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Early-onset preeclampsia (EOPE) is a complex pregnancy complication that poses significant risks to the health of both mothers and fetuses, and research on its pathogenesis and pathophysiology remains insuffcient. This study aims to explore the role of candidate genes and their potential interaction mechanisms in EOPE through bioinformatics analysis techniques. Two gene expression datasets, GSE44711 and GSE74341, were obtained from the Gene Expression Omnibus (GEO) to identify differentially expressed genes (DEGs) between EOPE and gestational age-matched preterm control samples. Functional enrichment analysis was performed utilizing the kyoto encyclopedia of genes and genomes (KEGG), gene ontology (GO), and gene set enrichment analysis (GSEA). A protein–protein interaction (PPI) network was constructed using the STRING database, and hub DEGs were identified through Cytoscape software and comparative toxicogenomics database (CTD) analysis. Furthermore, a diagnostic logistic model was established using these hub genes, which were confirmed through reverse transcription polymerase chain reaction (RT-PCR). Finally, immune cell infiltration was analyzed using CIBERSORT. In total, 807 DEGs were identified in the GSE44711 dataset (451 upregulated genes and 356 downregulated genes), and 787 DEGs were identified in the GSE74341 dataset (446 upregulated genes and 341 downregulated genes). These DEGs were significantly enriched in various molecular functions such as extracellular matrix structural constituent, receptor-ligand activity binding, cytokine activity, and platelet-derived growth factor. KEGG and GSEA annotation revealed significant enrichment in pathways related to ECM-receptor interaction, PI3K-AKT signaling, and focal adhesion. Ten hub genes were identified through the CytoHubba plugin in Cytoscape. Among these hub genes, three key DEGs (COL1A1, SPP1, and THY1) were selected using CTD analysis and various topological methods in Cytoscape. The diagnostic logistic model based on these three genes exhibited high efficiency in predicting EOPE (AUC = 0.922). RT-PCR analysis confirmed the downregulation of these genes in EOPE, and immune cell infiltration analysis suggested the significant role of M1 and M2 macrophages in EOPE. In conclusion, this study highlights the association of three key genes (COL1A1, SPP1, and THY1) with EOPE and their contribution to high diagnostic efficiency in the logistic model. Additionally, it provides new insights for future research on EOPE and emphasizes the diagnostic value of these identified genes. More research is needed to explore their functional and diagnostic significance in EOPE. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to investigate the association of the epithelial and lymphoid immune markers with the adverse perinatal conditions such as early-onset preeclampsia (EOPE), fetal growth restriction (FGR) and intrauterine fetal death (IUFD) in preeclampsia in the placentae of preeclamptic patients. Material and methods: A total of 60 pregnant patients were included in this study. The immunohistochemistry method was used to determine the expression levels of CD4, CD8, CD4 / CD8, CD68, P53, MDM2, CK18, CK19, E-cadherin, and β-catenin. Results: In our study, the increase in E-cadherin expression in the preeclamptic fetal-maternal placental region was associated with EOPE and FGR development preeclampsia and the decrease in the expression of CD4 and CD8, which are involved in the local immunomodulation, was associated with IUFD. Conclusions:Our data reveal that the increase in the expression of CK18, CK19, E-cadherin, and β-catenin and the decrease in CD4 and CD8 play a role in the pathogenesis of preeclampsia. [ABSTRACT FROM AUTHOR]

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.

Objective To identify the factors affecting expectant management of early-onset preeclampsia, and evaluate the correlation between expectant treatment and foetal growth restriction.Materials and Methods The retrospective study included 72 women who were admitted for early-onset preeclampsia between February 2018 to April 2021. Data included maternal clinical parameters, demographic and maternal and neonatal outcomes, which were analysed for correlation.Results Multiple logistic regression analysis demonstrated that the time interval from the onset of 24-h proteinuria to termination of pregnancy showed a strong correlation with the expectant treatment; Univariate logistic analysis confirmed that there was no correlation between expectant treatment and foetal growth restriction.Conclusion There was a negative correlation between the duration of 24-h proteinuria and the expectant treatment of patients with early-onset preeclampsia; Expectant treatment could not improve the development of foetal growth restriction in patients with early-onset preeclampsia.KEY MESSAGESThe duration of 24-h proteinuria affects the effectiveness of expectant management of early-onset preeclampsia.Expectant management can reduce adverse neonatal outcomes due to iatrogenic preterm delivery, but it cannot improve the occurrence of foetal growth restriction.

