Can thrombophilia worsen maternal and perinatal outcomes in cases of severe preeclampsia?

Baptista, Fernanda Spadotto; Bortolotto, Maria Rita de Figueiredo Lemos; Bianchini, Fabiola Roberta Marim; Krebs, Vera Lúcia Jornada; Zugaib, Marcelo; Francisco, Rossana Pulcineli Vieira

doi:10.1016/j.preghy.2017.12.012

Cited by 10 publications

(3 citation statements)

References 33 publications

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“…[43] Although these conditions are heterogeneous in their pathophysiology, hereditary and acquired thrombophilia has been shown to be associated with recurrent pregnancy loss and gestational vascular complications. [44] In the present study, KEGG pathway analysis revealed that the coagulation cascade was significantly activated through the intrinsic and extrinsic pathways in placentae after IVF-ET treatment compared to that in placentae from natural pregnancy. In early IVF-ET placentae, a state of hypercoagulability and the local formation of thrombi in the microvasculature draining the site of embryo implantation provide a competent barrier to protect the embryo from the maternal immune system.…”

Section: Discussionmentioning

confidence: 52%

Alterations in complement and coagulation pathways of human placentae subjected to in vitro fertilization and embryo transfer in the first trimester

et al. 2019

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The mechanisms underlying the potential risks of in vitro fertilization and embryo transfer (IVF-ET) have not been fully elucidated. The aim of this study was to explore changes in the complement and coagulation pathways in placentae subjected to IVF-ET in the first trimester compared to placentae from normal pregnancies. Four placenta samples in the first trimester were obtained from patients undergoing IVF-ET owing to oviductal factors only. An additional 4 control placentae were obtained from volunteers with normal pregnancies. A GeneChip Affymetrix HG-U133 Plus 2.0 Array was utilized to analyze the changes in gene expression between the normal and IVF-ET placentae. Differentially expressed genes (DEGs) were analyzed using the Database for Annotation and Visualization and Integrated Discovery bioinformatics resource, and gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were conducted. Using real-time PCR, we confirmed the obtained microarray data in 10 dysregulated genes. Five of the gene products were further analyzed by immunohistochemistry (IHC) to determine their protein expression and localization. A total of fifty DEGs were identified in the complement and coagulation pathways in the IVF-ET treated placentae: 38 upregulated and 12 down-regulated. KEGG pathway analysis indicated that IVF-ET manipulation substantially overactivated the coagulation and complement pathways, while urokinase plasminogen activator-and urokinase plasminogen activator receptor-mediated trophoblastic invasion and tissue remodeling were inhibited. Furthermore, the 5 proteins analyzed by IHC were found to be localized specifically to the placenta. This is the first study to compare DEGs relating to the placental complement and coagulation pathways from patients undergoing IVF-ET treatment compared to those undergoing normal pregnancy. These findings identified valuable biomarkers and potential novel therapeutic targets to combat the unfavorable effects of IVF-ET. Abbreviations: CD59 = CD59 molecule complement regulatory protein, CFD = complement factor D (adipsin), DAVID = Database for Annotation, Visualization and Integrated Discovery, DEG = differentially expressed gene, FGA = fibrinogen alpha chain, FGB = fibrinogen beta chain, FGG = fibrinogen gamma chain, GCOS = gene chip operating software, GEO = Gene Expression Omnibus, GO = gene ontology, IHC = immunohistochemistry, IVF-ET = in vitro fertilization and embryo transfer, PLAU = plasminogen activator urokinase, PLAUR = plasminogen activator urokinase receptor, PROC = protein C, qRT-PCR = quantitative real-time PCR, SERPINC1 = serpin peptidase inhibitor clade C member 1, SERPINE1 = serpin peptidase inhibitor clade E member 1, STRING = search tool for the retrieval of interacting genes, uPA = urokinase plasminogen activator, uPAR = urokinase plasminogen activator receptor.

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Section: Discussionmentioning

confidence: 52%

Alterations in complement and coagulation pathways of human placentae subjected to in vitro fertilization and embryo transfer in the first trimester

et al. 2019

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“…Chronic hypertension is an important risk factor for PE, and a blood hypercoagulable state serves as the pathological basis of PE [25]. Scholars have utilized MP screen-ing to monitor the blood hypercoagulable state in pregnant women, and satisfactory prediction rates have been reported [26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

Monitoring of Pregnancy-Induced Hypertension Syndrome Combined with Ultrasound Monitoring in Early Pregnancy to Prevent Chronic Hypertension with Preeclampsia

Xiao¹,

Liu²,

Liu³

et al. 2023

Clin. Exp. Obstet. Gynecol.

