Risk Of Early-onset Preeclampsia Research Articles

TNF-α inhibitor use during pregnancy and the risk of preeclampsia: population-based cohort study.

Although the clinical importance of preeclampsia is widely recognized, few treatment options are available for prevention. TNF-α inhibitors have been hypothesized to potentially prevent the disease. We aimed to examine whether exposure to TNF-α inhibitors during pregnancy reduces the risk of preeclampsia. We conducted a population-based pregnancy cohort study using nationwide samples of publicly (Medicaid data, 2000-2018) and commercially (MarketScan Research Database, 2003-2020) insured pregnant women linked to their liveborn infants. Exposure was ascertained based on a filled prescription or administration code for TNF-α inhibitors during the first and second trimester of pregnancy. The outcomes included early-onset preeclampsia, late-onset preeclampsia, and small-for-gestational age. For baseline confounding adjustment, we leveraged propensity score overlap weights to estimate risk ratios (RR). Among 4 315 658 pregnancies in the Medicaid and the MarketScan cohort, 2736 (0.063%) were exposed to TNF-α inhibitors during the first trimester and 1712 (0.040%) during the second trimester. After adjustment, the risk of early-onset preeclampsia was not decreased among mothers exposed during the first trimester compared with unexposed women with treatment indications [RR pooled : 1.25, 95% confidence interval (CI) 0.93-1.67]. Similarly, the risk of late-onset preeclampsia was not decreased among mothers exposed during the second trimester compared with unexposed women (RR pooled : 0.99, 95% CI 0.81-1.22). Contrary to the hypothesis, exposure to TNF-α inhibitors during pregnancy did not appear to be associated with a reduced risk of early-onset or late-onset preeclampsia. These findings do not support consideration of the use of TNF-α inhibitors for the prevention of preeclampsia.

Is artificial endometrial preparation more associated with early-onset or late-onset preeclampsia after frozen embryo transfer?

To explore whether the risks of early- or late-onset preeclampsia vary among frozen embryo transfer (FET) with different regimens for endometrial preparation and fresh embryo transfer (FreET). We retrospectively included a total of 24129 women who achieved singleton delivery during their first cycles of in vitro fertilization (IVF) between January 2012 and March 2020. The risks of early- and late-onset preeclampsia after FET with endometrial preparation by natural ovulation cycles (FET-NC) or by artificial cycles (FET-AC) were compared to that after FreET. After adjustment via multivariable logistic regression, the total risk of preeclampsia was higher in the FET-AC group compared to the FreET group [2.2% vs. 0.9%; adjusted odds ratio (aOR): 2.00; 95% confidence interval (CI): 1.45-2.76] and FET-NC group (2.2% vs. 0.9%; aOR: 2.17; 95% CI: 1.59-2.96).When stratified by the gestational age at delivery based on < 34weeks or ≥ 34weeks, the risk of late-onset preeclampsia remained higher in the FET-AC group than that in the and FreET group (1.8% vs. 0.6%; aOR: 2.56; 95% CI: 1.83-3.58) and the FET-NC group (1.8% vs. 0.6%; aOR: 2.63; 95% CI: 1.86-3.73). We did not find a statistically significant difference in the risk of early-onset preeclampsia among the three groups. An artificial regimen for endometrial preparation was more associated with an increased risk of late-onset preeclampsia after FET. Given that FET-AC is widely used in clinical practice, the potential maternal risk factors for late-onset preeclampsia when using the FET-AC regimen should be further explored, considering the maternal origin of late-onset preeclampsia.