To estimate incidence, risk of early and late-onset preeclampsia (PE) and understand their relationship with severity of COVID-19. 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. 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. Risk of early onset PE was higher in pregnant women with symptomatic COVID-19 as compared to asymptomatic women. [ABSTRACT FROM AUTHOR]

To identify the factors affecting expectant management of early-onset preeclampsia, and evaluate the correlation between expectant treatment and foetal growth restriction. The retrospective study included 72 women who were admitted for early-onset preeclampsia between February 2018 to April 2021. Data included maternal clinical parameters, demographic and maternal and neonatal outcomes, which were analysed for correlation. Multiple logistic regression analysis demonstrated that the time interval from the onset of 24-h proteinuria to termination of pregnancy showed a strong correlation with the expectant treatment; Univariate logistic analysis confirmed that there was no correlation between expectant treatment and foetal growth restriction. There was a negative correlation between the duration of 24-h proteinuria and the expectant treatment of patients with early-onset preeclampsia; Expectant treatment could not improve the development of foetal growth restriction in patients with early-onset preeclampsia. The duration of 24-h proteinuria affects the effectiveness of expectant management of early-onset preeclampsia. Expectant management can reduce adverse neonatal outcomes due to iatrogenic preterm delivery, but it cannot improve the occurrence of foetal growth restriction. [ABSTRACT FROM AUTHOR]

BackgroundEarly onset preeclampsia (EOSP, PE) is characterized by hypertension, proteinuria, and endothelial dysfunction. Oxidative stress-induced trophoblast dysfunction is a major pathology in PE. Placental exosomes are extracellular vesicles that are involved in “mother-placenta-foetal communication” and can regulate the biological functions of endothelial cells. Our study was designed to evaluate placental exosomes effects on endothelial cells.MethodsUmbilical cord blood from normal pregnant women and patients with PE were collected. A hypoxia/reoxygenation (H/R) model in human first trimester extravillous trophoblast cell (HTR8/SVneo) line to simulate the PE model of oxidative stress in vitro. Then, placental exosomes (i.e., NO-exo, H/R-exo, N-exo, and PE-exo) were extracted and identified. Finally, the effects of placental exosomes on the biological functions of human umbilical vein endothelial cells (HUVECs) were further evaluated by performing a series of experiments.ResultsPlacental exosomes had a double-membrane cup structure with diameters of 30–150 nm, and there was no obvious difference in placental exosomes. Compared with NO-exo and N-exo, H/R-exo and PE-exo inhibited HUVECs proliferation, tube formation and migration, increased permeability and apoptosis in vitro.ConclusionWe hypothesize that H/R-exo and PE-exo impair vessel development by disrupted biological functions in endothelial cells, which may result in vascular disorders in offspring.

