Abstract:Objectives
This study aims at identifying associations between therapeutics used during labor and the occurrence of postpartum preeclampsia (PPPE), a poorly understood entity.
Study Design and Main Outcome Measures
This is a case-control study of women who received an ICD-9 code for PPPE (cases) during the years 2009–2011, compared to women with a normotensive term pregnancy, delivery and postpartum period until discharge (controls), matched on age (±1 year) and delivery date (± 3 months). Cases were defined… Show more
“…The etiology and pathogenesis of PE are not clear [ 3 ], which has been reported to be associated with abnormal trophoblast invasion resulting in maternal endothelial dysfunction, chronic placental malperfusion and hypertension with adverse outcomes [ 4 ]. With the exception of fetal and placental delivery, there is no specific therapy for PE [ 5 ]. Therefore, it is urgent to explore the therapeutic targets to improve the prognosis of this disease.…”
Exosomes derived from human umbilical cord mesenchymal stem cells (hucMSCs) expressing microRNAs have been highlighted in human diseases. However, the detailed molecular mechanism of hucMSCs-derived exosomal miR-18b-3p on preeclampsia (PE) remains further investigation. We aimed to investigate the effect of exosomes and miR-18b-3p/leptin (LEP) on occurrence of PE. The morphology of the hucMSC and hucMSC-exosomes (Exos) was identified. The exosomes were infected with different lentivirus expressing miR-18b-3p to explore the role of miR-18b-3p in PE. The PE rat model was established by intraperitoneal injection of N-nitro-l-arginine methyl ester. The expression of LEP and miR-18b-3p was tested in PE rat placenta tissues. Also, the effect of exosomes on LEP and miR-18b-3p expression was detected. The systolic blood pressure (SBP), proteinuria, inflammatory factors, the weight of fetal rat and placenta and cell apoptosis in PE rats were detected. Finally, the relationship between miR-18b-3p and LEP was verified using dual-luciferase reporter gene assay and RNA pull-down assay. Exosomes, restoring miR-18b-3p or inhibiting LEP reduced SBP and proteinuria of PE rats as well as increased the weight of fetal rat and placenta, decreased serum levels of inflammatory factors as well as suppressed apoptotic cells of PE rats, exerting a suppressive effect on PE progression. miR-18b-3p was decreased and LEP was increased in placenta tissues of PE rats. LEP was the direct target gene of miR-18b-3p. Upregulation of miR-18b-3p or treatment of the exosomes suppressed LEP expression and reduced PE occurrence, while downregulation of miR-18b-3p had contrary effects. Downregulated LEP reversed the effect of miR-18b-3p reduction on PE rats. HucMSCs-derived exosomal miR-18b-3p targets LEP to participate in the occurrence and development of PE. This study may provide a novel theoretical basis for the mechanism and investigation of PE.
“…The etiology and pathogenesis of PE are not clear [ 3 ], which has been reported to be associated with abnormal trophoblast invasion resulting in maternal endothelial dysfunction, chronic placental malperfusion and hypertension with adverse outcomes [ 4 ]. With the exception of fetal and placental delivery, there is no specific therapy for PE [ 5 ]. Therefore, it is urgent to explore the therapeutic targets to improve the prognosis of this disease.…”
Exosomes derived from human umbilical cord mesenchymal stem cells (hucMSCs) expressing microRNAs have been highlighted in human diseases. However, the detailed molecular mechanism of hucMSCs-derived exosomal miR-18b-3p on preeclampsia (PE) remains further investigation. We aimed to investigate the effect of exosomes and miR-18b-3p/leptin (LEP) on occurrence of PE. The morphology of the hucMSC and hucMSC-exosomes (Exos) was identified. The exosomes were infected with different lentivirus expressing miR-18b-3p to explore the role of miR-18b-3p in PE. The PE rat model was established by intraperitoneal injection of N-nitro-l-arginine methyl ester. The expression of LEP and miR-18b-3p was tested in PE rat placenta tissues. Also, the effect of exosomes on LEP and miR-18b-3p expression was detected. The systolic blood pressure (SBP), proteinuria, inflammatory factors, the weight of fetal rat and placenta and cell apoptosis in PE rats were detected. Finally, the relationship between miR-18b-3p and LEP was verified using dual-luciferase reporter gene assay and RNA pull-down assay. Exosomes, restoring miR-18b-3p or inhibiting LEP reduced SBP and proteinuria of PE rats as well as increased the weight of fetal rat and placenta, decreased serum levels of inflammatory factors as well as suppressed apoptotic cells of PE rats, exerting a suppressive effect on PE progression. miR-18b-3p was decreased and LEP was increased in placenta tissues of PE rats. LEP was the direct target gene of miR-18b-3p. Upregulation of miR-18b-3p or treatment of the exosomes suppressed LEP expression and reduced PE occurrence, while downregulation of miR-18b-3p had contrary effects. Downregulated LEP reversed the effect of miR-18b-3p reduction on PE rats. HucMSCs-derived exosomal miR-18b-3p targets LEP to participate in the occurrence and development of PE. This study may provide a novel theoretical basis for the mechanism and investigation of PE.