Increased risk of early-onset preeclampsia in pregnant women with COVID-19

ABSTRACT Objective To estimate incidence, risk of early and late-onset preeclampsia (PE) and understand their relationship with severity of COVID-19. Methods Pregnant women with COVID-19 (n = 1929) were enrolled from 1 April 2020 to 24 February 2022. Primary outcome measure was incidence and risk of early onset PE in women with COVID-19. Results The incidence of early and late-onset PE was 11.4% and 5.6%. Moderate to severe COVID-19 was associated with eight times higher risk of early onset PE [aOR = 8.13 (1.56–42.46), p = 0.0129] compared to asymptomatic group. Conclusions Risk of early onset PE was higher in pregnant women with symptomatic COVID-19 as compared to asymptomatic women.

155. Antihistamine use in pregnancy and risk of early-onset preeclampsia

Introduction:/aims: Pregestational maternal allergy is an isolated risk factor for early-onset preeclampsia. The aim of this study was to assess the association between maternal use of antihistamines and early-onset preeclampsia, Methods: A population-based cohort study with data from the Medical Birth Registry of Norway and the Norwegian Prescription Database 2004-2016. We divided the prescription of antihistamines into pregestational (last six months before conception), first half of pregnancy (from conception to week 20) and second half of pregnancy (from week 20 to 36).

Endothelial Cell Activation and Thrombin Generation Assessment for the Risk of Severe Early Onset Preeclampsia. the ROADMAP-EOP Study

Background The ROADMAP-EOP study aimed to identify clinically relevant biomarkers of hypercoagulability for the identification of pregnant women at risk of early onset preeclampsia worsening. Methods The ROADMAP-EOP observational single center retrospective case–control study was conducted in Greece (Centre for Human Reproduction, Genesis Athens Clinic, Athens, Greece) from July 2020 to July and enrolled pregnant women diagnosed with EOP stratified in mild EOP group (n = 34) and severe EOP group (n = 15) as well as women with uncomplicated pregnancy (control group; n = 35). All women were assessed with thromboelastometry (ROTEM®), Calibrated Automated Thrombogram®, tissue factor activity (TFa), procoagulant phospholipid dependentclotting time (Procoag-PPL®), Proteins S (PS), TFPI, D-dimer, antithrombin (AT), thrombomodulin (TM), fibrinogen, prothrombin time (PT) and activated partial thromboplastin time (aPTT). The primary study end-point was severe earlyonset preeclampsia. Principal component analysis (PCA) was performed. Results The PCA analysis showed that a score composed of the lag-time, ttPeak and Procoag-PPL accurately predicted severe EOP (sensitivity 71.4%, specificity 61.8%, and AUC of the ROC analysis 0.953). Conclusion The pilot ROADMAP-EOP shows that activation of endothelial cells and blood hypercoagulability are driven events in the worsening of EOP. Among a large panel of biomarkers and coagulation assays, thrombingeneration test and procoagulant phospholipid dependent clotting time emerged as clinically relevant for the evaluation of the risk of severe EOP. This methodology for the development of a new clinic-biological risk assessment model for prompt identification of pregnant women at risk of severe EOP must be validated in a large multi-centerprospective study.

Gene variants and haplotypes of Vitamin D biosynthesis, transport, and function in preeclampsia

ABSTRACT Objective: To find whether the gene variants and haplotypes of cytochrome (CYP) 27B1 (1α-hydroxylase), group-specific component (GC) that is a vitamin D binding protein, vitamin D receptor (VDR), peroxisome proliferator-activated receptor γ (PPARγ) and retinoid-X receptor (RXR) affect the risk of preeclampsia. Methods: In a case–control study 100 women with preeclampsia and 100 healthy pregnant women were investigated for gene variants and haplotypes of vitamin D biosynthesis, transport, and function using the polymerase chain reaction-restriction fragment length polymorphism method. Results: The frequency of gene variants of PPARγ Pro12Ala and RXR -α (A/G, rs749759) were not significantly different comparing patients and controls. The TT genotype of CYP 27B1 (G > T) was associated with 2.2-fold (95% CI 1.04–4.7, p = 0.039) increased risk of early-onset preeclampsia. Also, the TT genotype of GC rs7041 (T > G) increased the risk of preeclampsia [OR = 2.13 (95% CI 1.09–4.17, p = 0.027)]. The VDR ApaI GT genotype elevated susceptibility to preeclampsia (OR = 2.55, p = 0.04). Further, the presence of VDR ApaI GT+TT genotype was associated with higher levels of body mass index, and systolic blood pressure, and lower level of 25 (OH)-D3. In the presence of haplotype CYP T, VDR T, and RXR A (TTA) compared to haplotype GTG the risk of preeclampsia was 6.71-fold (p = 0.044). Conclusions: The present study indicated an association between the CYP 27B1, GC, and VDR ApaI variants with the risk of preeclampsia. Also, the variants of the latter polymorphism influenced BMI, blood pressure, and vitamin D levels.