Objectives: To develop a multivariate model for risk factors specific to early onset preeclampsia (EOP) and late onset preeclampsia (LOP) in our entire population (singleton and twin pregnancies). Material and methods: 20 year-observational population-based historical cohort study (2001–2020). All consecutive births delivered at the Centre Hospitalier Universitaire Hospitalier Sud Reunion’s maternity ward. A standardized validated epidemiological perinatal database was used. Results: During the 20-year period, there were 81,834 pregnancies and 83,497 infants born, 1232 dichorionic and 350 monochorionic twin pregnancies. There were 2120 cases of preeclampsia, of which 2001 were preeclamptic singleton pregnancies and 119 twin pregnancies (incidence 7.5% in twin pregnancies vs. 2.5% singletons, OR 3.0, p < 0.001). Independent risk factors for EOP and LOP in a multivariate model (controlling for the two major confounders: maternal ages—both risks for EOP and LOP, and maternal pre-pregnancy BMI—specific risk factor for LOP) were: history of preeclampsia (adjusted OR (aOR) 11.7 for EOP, 7.8 for LOP, p < 0.0001), chronic hypertension (aOR 7.3 for EOP, 3.9 for LOP, p < 0.0001), history of perinatal death (aOR 2.2 for EOP, p < 0.0001 and 1.48 for LOP, p = 0.007), primipaternity (aOR 3.0 for EOP and 3.6 for LOP, p = 0.001), dizygotic twin pregnancies (aOR 3.7 for EOP, p < 0.0001 and 2.1 for LOP, p = 0.003), monozygotic twin pregnancies (aOR 3.98 for EOP, p = 0.003 and non-significant (NS) for LOP), ovulation induction (aOR 5.6 for EOP, p = 0.004 and NS for LOP), and in vitro fertilization (aOR 2.8 for EOP, p = 0.05 and NS for LOP). Specific to LOP and NS for EOP: renal diseases (aOR for LOP 2.9, p = 0.007) and gestational diabetes mellitus (aOR 1.2, p = 0.04). Conclusions: Maternal ages over 35 years, chronic hypertension, history of preeclampsia, ovulation induction, in vitro fertilizations, history of perinatal deaths and twin pregnancy (in our experience, especially mono zygotic twin pregnancies) are significant risk factors for EOP. New paternity is an independent factor for both EOP and LOP.

Background: Recent advancement on experiment concluded that etiology of pre-eclampsia (PE) could be explained by the "two-stage" theory. The theory of which explained that pre-eclampsia occurs due to abnormalities in spiral arteries development and release of inflammatory response. Failure of spiral arteries development, the lesion of damage could be due to ischemia-reperfusion or hypoxia-reoxygenation. Hypoxia in pre-eclamptic placenta leads to metabolic change to anaerobic in glycolysis. Lactate dehydrogenase (LDH) has important role in anaerobic glycolysis that catalyzes the conversion of lactate to pyruvate during hypoxia. On the other hand, phosphoenolpyruvate carboxy kinase (PEPCK) is merely an enzyme of gluconeogenesis. This research conduct to reveal that in early onset pre-eclampsia the placenta still hypoxic and undergoes gluconeogenesis even after delivery, through metabolic enzyme of LDH and PEPCK level. Methods: This cross-sectional study compared early onset PE (< 34 weeks) with normal term placenta. We measured LDH enzyme activity using colorimetric assay and PEPCK protein using ELISA method. Results: Result show that placental LDH specific activity was increased significantly in PE with median 2.750 (0.030 - 5.680) U/mg compared to normal term placenta 0.255 (0.032 - 1.194) U/mg (Mann-Whitney, p< 0.001). PEPCK level was significantly increased in PE 8.998 (1.737-44.914) ng/mg compared to normal term placenta 1.552 (0.741-8.832) ng/mg (Mann-Whitney, p< 0.001). Conclusions: We conclude that anaerobic glycolysis and gluconeogenesis pathway are increased in early onset PE placenta as adaptation mechanism to hypoxic condition. [ABSTRACT FROM AUTHOR]

Preterm birth is the principal contributor to neonatal death and morbidity worldwide. We previously described a plasma cell-free RNA panel that between 16 and 20 weeks of pregnancy had potential to predict spontaneous preterm birth (sPTB) ≤ 32 weeks caused by preterm labor (PTL) or preterm premature rupture of membranes (PPROM). The present study had three objectives: (1) estimate the RNA panel prognostic accuracy for PTL/PPROM ≤ 32 weeks in a larger series; (2) improve accuracy by adding clinical characteristics to the predictive model; and (3) examine the association of the RNA panel with preeclampsia. We studied 289 women from Memphis TN prospectively sampled 16.0–20.7 weeks and found: (1) PSME2 and Hsa-Let 7g were differentially expressed in cases of PTL/PPROM ≤ 32 weeks and together provided fair predictive accuracy with AUC of 0.76; (2) combining the two RNAs with clinical characteristics improved good predictive accuracy for PTL/PPROM ≤ 32 weeks (AUC 0.83); (3) NAMPT and APOA1 were differentially expressed in women with 'early-onset preeclampsia' (EOP) and together provided good predictive accuracy with AUC of 0.89; and (4) combining the two RNAs with clinical characteristics provided excellent predictive accuracy (AUC 0.96). Our findings suggest an underlying common pathophysiological relationship between PTL/PPROM ≤ 32 weeks and EOP and open inroads for the prognostication of high-risk pregnancies. [ABSTRACT FROM AUTHOR]