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Background: This study explored the guiding value of monitoring pregnancy-induced hypertension syndrome (MP) for blood hypercoagulability in combination with ultrasound monitoring of uterine artery blood flow in early pregnancy and fetal growth and development in the second and third trimesters, with the goal of preventing chronic hypertension with preeclampsia (PE) and its clinical effects. Methods: The medical records of 189 pregnant patients with chronic hypertension between June 2016 and June 2021 were retrospectively analyzed; among them, 98 constituted the intervention group. The intervention group received MP screening for blood hypercoagulability in combination with ultrasound monitoring of uterine artery blood flow in early pregnancy and fetal growth and development in the second and third trimesters of pregnancy. Those with abnormalities were given timely symptomatic (low-molecular-weight heparin with or without aspirin) and supportive treatment. The remaining 91 patients who did not receive timely monitoring and intervention constituted the control group. Fetal outcomes and PE rates were compared between groups. Results: The PE incidence in the intervention group was significantly lower than that in the control group (p < 0.01), and the premature delivery of low-birth-weight neonates, fetal loss and neonatal asphyxia incidences were also significantly lower in the intervention group than the control group (p < 0.05). Conclusions: MP screening for blood hypercoagulability combined with ultrasound monitoring of uterine artery blood flow can effectively prevent PE occurrence in pregnant patients with chronic hypertension and significantly improve fetal outcomes. Additionally, MP screening is noninvasive and easy to use at a low cost.

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“…[2][3][4][5], що спровоковані різноманітними тромбоемболічними розладами, які відповідальні за прееклампсію, фетоплацентарну недостатність, затримку внутрішньоутробного розвитку плоду та його втрату й інш. [6][7][8][9]. На сьогодні вже доведено вірогідний взаємозв'язок між антифосфоліпідними антитілами та втратою вагітності, але, переконливих даних щодо інших факторів ризику розвитку тромбозу менш достатньо.…”

Section: Introduction/вступunclassified

Analysis of the State of Platelet Aggregation in Pregnant Women With Thrombophilia and Burdened Obstetric History

Zalyubovska

Hryshchenko

2021

EUMJ

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The analysis of platelet aggregation in pregnant women with thrombophilia and burdened obstetric history was performed. It has been determined that the development of adverse effects of pregnancy is significantly influenced by conditions such as placental abruption, fetal growth retardation, preeclampsia and fetal death, which are provoked by an abnormal vascular network of the placenta and hemostasis disorders caused by various thromboembolic disorders due to thrombophilia. Therefore, in recent years, the problem of thrombophilia has attracted much attention as a risk factor for pregnancy complications caused by various thromboembolic disorders, which are responsible for preeclampsia, fetoplacental insufficiency, fetal growth retardation and fetal loss, and others. Given the above, the aim of the work was to analyze the state of platelet aggregation of pregnant women with thrombophilia and burdened obstetric history. To achieve this goal, a study of pregnant women with thrombophilia and burdened obstetric history was conducted: 137 pregnant women, which were divided into two study groups – the main group, which included 101 pregnant women with a burdened obstetric history and thrombophilia, and the control group, which included 36 pregnant women with a burdened obstetric history without thrombophilia. The analysis of platelet aggregation of pregnant women with thrombophilia and burdened obstetric history was performed. It was found that the degree of platelet aggregation with the addition of an inducer of adenosine diphosphate at a concentration of 0.0625 prevailed in the control group as compared with pregnant women with thrombophilia (26.3 [24.3; 28.4] % and 21,4 [14,6; 31,1] % in contrast to the aggregation time and its speed (which were lower in the controls (58.0 [54.0; 72.0] s and 22.9 [20.4; 24.9] min) as compared with the main group (71.0 [48.0; 530.5] s) (and 26.5 [14.5; 38.3] min)). It was found that at a concentration of adenosine diphosphate of 0.125, all indicators of platelet aggregation prevailed in the main group (degree of aggregation (35.4 [25.6; 52.5] %; U = 1236.0; p = 0.004), its time (115.0 [47.0; 324.0] s; U = 1623.5; p = 0.341) and speed (45.2 [32.1; 57.5] min; U = 968.5; p < 0.001) compared to the controls (30.1 [26.7; 31.2] %, 84,0 [78.0; 103.5] s and 26.4 [30.4; 35.8] min). It was determined that the concentration of adenosine diphosphate of 0.250 caused an increase in the aggregation time in the control group as compared to the main group (225.5 [196.5; 269.3] s and 181.0 [57.0; 347.0] s; U = 1554.5; p = 0,198) in contrast to the degree [43,3 [39,6; 48.8] % and 51.1 [35.4; 63.8] %; U = 1417.0; p = 0.050) and aggregation rates (57.8 [42.8; 67.0] min and 40.1 [34.4; 47.9] min; U = 786.5; p < 0.001). It was also found that the maximum concentration of adenosine diphosphate (0.500) caused a significant (U = 11178.0; p = 0.002) increase in the aggregation time in the controls (329.0 [269.5; 390.0] s) compared to the main group (211.0 [72.5; 381.0] s) in contrast to the degree and rate of aggregation [51.9 [50.1; 54.3] %; U = 1606.5; p = 0.300 and 42.7 (38.8; 49.4] min; U = 923.5; p < 0.001 and 55.1 [38.6; 69.0] % and 63.6 [44.7; 72.6] min).

show abstract

Can thrombophilia worsen maternal and perinatal outcomes in cases of severe preeclampsia?

Cited by 10 publications

References 33 publications

Alterations in complement and coagulation pathways of human placentae subjected to in vitro fertilization and embryo transfer in the first trimester

Alterations in complement and coagulation pathways of human placentae subjected to in vitro fertilization and embryo transfer in the first trimester

Monitoring of Pregnancy-Induced Hypertension Syndrome Combined with Ultrasound Monitoring in Early Pregnancy to Prevent Chronic Hypertension with Preeclampsia

Analysis of the State of Platelet Aggregation in Pregnant Women With Thrombophilia and Burdened Obstetric History

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