Genetic polymorphism in DGCR8 is associated with late onset of preeclampsia

BackgroundPE (preeclampsia) is a heterogeneous disorder with early onset PE (EOPE) and late onset PE (LOPE) subtypes. Associations between maternal miRNAs biosynthesis genes polymorphisms and risk of PE have been previously observed. However, the impact of polymorphisms in DGCR8 which is indispensable in miRNA maturing processing on the susceptibility to preeclampsia (PE) has not been elucidated yet. We, therefore, conducted a case-control study to evaluate the impact of polymorphisms in DGCR8 on the risk of EOPE and LOPE.MethodsA total of 66 patients diagnosed with EOPE, 206 with LOPE and 330 healthy controls were recruited. Five SNPs in DGCR8 were genotyped including rs1558496, rs1640299, rs720012, rs720014, and rs9606241. Logistic regression was used to estimate the OR and the 95% CI for the associations.ResultsIncreased risk of LOPE has been observed among patients with rs1640299 TG genotype (OR = 1.98 (95%CI: 1.38, 2.87), p = 2.32e-4) and rs720014 TC genotype (OR = 2.49 (95%CI: 1.72, 3.60), p = 1.40e-7). The DGCR8 rs1558496/ rs1640299/ rs720012/ rs720014/ rs9606241 haplotype T-G-A-C-A and T-G-A-C-G were associated with increased risk of LOPE (OR = 2.20 (95%CI: 1.49, 3.25), p = 5.90e-5, and 1.58 (95%CI: 1.06, 2.36), p = 0.024, respectively). And the haplotype T-T-G-T-A was associated with lower risk of LOPE (OR = 0.74 (95%CI: 0.58, 0.95), p = 0.018). These significant associations retained after false-positive discovery rate correction. However, none of the tested SNPs or haplotypes in DGCR8 gene is associated with risk of EOPE (p > 0.05).ConclusionsPolymorphisms in DGCR8 might participate in the pathological process of preeclampsia. The rs1640299 T > G and rs720014 T > C polymorphisms are associated with late onset preeclampsia susceptibility.

Does low dose aspirin prescribed for risk of early onset preeclampsia reduce the prevalence of preterm prelabor rupture of membranes?

Background: Placental dysfunction, inflammation and degradation of fetal membranes has been hypothesized as a cause of preterm prelabor of rupture of membranes.Objective: To examine the effect of aspirin, an anti-inflammatory agent, on the prevalence of preterm prelabor rupture of membranes (PPRoMs).Methods: A retrospective analysis was conducted to examine the effect of aspirin on the prevalence of PPRoM. Aspirin (150 mg, nocte) was prescribed to women who were identified through a screening program at 11–13+6 weeks’ gestation as being at high risk for developing early-onset preeclampsia. Women who were at low risk for developing preeclampsia did not receive aspirin. The prevalence of PPRoM was compared with an observational cohort.Results: In the observational cohort, there were 3027 women, including 32 (1.1%) cases of PPRoM. The prevalence of PPRoM in the high risk group was 3.1% (4/128) and was statistically significantly higher compared to the low risk group (1.0%) (28/2899). The relative risk was 3.02 (95% CI 1.2–7.7; p= .04). In the interventional cohort, there were 7280 women, with 114 (1.6%) cases of PPRoM. The prevalence of PPRoM in the high risk group who were treated with aspirin was 1.8% (14/766) compared to 1.5% (100/6516) in the low risk group (p= .54). The prevalence of PPRoM in high risk patients in the observational group (who did not receive aspirin) compared with the high risk patients in the interventional group (who were treated with aspirin) was not statistically significant (p= .31).Conclusions: PPRoM is significantly associated with a description of high risk for ePET; although, this algorithm is not a good screening tool for predicting PPRoM. Aspirin treatment of women deemed high risk for ePET is safe in the context of PPRoM and there may be some reduction in prevalence of PPRoM in treated high risk women; although, this study was not powered to demonstrate a small reduction in the prevalence of PPRoM. The findings merit further investigation through a larger prospective study with adequate sample size.