Abstract Background The data on the association between the microbiota-dependent metabolite trimethylamine-N-oxide (TMAO) during pregnancy and risk of preeclampsia (PE) is limited. Methods We, therefore, conducted a prospective nested case control study during Sep 2017 to Dec 2018 to examine the association between plasma TMAO measured during pregnancy and the risk of PE. Total of 17 patients diagnosed with early onset PE (EOPE), 49 with late onset PE (LOPE) and 198 healthy controls were enrolled. Blood samples were collected at 15–23 weeks gestation and time at delivery. The Logistic regression model was used to assess the odds ratio (OR) and 95% confidence interval (CI) for TMAO and risk of PE, EOPE, LOPE, mild PE, and severe PE. Results We found that the mean TMAO levels of overall subjects in the second trimester (T2) and at the time of delivery (TD) were 90.39 μg/m3 (standard deviation (SD) =45.91) and 175.01 μg/m3 (SD = 160.97), respectively. No significant spearman correlation was found between the TMAO in those two periods (p > 0.05). T2 TMAO was not significantly associated with risk of PE or risk of any PE subtypes (p > 0.05). However, TD TMAO was significant associated with risk of PE, EOPE and severe PE (adjusted OR and 95%CI were 1.24(1.09, 1.40), 1.62(1.29, 2.03), and 1.41(1.17, 1.70)) per 50 μg/m3 increment, respectively). Conclusion Our study found that plasma TMAO level would alter over the course of pregnancy. The major role of TMAO in PE development might be in the accelerating process not in the initiation.

Abstract Objective PPARγ is a ligand-binding transcription factor that has been reported to be implicated in lipid metabolism, immune function, and cellular growth and differentiation. It has been suspected to play a role in the pathophysiology of preeclampsia, although the mechanism is yet to be elaborated. This study aims to investigate the expression of PPARγ in early onset preeclampsia (EOPE), late onset preeclampsia (LOPE), and normal pregnancy. We conducted this study using primary trophoblastic cell culture incubated with serum from EOPE, LOPE, and normal pregnancy. The expression of PPARγ in these cells was analyzed using Western Blot. Statistical analysis was performed using one-way ANOVA and Bonferroni’s post hoc test. p 0.05). In contrast, expression of PPAR-γ was increased in those cells induced by serum from LOPE (p

Abstract Background Previous studies showed that thyroid dysfunction in women with gestational hypertension could negatively affect maternal and fetal outcomes. In this study, we aimed to investigate whether thyroid dysfunction assessed in the second half trimester contributed to neonatal outcomes of pregnancy in different subtypes of gestational hypertension disease. Methods We performed a retrospective case-control study and collected data from 135 singleton pregnant women with gestational hypertension disease and their offspring who delivered in Renmin Hospital of Wuhan University from January 2015 to June 2017. We classified the patients based on the severity of the preeclampsia into three groups: pregnant induced hypertension (PIH), mild preeclampsia (MPE) and severe preeclampsia (SPE). Based on the onset time of preeclampsia, we classified the patients into PIH, early onset preeclampsia (EPE) and late onset preeclampsia. Demographic data and levels of thyroid hormones, as well as the adverse maternal and neonatal outcomes were collected from Electronic Medical Records. Logistic regression was used to estimate the associations between thyroid dysfunction and neonatal outcomes in these patients. Results Gestational weeks and neonatal birthweight were significantly lower, while incidence of preterm birth was significantly higher in the SPE and EPE groups than those in the PIH group (P

