Table 1.
Demographic characteristics of the study population.
Fig 1.
Sensitivity for early preeclampsia using multi-protein markers.
Sensitivity (y-axis) at a 10% FPR are shown by gestational-age interval (x-axis) for early preeclampsia (PE), early PE with placental lesions consistent with MVM, and severe early PE. The vertical bars represent the average (with 95% confidence intervals) of sensitivity obtained from 200 bootstrap iterations. Early PE: early preeclampsia; FPR: false-positive rate; MVM: maternal vascular malperfusion.
Table 2.
Summary of bootstrap results for prediction of early preeclampsia vs normal pregnancy.
Fig 2.
Longitudinal maternal plasma abundance of MMP-7 and gpIIbIIIA in normal pregnancy and early preeclampsia.
Each line corresponds to a single patient (grey = normal pregnancy, red = early preeclampsia). Individual dots represent samples at 8–16 weeks (A, B) and 16.1–22 weeks (C, D) of gestation. Samples taken at the time of diagnosis with early preeclampsia are marked with an “x” and were not included in the analysis but only displayed. The thick black line represents the mean value in normal pregnancy. AUC: area under the receiver operating characteristic curve of the protein using data in the current interval; early PE: early preeclampsia; FC: fold change; gpIIbIIIa: glycoprotein IIb/IIIa; MMP-7: matrix metalloproteinase 7; MoM: multiples of the mean; p: the nominal significance p-value comparing mean MoM values between groups with a moderated t-test. Log2FC is the log (base 2) of the fold change between the cases and control groups, with negative values denoting lower MoM values in cases than in controls.
Fig 3.
Longitudinal maternal plasma abundance of siglec−6 (A), PlGF (B), VEGF121 (C), and activin-A (D) in normal pregnancy and early preeclampsia cases, highlighting differences at 22.1–28 weeks. AUC: area under the receiver operating characteristic curve; early PE: early preeclampsia; FC: fold change; PlGF: placental growth factor; Siglec-6: sialic acid binding immunoglobulin-like lectin; VEGF121: vascular endothelial growth factor A, isoform 121.
Fig 4.
Longitudinal maternal plasma ALCAM abundance in normal pregnancy and early preeclampsia cases, highlighting differences at 28.1–32 weeks.
ALCAM: activated leukocyte cell adhesion molecule; AUC: area under the receiver operating characteristic curve; early PE: early preeclampsia; FC: fold change; MVM: maternal vascular malperfusion.
Fig 5.
Longitudinal maternal plasma ACE2 abundance in normal pregnancy and early preeclampsia cases, highlighting differences at 8–16 weeks of gestation.
See Fig 2 legend for more details. ACE2: angiotensin-converting enzyme 2; AUC: area under the receiver operating characteristic curve; early PE: early preeclampsia; FC: fold change; MVM: maternal vascular malperfusion.
Fig 6.
Longitudinal maternal plasma abundance of siglec-6 (A) and activin-A (B) in normal pregnancy and early preeclampsia, highlighting differences at 22.1–28 weeks. Blue dots correspond to samples taken from late preeclampsia cases. AUC: area under the receiver operating characteristic curve; early PE: early preeclampsia; FC: fold change; late PE: late preeclampsia; Siglec-6: sialic acid binding immunoglobulin-like lectin.
Table 3.
Summary of bootstrap results for prediction of early preeclampsia versus normal pregnancy and late preeclampsia.
Fig 7.
A summary of differential protein abundance between early preeclampsia and normal pregnancy throughout gestation.
The values shown using a color scheme represent the log2 fold change in MoM values between the cases and controls (green = lower, red = higher mean MoM in cases versus controls). Fold changes >1.5 (absolute log2 fold change >0.58) were reset to 1.5 to enhance visualization of the data.
Table 4.
Biological processes enriched in proteins with a differential abundance between early preeclampsia and normal pregnancy.