M1 macrophages are involved in folliculogenesis and M2 macrophages play an essential role for successful implantation

Early administration of low dose acetyl salicylic acid (Aspirin) in high risk women reduces the risk of early onset preeclampsia. This study aims to investigate the effect of aspirin on trophoblast integration and the its effect on angiogenic and invasive pathways in an in-vitro model of preeclampsia. Red fluorescent-labeled human uterine myometrial microvascular endothelial cells (UtMVECs) were seeded on matrigel to form endothelial networks. Green fluorescent-labeled trophoblastic HTR-8/SVneo cells were co-cultured with the endothelial networks with/without TNF-a (0.5 ng/mL) and/or aspirin (0.1 mM) for 24 h. Fluorescent images were captured and quantified by Image J to examine the effects of TNF-a and aspirin on the trophoblast-endothelial integration. Conditioned media were collected to measure free VEGF, PlGF and sFlt-1 by ELISA and PGF1a by Enzyme immunoassay (EIA). Cells were retrieved to examine mRNA expression of angiogenic factors (VEGF, PlGF and sFlt-1), invasion markers (MMP-2 and TIMP-1), endothelial cell activation markers (E-selectin and VCAM), eNOS and cyclooxygenase (COX)-2 by quantitative PCR. Aspirin reversed the inhibitory effect of TNF-a on trophoblast cell integration into endothelial cellular networks. TNF-a increased PGF1a production (128 ± 11%, p < 0.05), whilst aspirin reversed the TNF-a effect on PGF1a production (19 ± 4%, p < 0.01). TNF-a decreased the mRNA expression of PlGF, eNOS, MMP-2 and TIMP-1, and stimulated COX2, E-selectin and VCAM mRNA expression. Aspirin did not reverse the TNF-a effect on these molecules. Aspirin improves trophoblast cell integration into endothelial cellular networks by inhibiting the effect of TNF-a via PGI2 with no significant effect on antiangiogenic, invasive or endothelial activation markers.

The effect of acetyl salicylic acid (Aspirin) on trophoblast-endothelial interaction in vitro

Early administration of low dose acetyl salicylic acid (Aspirin) in high risk women reduces the risk of early onset preeclampsia. This study aims to investigate the effect of aspirin on trophoblast integration and the its effect on angiogenic and invasive pathways in an in-vitro model of preeclampsia. Red fluorescent-labeled human uterine myometrial microvascular endothelial cells (UtMVECs) were seeded on matrigel to form endothelial networks. Green fluorescent-labeled trophoblastic HTR-8/SVneo cells were co-cultured with the endothelial networks with/without TNF-a (0.5ng/mL) and/or aspirin (0.1mM) for 24h. Fluorescent images were captured and quantified by Image J to examine the effects of TNF-a and aspirin on the trophoblast-endothelial integration. Conditioned media were collected to measure free VEGF, PlGF and sFlt-1 by ELISA and PGF1a by Enzyme immunoassay (EIA). Cells were retrieved to examine mRNA expression of angiogenic factors (VEGF, PlGF and sFlt-1), invasion markers (MMP-2 and TIMP-1), endothelial cell activation markers (E-selectin and VCAM), eNOS and cyclooxygenase (COX)-2 by quantitative PCR. Aspirin reversed the inhibitory effect of TNF-a on trophoblast cell integration into endothelial cellular networks. TNF-a increased PGF1a production (128±11%, p<0.05), whilst aspirin reversed the TNF-a effect on PGF1a production (19±4%, p<0.01). TNF-a decreased the mRNA expression of PlGF, eNOS, MMP-2 and TIMP-1, and stimulated COX2, E-selectin and VCAM mRNA expression. Aspirin did not reverse the TNF-a effect on these molecules. Aspirin improves trophoblast cell integration into endothelial cellular networks by inhibiting the effect of TNF-a via PGI2 with no significant effect on antiangiogenic, invasive or endothelial activation markers.