Background: Conservative management of early-onset severe preeclampsia is gaining widespread acceptance among obstetricians despite well-known maternal risks associated with it. There is limited data on the outcome of pregnancy of women managed with this modality of management in Nigerian setting. Objective: We determined the maternal and perinatal outcome of women managed conservatively for early-onset severe preeclampsia. Materials and Methods: This was a 7-year retrospective study of 118 women with early-onset severe preeclampsia that were managed conservatively at the Alex Ekwueme Federal University Teaching Hospital, Abakaliki. The data were entered and analyzed using the SPSS software version 22.0 (SPSS Inc., Chicago, IL, USA). Results: The median duration of expectant management was 12 days (range 3–20 days). The mean gestational age at delivery was 33.4 ± 2.5 weeks. The most common indication for delivery was uncontrolled hypertension (35.6%). Adverse maternal outcomes found in the study included abruptio placentae (11%), acute renal failure (2.5%), pulmonary edema (0.8%), eclampsia (11.9%), disseminated intravascular coagulation (2.5%), Haemolysis, elevated liver enzymes and low platelet (HELLP) syndrome (2.5%), and maternal death (2.5%). Perinatal mortality occurred in 68 (57.6%) cases in the study. Perinatal survival improved significantly with gestational age, with reductions in perinatal mortality of approximately 50% per week between 28 and 34 weeks' gestation on admission. Conclusion: Delayed delivery of women with early-onset severe preeclampsia improved perinatal outcome in this study, but it was associated with considerable maternal morbidity and mortality. Therefore, proper patient selection, adequate counseling of women on the risks and benefit of conservative management, close maternal monitoring, and the presence of advanced neonatal care are necessary to optimize pregnancy outcome when this management modality is adopted.

Preterm birth is the principal contributor to neonatal death and morbidity worldwide. We previously described a plasma cell-free RNA panel that between 16 and 20 weeks of pregnancy had potential to predict spontaneous preterm birth (sPTB) ≤ 32 weeks caused by preterm labor (PTL) or preterm premature rupture of membranes (PPROM). The present study had three objectives: (1) estimate the RNA panel prognostic accuracy for PTL/PPROM ≤ 32 weeks in a larger series; (2) improve accuracy by adding clinical characteristics to the predictive model; and (3) examine the association of the RNA panel with preeclampsia. We studied 289 women from Memphis TN prospectively sampled 16.0–20.7 weeks and found: (1) PSME2 and Hsa-Let 7g were differentially expressed in cases of PTL/PPROM ≤ 32 weeks and together provided fair predictive accuracy with AUC of 0.76; (2) combining the two RNAs with clinical characteristics improved good predictive accuracy for PTL/PPROM ≤ 32 weeks (AUC 0.83); (3) NAMPT and APOA1 were differentially expressed in women with ‘early-onset preeclampsia’ (EOP) and together provided good predictive accuracy with AUC of 0.89; and (4) combining the two RNAs with clinical characteristics provided excellent predictive accuracy (AUC 0.96). Our findings suggest an underlying common pathophysiological relationship between PTL/PPROM ≤ 32 weeks and EOP and open inroads for the prognostication of high-risk pregnancies.

Objective: To compare the level of serum heme oxygenase 1 (HO-1), soluble FMS like tyrosine kinase (sFlt-1), and neonatal outcome in early onset preeclampsia (EO-PE), late onset preeclampsia (LO-PE), and normal pregnancy (NP). Methods: In this prospective observational case control study, HO-1 and sFlt-1 levels were measured in blood samples within 24 h of hospital admission. Preeclampsia cases were divided into two groups based on gestational age at delivery: EO-PE (

Background: The data on the association between the microbiota-dependent metabolite trimethylamine-N-oxide (TMAO) during pregnancy and risk of preeclampsia (PE) is limited.Methods: We, therefore, conducted a prospective nested case control study during Sep 2017 to Dec 2018 to examine the association between plasma TMAO measured during pregnancy and the risk of PE. Total of 17 patients diagnosed with early onset PE (EOPE), 49 with late onset PE (LOPE) and 198 healthy controls were enrolled. Blood samples were collected at 15-23 weeks gestation and time at delivery. The Logistic regression model was used to assess the odds ratio (OR) and 95% confidence interval (CI) for TMAO and risk of PE, EOPE, LOPE, mild PE, and severe PE.Results: We found that the mean TMAO levels of overall subjects in the second trimester (T2) and at the time of delivery (TD) were 90.39 μg/m3 (standard deviation (SD) =45.91) and 175.01 μg/m3 (SD = 160.97), respectively. No significant spearman correlation was found between the TMAO in those two periods (p > 0.05). T2 TMAO was not significantly associated with risk of PE or risk of any PE subtypes (p > 0.05). However, TD TMAO was significant associated with risk of PE, EOPE and severe PE (adjusted OR and 95%CI were 1.24(1.09, 1.40), 1.62(1.29, 2.03), and 1.41(1.17, 1.70)) per 50 μg/m3 increment, respectively).Conclusion: Our study found that plasma TMAO level would alter over the course of pregnancy. The major role of TMAO in PE development might be in the accelerating process not in the initiation. [ABSTRACT FROM AUTHOR]

