baseline, women underwent assessment of blood pressure, PAPP-A, PLGF, and ACR, repeated 9 to 10 weeks postaspirin, in addition to fetal growth assessment. Gross and histopathological placental analyses were performed in line with Amsterdam criteria. Results A total of 445 subjects were included (aspirin n = 163 [36.6%]; no aspirin n = 282 [63.4%]). Although the fetal-to-placental weight ratio was significantly greater in the aspirin group (7.5 [±1.3] vs. 7.3 [±1.4], p = 0.045), as was change in ultrasound assessed estimated fetal weight from second to third trimesters (1,624.5 g [±235.1] vs. 1,606.2 [±189.4], p = 0.042), this was invalidated by the lack of a difference in birth weight. Aspirin did not significantly impact on change in serum or urine preeclampsia biomarkers, maternal blood pressure, or placental histopathology. Conclusion Aspirin use in low-risk pregnancy does not appear to impact on preeclampsia biomarkers, fetal growth, or placental pathology.

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“…We excluded pregnancies where the gestational age was over 43 weeks; gestational age was calculated based on the last menstrual period to the nearest week. Within each gestational age category (described below), birthweights and placental weights were corrected for maternal race, offspring sex and gestational age using a general linear model, after first removing the top and bottom 0.5% of raw birthweights and placenta weights within each gestational age category to objectively exclude biologically implausible values [40]. Pregnancies ending before 24 weeks were excluded from all analyses except those of spontaneous abortions.…”

Section: Methodsmentioning

confidence: 99%

Pregnancy complications recur independently of maternal vascular malperfusion lesions

Christians

Muñoz

2020

PLoS ONE

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Background Spontaneous abortions, intrauterine growth restriction, and preeclampsia are thought to be caused by defective placentation and are associated with increased risk of adverse outcomes in subsequent pregnancies. However, it is not known whether the recurrence of adverse outcomes is associated with the recurrence of placental pathology. We hypothesized that recurrent maternal vascular malperfusion (MVM) underlies the recurrence of adverse outcomes.

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The problem with using the birthweight:placental weight ratio as a measure of placental efficiency

Cited by 27 publications

References 24 publications

Pathologic placental lesions in early and late fetal growth restriction

Pathologic placental lesions in early and late fetal growth restriction

Evaluation of the Effect of Low-Dose Aspirin on Biochemical and Biophysical Biomarkers for Placental Disease in Low-Risk Pregnancy: Secondary Analysis of a Multicenter RCT

Pregnancy complications recur independently of maternal vascular malperfusion lesions

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