Polymorphisms in Inflammatory Mediator Genes and Risk of Preeclampsia in Taiyuan, China.

Excessive maternal inflammatory response is involved in the pathogenesis of preeclampsia. Few epidemiologic studies have investigated the associations between genetic variations in the inflammatory mediator genes and preeclampsia risk, and these studies have reached inconsistent results. We examined 31 single-nucleotide polymorphisms in IL-1A, IL-1B, IL-1R1, IL-2RA, IL-5RA, IL-6, IL-6R, TNFSF11, TNFRSF11A, IL-28RA, IRAK4, and KIT genes and the risk of preeclampsia and its clinical subtypes in a nested case-control study including 203 preeclampsia cases and 233 controls. We found that IL-1R1, IL-5RA, IL-6R, and TNFSF11 were associated with the risk of preeclampsia. Although the significant associations observed for preeclampsia overall were mainly seen for late-onset preeclampsia and severe preeclampsia, IL-6R (rs2229238) and TNFSF11 (rs9525643) polymorphisms were associated with the risk of early-onset preeclampsia. TNFSF11 (rs2200287 and rs2148072) polymorphisms were associated with risk of mild preeclampsia. Our study provided the first evidence that genetic variations in inflammatory mediator genes IL-1R1, IL-6R, TNFSF11, and IL-5RA were associated with preeclampsia risk, and the risk varied by preeclampsia subtypes.

Plasma biomarkers for the identification of women at risk for early-onset preeclampsia

ABSTRACTBackground: To identify potential biomarkers in the 1st trimester of pregnancy for the identification of women destined to develop early onset preeclampsia (EOPE).Methods: Blood samples were obtained from pregnant women at 11–13 weeks of gestation. Women were followed up until delivery. Five samples from EOPE complicated pregnancies and 5 from unaffected ones were analysed using 2-DE and MALDI-TOF-TOF MS/MS. The altered expression of selected proteins was verified by ELISA in an extended sample cohort.Results: Twelve proteins were differentially expressed in the plasma of women who subsequently developed EOPE as compared to controls. Alpha-1-antitrypsin (A1AT), CD5 antigen-like molecule (CD5L) Keratin, type I cytoskeletal 9 (K1C9), Myeloid cell nuclear differentiation antigen (MNDA), Transferrin (TRFE) and Vitamin D-binding protein (VTDB) were up-regulated with fold changes 3.14, 2.18, 1.53, 1.53, 4.26 3.38 respectively, whereas Alpha-2-HS-glycoprotein (FETUA), Beta-2-glycoprotein 1 (APOH), Complement factor B (CFAB), Haptoglobin (HPT), Vitronectin (VTNC) and Zinc-alpha-2-glycoprotein (ZA2G) were down-regulated with fold changes -0.38, -0.76, -0.24, -0.47, -0.23, and -0.50 respectively. The down-regulation of APOH, VTNC and HPT was verified using ELISA.Conclusions: The differentially expressed proteins represent potential biomarkers for the early screening for EOPE. Follow-up experiments however are necessary for evaluation.