Objective: PPARγ is a ligand-binding transcription factor that has been reported to be implicated in lipid metabolism, immune function, and cellular growth and differentiation. It has been suspected to play a role in the pathophysiology of preeclampsia, although the mechanism is yet to be elaborated. This study aims to investigate the expression of PPARγ in early onset preeclampsia (EOPE), late onset preeclampsia (LOPE), and normal pregnancy. We conducted this study using primary trophoblastic cell culture incubated with serum from EOPE, LOPE, and normal pregnancy. The expression of PPARγ in these cells was analyzed using Western Blot. Statistical analysis was performed using one-way ANOVA and Bonferroni's post hoc test. p < 0.05 is considered significant. Results: Serum from normal pregnant women and EOPE did not induce any difference in the expression of PPAR-γ (p > 0.05). In contrast, expression of PPAR-γ was increased in those cells induced by serum from LOPE (p < 0.001). Therefore, we conclude that hypothetically PPAR-γ might play role in the pathophysiology of LOPE but not in EOPE. Other possibility is the activity of PPAR-γ in EOPE is inversely correlated with its expression, therefore the high enzymatic activity of PPAR-γ is tightly regulated by attenuating its expression. [ABSTRACT FROM AUTHOR]

Background: Previous studies showed that thyroid dysfunction in women with gestational hypertension could negatively affect maternal and fetal outcomes. In this study, we aimed to investigate whether thyroid dysfunction assessed in the second half trimester contributed to neonatal outcomes of pregnancy in different subtypes of gestational hypertension disease.Methods: We performed a retrospective case-control study and collected data from 135 singleton pregnant women with gestational hypertension disease and their offspring who delivered in Renmin Hospital of Wuhan University from January 2015 to June 2017. We classified the patients based on the severity of the preeclampsia into three groups: pregnant induced hypertension (PIH), mild preeclampsia (MPE) and severe preeclampsia (SPE). Based on the onset time of preeclampsia, we classified the patients into PIH, early onset preeclampsia (EPE) and late onset preeclampsia. Demographic data and levels of thyroid hormones, as well as the adverse maternal and neonatal outcomes were collected from Electronic Medical Records. Logistic regression was used to estimate the associations between thyroid dysfunction and neonatal outcomes in these patients.Results: Gestational weeks and neonatal birthweight were significantly lower, while incidence of preterm birth was significantly higher in the SPE and EPE groups than those in the PIH group (P < 0.001). Thyroid dysfunction was more frequent in the SPE group than in the MPE group (P = 0.01). Incidences of both preterm birth and low birth weight were significantly higher in patients with thyroid dysfunction (P = 0.008, P = 0.047 respectively). After adjustment, both severity of gestational hypertension (OR = 4.360, 95%CI [2.050, 9.271], P < 0.001; OR = 4.023, 95%CI [1.933, 8.372], P < 0.001) and thyroid dysfunction (OR = 3.011, 95%CI [1.248, 7.262], P = 0.014; OR = 11.306, 95%CI [1.040, 122.889], P = 0.046) were associated with higher risk of preterm birth and low birth weight, while the onset time of preeclampsia (OR = 0.031, 95%CI [0.009, 0.110], P < 0.001; OR = 0.097, 95%CI [0.033, 0.282], P < 0.001) was negatively associated with the risk of preterm birth and low birth weight.Conclusion: Severe and early onset preeclampsia, as well as thyroid dysfunction are associated with higher risk of preterm birth and low neonatal birth weight. Therefore, our data suggest that monitoring thyroid hormones in women with preeclampsia might help to predict adverse neonatal outcomes. [ABSTRACT FROM AUTHOR]

