thromboplastin and Pre-Eclampsia
thromboplastin has been researched along with Pre-Eclampsia* in 59 studies
Reviews
11 review(s) available for thromboplastin and Pre-Eclampsia
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Impact of haemostatic mechanisms on pathophysiology of preeclampsia.
Preeclampsia (PE) is disorder of new onset hypertension and proteinuria during the second half of pregnancy. There is increasing evidence to implicate placental over-expression of tissue factor and PAR-1 in the pathophysiology of PE. Excessive activation of platelets, neutrophils and the complement system may also contribute to the placental pathology and maternal endothelial responsible for the symptoms of PE. Increased knowledge in this field may identify new therapeutic strategies for the treatment of PE. Topics: Antibodies, Antiphospholipid; Blood Platelets; Complement Activation; Female; Hemostasis; Humans; Neutrophils; Placenta; Platelet Activation; Pre-Eclampsia; Pregnancy; Thromboplastin; Trophoblasts | 2017 |
The role of decidual cells in uterine hemostasis, menstruation, inflammation, adverse pregnancy outcomes and abnormal uterine bleeding.
Human pregnancy requires robust hemostasis to prevent hemorrhage during extravillous trophoblast (EVT) invasion of the decidualized endometrium, modification of spiral arteries and post-partum processes. However, decidual hemorrhage (abruption) can occur throughout pregnancy from poorly transformed spiral arteries, causing fetal death or spontaneous preterm birth (PTB), or it can promote the aberrant placentation observed in intrauterine growth restriction (IUGR) and pre-eclampsia; all leading causes of perinatal or maternal morbidity and mortality. In non-fertile cycles, the decidua undergoes controlled menstrual bleeding. Abnormal uterine bleeding (AUB) accompanying progestin-only, long-acting, reversible contraception (pLARC) accounts for most discontinuations of these safe and highly effective agents, thereby contributing to unwanted pregnancies and abortion. The aim of this study was to investigate the role of decidual cells in uterine hemostasis, menstruation, inflammation, adverse pregnancy outcomes and abnormal uterine bleeding.. We conducted a critical review of the literature arising from PubMed searches up to December 2015, regarding in situ and in vitro expression and regulation of several specific proteins involved in uterine hemostasis in decidua and cycling endometrium. In addition, we discussed clinical and molecular mechanisms associated with pLARC-induced AUB and pregnancy complications with abruptions, chorioamnionitis or pre-eclampsia.. Progestin-induced decidualization of estradiol-primed human endometrial stromal cells (HESCs) increases in vivo and in vitro expression of tissue factor (TF) and type-1 plasminogen activator inhibitor (PAI-1) while inhibiting plasminogen activators (PAs), matrix metalloproteinases (MMPs), and the vasoconstrictor, endothelin-1 (ET-1). These changes in decidual cell-derived regulators of hemostasis, fibrinolysis, extracellular matrix (ECM) turnover, and vascular tone prevent hemorrhage during EVT invasion and vascular remodeling. In non-fertile cycles, progesterone withdrawal reduces TF and PAI-1 while increasing PA, MMPs and ET-1, causing menstrual-associated bleeding, fibrinolysis, ECM degradation and ischemia. First trimester decidual hemorrhage elicits later adverse outcomes including pregnancy loss, pre-eclampsia, abruption, IUGR and PTB. Decidual hemorrhage generates excess thrombin that binds to decidual cell-expressed protease-activated receptors (PARs) to induce chemokines promoting shallow placentation; such bleeding later in pregnancy generates thrombin to down-regulate decidual cell progesterone receptors and up-regulate cytokines and MMPs linked to PTB. Endometria of pLARC users display ischemia-induced excess vasculogenesis and progestin inhibition of spiral artery vascular smooth muscle cell proliferation and migration leading to dilated fragile vessels prone to bleeding. Moreover, aberrant TF-derived thrombin signaling also contributes to the pathogenesis of endometriosis via induction of angiogenesis, inflammation and cell survival.. Perivascular decidualized HESCs promote endometrial hemostasis during placentation yet facilitate menstruation through progestational regulation of hemostatic, proteolytic, and vasoactive proteins. Pathological endometrial hemorrhage elicits excess local thrombin generation, which contributes to pLARC associated AUB, endometriosis and adverse pregnancy outcomes through several biochemical mechanisms. Topics: Decidua; Embryo Implantation; Endometrium; Female; Hemostasis; Humans; Menstrual Cycle; Plasminogen Activator Inhibitor 1; Pre-Eclampsia; Pregnancy; Pregnancy Outcome; Progestins; Thromboplastin; Uterine Hemorrhage | 2016 |
The role of tissue factor in normal pregnancy and in the development of preeclampsia: A review.
Tissue factor (TF) is a key element for normal gestation, especially in the first trimester. TF levels are hence raised in pregnancy, producing an adaptive hypercoagulable state. Potentiated hypercoagulability however, is associated with disorders of pregnancy such as pre-eclampsia but the results of TF and its inhibitor, tissue factor pathway inhibitor (TFPI), measurement, in pre eclampsic women are ambiguous and the data conflicting. This review covers the current knowledge status of the role of TF assessment in pregnancy with a focus on its diagnostic utility.. A review of the literature using the following key words: tissue factor, thrombosis, inflammation, pregnancy, preeclampsia.. The published literature shows raised and unchanged TF levels in various studies of pre-eclampsia along with equally conflicting data for TFPI. The various study designs and methods used in these studies makes valid comparison difficult. Meta analysis of 34 randomized trials showed that low-dose aspirin in early phases of gravidity (starting from the 16th week or earlier) significantly reduces the incidence of preeclampsia.. Overall, the results of the literature search together with knowledge of the structure and biological effects of TF, suggest that measuring the level of plasma TF/TFPI is not ideal for determining the actual levels of TF in the uteroplacental circulation. The current view that endothelial dysfunction is the trigger for preeclampsia, suggests that aspirin may be an effective prophylaxis. Further research will be necessary: measuring the expression of tissue factor on monocytes using flowcytometry and comparing the development of this expression during normal pregnancy and pregnancy complicated by preeclampsia, for example. Another possibility is immunohistochemical determination of the level of TF expression directly in placental tissue. Topics: Blood Coagulation; Female; Humans; Pre-Eclampsia; Pregnancy; Randomized Controlled Trials as Topic; Thromboplastin | 2015 |
Angiotensin II type 1 receptor autoantibody (AT1-AA)-mediated pregnancy hypertension.