“…Overall, studies have not shown an increased risk of postpartum PE associated with the use of epidural anesthesia and pharmacologic agents that might be hypothesized to raise BP, such as vasopressors or ergot derivatives in labor or after delivery. 14,15 Clinical Presentation As noted earlier, postpartum PE can develop after a pregnancy with no antecedent diagnosis of a hypertensive disorder of pregnancy or after a pregnancy complicated by gestational hypertension or in women with underlying chronic hypertension. Approximately 60% of patients with new, delayed-onset postpartum PE have no antecedent diagnosis of a hypertensive disorder of pregnancy.…”
Section: Risk Factors Demographicsmentioning
confidence: 96%
“…8,13e16 Higher rates of intravenous (IV) fluid infusion on labor and delivery are also associated with an increased risk of postpartum PE. 15 To the best of our knowledge, published studies do not distinguish between prelabor cesarean deliveries and intrapartum cesarean deliveries, which would likely affect the amount of IV fluids administered. Women who receive greater volumes of IV crystalloids during labor and delivery may shift more fluid to the interstitial compartment and may subsequently be more likely to develop volume overload and hypertension when the fluid is remobilized to the intravascular space after delivery.…”
Section: Risk Factors Demographicsmentioning
confidence: 97%
“…Black women have a 2-to 4-fold increased risk of postpartum PE compared with women of other races. 8,15 Unlike antepartum PE, postpartum PE does not seem to be more common among primiparous women. 8,16 Postpartum PE develops more commonly among women with a history of a hypertensive disorder in a previous pregnancy.…”
“…Elevated maternal pre-pregnancy BMI can lead to a higher risk of maternal and fetal morbidities and mortality [7][8][9][10][11][12][13]. It is controversial whether or not obesity impacts the response to assisted reproductive technology (ART) treatments [14][15][16][17][18].…”
Background: The purpose of this study was to assess whether increased body mass index (BMI) negatively affects assisted reproductive technology (ART) outcomes among gestational carriers. Methods: A retrospective matched case-control cohort, including all gestational carrier (GC) cycles performed at CReATe Fertility Centre (Toronto, ON, Canada) between 2003 and 2016. Setting: A Canadian fertility clinic, with a large surrogacy program. Patients: All gestational carriers that had undergone a cycle completed to a transfer at our clinic, and had BMI and outcome data available, were matched by BMI to infertile patients treated at our clinic during the same years provided they had undergone a cycle completed to a transfer, and had outcomes data available. Interventions: None. Main outcome measures: Clinical pregnancies rates, miscarriage rates and live birth rates. Results: BMI was not a reliable prediction factor of any of the measured outcomes. Importantly, the gestational carrier population had better outcomes and a significantly lower overall incidence of maternal, fetal and neonatal complications when compared with infertile patients, treated at our clinic during the same years. Conclusion: BMI is not a reliable predictor of outcomes among gestational carriers.
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