Association between Val158Met COMT, TNF-α -857 C>T, TNFR1 36 A>G, IL-1α 4845 G>T and IL-10 -1082 A>G polymorphisms and risk of early-onset preeclampsia and its complications

Background/Aim. Preeclampsia (PE) belongs to the group of hypertensive disorders in pregnancy with the global average incidence of 2.16%. It is considered as one of the leading causes of maternal and neonatal morbidity and mortality worldwide. The goal of this study was to assess the potential association between Val158Met catechol-o-methyltransferase (COMT), tumor necrosis factor-alpha (TNF-α) -857 C>T, tumor necrosis factor receptor 1 (TNFR1) 36 A>G, interleukin-1alpha (IL-1α) 4845 G>T and interleukin-10 (IL-10) -1082 A>G polymorphisms and risk of early-onset preeclampsia (PE) and its complications. Methods. The study included 47 early-onset PE patients, which were grouped by disease severity and by size for gestational age and 47 control cases. The Val158Met polymorphism was genotyped by polymerase chain reaction – restriction fragment length polymorphism (PCR-RFLP) analysis and inflammatory cytokine polymorphisms by the Sanger sequencing method. Results. The COMT Met allele as well as IL-1α T showed a protective role, decreasing the risk of early-onset PE after age and body mass index (BMI) adjustments. The detected interactions between the COMT Met and IL-10 A alleles, as well as between the COMT Met and TNF-α T alleles were insignificant after age and BMI adjustments. Conclusion. COMT and IL-1α may be used as candidate genes for early-onset PE and its severe form and small for gestational age (SGA) complications.

Polymorphisms in complement genes and risk of preeclampsia in Taiyuan, China.

Altered immune response may be a part of the pathogenesis of preeclampsia. The few epidemiologic studies that have investigated the associations between genetic variations in the complement system genes and preeclampsia risk have reached inconsistent results. The aim of this study is to determine if polymorphisms in the complement system genes could influence the risk of preeclampsia. We examined 51 SNPs in the C3, C5, C6, MASP1, MBL2 and CD55 genes and the risk of preeclampsia and its clinical subtypes in a nested case-control study of 203 preeclampsia cases and 233 controls. Both C6 and MASP1 were associated with the risk of preeclampsia. C6 (rs7444800, rs4957381) and MASP1 (rs1108450, rs3774282, rs698106) polymorphisms were associated with the risk of early-onset preeclampsia and severe preeclampsia, while MASP1 (rs1357134, rs698090) polymorphisms were associated with the risk of late-onset preeclampsia and severe preeclampsia. Our study provided novel evidence that genetic variations in complement genes C6 and MASP1were associated with preeclampsia risk, and that the risk varied by preeclampsia subtypes.

Investigations into the association between polymorphisms in the interleukin-10 gene and risk of early-onset preeclampsia.

In this case-control study, we assessed the influence of IL-10 -1082A/G and -819T/C on the development of preeclampsia. The IL-10 -1082A/G and -819T/C polymorphisms were assessed by polymerase chain reaction-restriction fragment length polymorphism. The genotype distributions of the IL-10 -1082A/G and -819T/C polymorphisms in the control subjects were in conformance with Hardy-Weinberg equilibrium (HWE; P = 0.46 and 0.17). Unconditional logistic regression analyses revealed that individuals carrying the CC genotype of IL-10 -819T/C were associated with an increased risk of preeclampsia compared to the TT genotype. The odds ratio (95% confidence interval) for the CC genotype of IL-10 -819T/C was 1.71 (1.07-3.27) compared to the TT genotype. In conclusion, the results of our study indicated that the IL-10 -819T/C polymorphism was associated with an increased risk of preeclampsia in a Chinese population.