It is generally accepted today that there are two different types of preeclampsia: an early‐onset or placental type and a late‐onset or maternal type. In the latent phase, the first one presents with a low output/high resistance circulation eventually leading in the late second or early third trimester to an intense and acutely aggravating systemic disorder with an important impact on maternal and neonatal mortality and morbidity; the other type presents initially as a high volume/low resistance circulation, gradually evolving to a state of circulatory decompensation usually in the later stages of pregnancy, with a less severe impact on maternal and neonatal outcome. For both processes, numerous dysfunctions of the heart, kidneys, arteries, veins and interconnecting systems are reported, most of them presenting earlier and more severely in early‐ than in late‐onset preeclampsia; however, some very specific dysfunctions exist for either type. Experimental, clinical and epidemiological observations before, during and after pregnancy are consistent with gestation‐induced worsening of subclinical pre‐existing chronic cardiovascular dysfunction in early‐onset preeclampsia, and thus sharing the pathophysiology of cardiorenal syndrome type II, and with acute volume overload decompensation of the maternal circulation in late‐onset preeclampsia, thus sharing the pathophysiology of cardiorenal syndrome type 1. Cardiorenal syndrome type V is consistent with the process of preeclampsia superimposed upon clinical cardiovascular and/or renal disease, alone or as part of a systemic disorder. This review focuses on the specific differences in haemodynamic dysfunctions between the two types of preeclampsia, with special emphasis on the interorgan interactions between heart and kidneys, introducing the theoretical concept that the pathophysiological processes of preeclampsia can be regarded as the gestational manifestations of cardiorenal syndromes. [ABSTRACT FROM AUTHOR]

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A single, healthy, 44-year-old perimenopausal woman pursuing a pregnancy, employed donor embryos, resulting to a dichorionic diamniotic twin pregnancy. In the 18th week of gestation severe symptoms indicated early onset preeclampsia reporting severe hypertension (BP 180/90 mmHg), intense headaches and nausea as well as elevated 24-h urine protein levels (1.5 g/day). Concurrently diagnosis of an IUGR fetus was concluded. Standard pharmaceutical administration for treating preeclampsia was ordered. Persistence of symptoms indicated recommendation for pregnancy termination, however the patient opted against this. Selective embryo reduction was performed as the last resort prior to pregnancy termination. Following selective reduction the headaches and nausea were successfully subdued and the patient’s blood pressure was adjusted (mean BP 130/80 mmHg). This enabled further progression of pregnancy for an impressive 11 week-period, and a live birth on the 30th week. To conclude, only a few rare cases have been reported with diagnosis of early onset preeclampsia prior to the 20th week mark and none report live births. Albeit termination of pregnancy was recommended, the management of selective reduction of the IUGR fetus enabled successful treatment of preeclampsia coupled by a live birth of a healthy infant without any perinatal or postnatal complications reported.

Background: Preeclampsia (PE) is a multisystemic metabolic disease with an undetermined etiology. PE is a worldwide cause of maternal and perinatal morbidity, subdivided into early (EoPE) and late-onset (LoPE) according to 34 wk of gestation as a divider. Many researchers investigated biomarkers for predicting PE to halt its consequences on the feto-maternal outcome. Elabela (Ela) is a newly discovered peptide hormone that was implicated in PE pathogenesis. Earlier rodent studies discussed Ela's role in controlling blood pressure. Moreover, Ela deficiency was associated with PE development., Aim: To test whether plasma Ela could serve as a reliable marker for predicting PE based on the time of onset (EoPE vs LoPE) compared to age and body mass matched healthy controls since no definitive treatment exists for PE but to terminate a pregnancy., Methods: This case-control study recruited ( n = 90) pregnant who fulfilled inclusion criteria; they were allocated into three groups: EoPE (30/90) (< 34 wk of gestation); LoPE (30/90) (≥ 34 wk of gestation); and healthy pregnant (30/90). Demographic criteria; biochemical, hematological, and maternal plasma Ela levels were recorded for comparison., Results: Serum Ela was significantly reduced in EoPE compared to LoPE and healthy controls ( P = 0.0023). The correlation confirmed a strong inverse relationship with mean atrial blood pressure ( r = -0.7, P < 0.001), while gestational age and platelets count showed a moderate correlation with ( r = 0.4 with P < 0.0001). No correlation was confirmed between the body mass index (BMI) and urine albumin. The predictive ability of 25 centile serum Ela had an Odds ratio of 5.21, 95% confidence interval (1.28, 21.24), P = 0.02 for predicting EoPE. The receiver operator characteristic curve defined the Ela cutoff value at > 9.156 with 96.7% and 93.3% sensitivity and specificity, P < 0.0001 in predicting EoPE., Conclusion: A strong correlation of serum Ela with PE parameters with excellent sensitivity and specificity in distinguishing EoPE independent of the BMI, age, and blood pressure which makes Ela a recommendable marker in screening. Further research is warranted to explore prognostic and therapeutic applications for Ela in PE., Competing Interests: Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article., (©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.)