Associations of Personal and Family Preeclampsia History With the Risk of Early-, Intermediate- and Late-Onset Preeclampsia

Preeclampsia encompasses multiple conditions of varying severity. We examined the recurrence and familial aggregation of preeclampsia by timing of onset, which is a marker for severity. We ascertained personal and family histories of preeclampsia for women who delivered live singletons in Denmark in 1978-2008 (almost 1.4 million pregnancies). Using log-linear binomial regression, we estimated risk ratios for the associations between personal and family histories of preeclampsia and the risk of early-onset (before 34 weeks of gestation, which is typically the most severe), intermediate-onset (at 34-36 weeks of gestation), and late-onset (after 36 weeks of gestation) preeclampsia. Previous early-, intermediate-, or late-onset preeclampsia increased the risk of recurrent preeclampsia with the same timing of onset 25.2 times (95% confidence interval (CI): 21.8, 29.1), 19.7 times (95% CI: 17.0, 22.8), and 10.3 times (95% CI: 9.85, 10.9), respectively, compared with having no such history. Preeclampsia in a woman's family was associated with a 24%-163% increase in preeclampsia risk, with the strongest associations for early- and intermediate-onset preeclampsia in female relatives. Preeclampsia in the man's family did not affect a woman's risk of early-onset preeclampsia and was only weakly associated with her risks of intermediate- and late-onset preeclampsia. Early-onset preeclampsia appears to have the largest genetic component, whereas environmental factors likely contribute most to late-onset preeclampsia. The role of paternal genes in the etiology of preeclampsia appears to be limited.

Endostatin levels and the risk of subsequent preeclampsia

ObjectiveTo evaluate endostatin, an anti-angiogenic factor, in relation to the risk of preeclampsia (PE). Study designIn this case control study, serum samples were collected at 11–17 weeks and 18–26 weeks’ gestation. Endostatin levels were expressed as adjusted multiples of the median (MoM). Logistic regression was used to calculate adjusted odds ratios (aORs) for the prediction of PE. ResultsA total of 77 women with PE and 150 controls were studied. Endostatin levels were significantly higher in women with PE compared to controls in both the first and the second trimester. At a cut-off level of 75th percentile of endostatin MoMs, the aORs for PE were 1.33 (95% confidence interval [CI], 0.68–2.58) at 11–17 weeks and 1.77 (95% CI, 0.94–3.34) at 18–26 weeks, after adjustment for ethnicity and chronic hypertension. The aORs for early-onset PE were 3.51 (95% CI, 1.18–10.43) at 11–17 weeks and 2.17 (95% CI, 0.67–7.06) at 18–26 weeks. ConclusionsHigher endostatin levels are associated with an increased risk of early onset PE. Endostatin alone, however, has a poor predictive value for clinical usefulness.

Serum placental growth factor as a predictor of early onset preeclampsia in overweight/obese pregnant women

The purpose of this study was to analyze whether maternal serum placental growth factor (PlGF) could predict early onset preeclampsia (<32 weeks of gestation) in overweight/obese pregnant women, and whether it could do it more effectively than in normal/underweight pregnant women. A prospective cohort study was conducted on 1678 pregnant women with singleton pregnancies, who were grouped as underweight, normal, overweight, and obese on the basis of body mass index, followed by serum PlGF estimation at 20 to 22 weeks of gestation. A cut-off value of <144 pg/mL for PlGF was determined by Receiver Operating Characteristic curve analysis to identify risk of early onset preeclampsia. Univariate logistic regression analysis revealed significantly stronger association between PlGF <144 pg/mL and early onset preeclampsia in overweight/obese pregnant women (odds ratio 7.64; 95% confidence interval 5.34–10.12; P = .000) than in normal/underweight pregnant women (odds ratio 2.95; 95% confidence interval 1.74–4.26; P = .007). Weight and PlGF levels in study women had a significant negative correlation (r = 0.663; P = .002). Serum PlGF in early second trimester could be an effective predictor of early onset preeclampsia in overweight/obese pregnant women and may be more effective than in normal/underweight pregnant women.