Introduction: Preeclampsia is a leading cause of maternal and perinatal mortality and morbidity, but signs and symptoms are non-specific and may vary. The root cause is imbalance of circulating angiogenic factors of placental (syncytiotrophoblast) origin, with consequent low levels of placental growth factor (PlGF) which may aid in diagnosis and prediction of disease. Aims and Objectives: To study the incidence of women at risk of developing early-onset preeclampsia by plasma placental growth factor biomarker assay in high-risk patients, to assess the maternal outcome in patients with PlGF values below cutoff for presenting gestational age, to calculate sensitivity, specificity, positive predictive value and negative predictive value of PlGF assay in predicting preeclampsia and to conclude whether PlGF biomarker assay can be an effective screening test in high-risk patients for prediction of early-onset preeclampsia. Materials and Methods: The study was carried out in the Department of Obstetrics and Gynecology at a tertiary care center. It is a prospective study, and study period extended from April 2012 to October 2013. One hundred pregnant women with 20- to 34-week gestational age with possible high risk of developing preeclampsia attending the antenatal clinics and high-risk OPDs were screened in the present study after explaining the nature of the study. PLGF concentration was quantitated using plasma and processed in Triage kit device (fluorescence immunoassay device). PLGF concentration was categorized against a specific range for specific gestation, and values below the range or <12 pg/ml were considered screened positives. The cases were followed up till delivery. Results: Twenty-two cases were screened positive, of which 20 developed preeclampsia with a strong positive prediction value of more than 90 %. Conclusion: PLGF is a strong predictor and a useful assay for early-onset preeclampsia. [ABSTRACT FROM AUTHOR]

Background: Early onset preeclampsia (EOSP, PE) is characterized by hypertension, proteinuria, and endothelial dysfunction. Oxidative stress-induced trophoblast dysfunction is a major pathology in PE. Placental exosomes are extracellular vesicles that are involved in "mother-placenta-foetal communication" and can regulate the biological functions of endothelial cells. Our study was designed to evaluate placental exosomes effects on endothelial cells., Methods: Umbilical cord blood from normal pregnant women and patients with PE were collected. A hypoxia/reoxygenation (H/R) model in human first trimester extravillous trophoblast cell (HTR8/SVneo) line to simulate the PE model of oxidative stress in vitro . Then, placental exosomes (i.e., NO-exo, H/R-exo, N-exo, and PE-exo) were extracted and identified. Finally, the effects of placental exosomes on the biological functions of human umbilical vein endothelial cells (HUVECs) were further evaluated by performing a series of experiments., Results: Placental exosomes had a double-membrane cup structure with diameters of 30-150 nm, and there was no obvious difference in placental exosomes. Compared with NO-exo and N-exo, H/R-exo and PE-exo inhibited HUVECs proliferation, tube formation and migration, increased permeability and apoptosis in vitro ., Conclusion: We hypothesize that H/R-exo and PE-exo impair vessel development by disrupted biological functions in endothelial cells, which may result in vascular disorders in offspring., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Gu, Zhang, Jiang, Chen, Wan, Lv, Lu, Zhou, Wang and Li.)