Autoantibodies can cause complications in pregnancy. Preeclampsia is the leading cause of maternal and fetal morbidity and mortality during pregnancy. Overall, 5-10% of all pregnancies worldwide develop preeclampsia. Women who developed preeclampsia and their children have an increased risk to suffer from cardiovascular diseases later in life. In preeclampsia, agonistic autoantibodies against the angiotensin II type 1 receptor autoantibodies (AT1-AA) are described. They induce NADPH oxidase and the MAPK/ERK pathway leading to NF-κB and tissue factor activation. AT1-AA are detectable in animal models of preeclampsia and are responsible for elevation of soluble fms-related tyrosine kinase-1 (sFlt1) and soluble endoglin (sEng), oxidative stress, and endothelin-1, all of which are enhanced in preeclamptic women. AT1-AA can be detected in pregnancies with abnormal uterine perfusion and increased resistance index as well as in patients with systemic sclerosis and renal allograft rejection. This review discusses the current knowledge about the AT1-AA, its signaling, and their impact in pregnancy complications and other autoimmune disorders. Topics: Animals; Antigens, CD; Autoantibodies; Endoglin; Endothelin-1; Enzyme Activation; Female; Humans; MAP Kinase Signaling System; Mice; NADPH Oxidases; NF-kappa B; Oxidative Stress; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Rats; Receptor, Angiotensin, Type 1; Receptors, Cell Surface; Thromboplastin; Vascular Endothelial Growth Factor Receptor-1 | 2013 |
Role of tissue factor in feto-maternal development: a xiphos.
In this review, the dual role of tissue factor (TF) in pregnancy is described. On the one hand, TF is required for embryonic and placental development in a successful pregnancy, and on the other hand, pathologic expression of TF can lead to serious pregnancy complications in humans and mice. Human studies show increased TF levels in plasma, amniotic fluid and and/or placentas of abnormal pregnancies affected by miscarriages, preterm birth, or pre-eclampsia. Interestingly, using two mouse models, we found that blood-borne TF plays a crucial role in the pathogenesis of pregnancy complications. TF on neutrophils and monocytes is a critical mediator in trophoblast injury and embryo damage in pregnancy loss induced by antiphospholipid antibodies and in the antibody-independent CBA/J × DBA/2 model of miscarriages. Blockade of TF or genetic diminution prevented pregnancy complications, suggesting that TF may be a good target for therapy in patients with recurrent miscarriages, pregnancy loss, and pre-eclampsia. In addition, statins, which downregulate TF, may constitute a good therapeutic option for women with pregnancy complications. Clinical trials should be conducted to confirm these observations in women. Topics: Animals; Female; Fetal Development; Humans; Mice; Mice, Inbred CBA; Mice, Inbred DBA; Pre-Eclampsia; Pregnancy; Pregnancy Outcome; Thromboplastin | 2011 |
Tissue factor dependent pathway and the diagnosis of pre-eclampsia.
Pre-eclampsia (P-EC) is a major contributor to perinatal and maternal morbidity and mortality worldwide. Its etiology and pathogenesis remains poorly understood, and differential diagnosis is problematic. During a normal pregnancy, coagulation activation is essential for physiological placental hemostasis, but women with P-EC tend to be more hypercoagulable than normal pregnant women. A common proposed mechanism for P-EC is utero-placental thrombosis. Indeed, multiple placental microthrombi are frequently observed in women with P-EC, and these may compromise placental perfusion and fetal development. This suggests that predisposing factors to thrombosis could contribute to the development of P-EC. Thus studying circulating hemostatic proteins may help elucidate some of the pathogenesis of P-EC and may provide a rational basis for its differential diagnosis and effective treatment. Preliminary studies by our group on third-trimester women suggest that raised circulating factor VII (FVII) is a selective marker for P-EC when women with P-EC were compared with healthy nonpregnant or normal pregnant women groups. Plasma FVII levels have shown good sensitivity and specificity for P-EC of 90% and 80%, respectively. However, significant comparable changes in the other tissue factor (TF)-dependent pathway factors (activated FVII), TF, and tissue factor pathway inhibitor were not observed. Thus we propose the use of plasma FVII as a potential marker of P-EC. Topics: Biomarkers; Factor VII; Female; Hemostasis; Humans; Lipoproteins; Pre-Eclampsia; Pregnancy; Pregnancy Trimester, Third; Sensitivity and Specificity; Thromboplastin | 2011 |
Coagulation and fibrinolysis in amniotic fluid: physiology and observations on amniotic fluid embolism, preterm fetal membrane rupture, and pre-eclampsia.
Two dangerous obstetric complications, amniotic fluid embolism and preterm prelabor rupture of membranes (PROM), can be caused by amniotic fluid (AF) constituents. Disseminated intravascular coagulation (DIC) is related to the former complication, whereas local thrombin/plasmin-dependent collagenolysis in the decidua and fetal membranes is associated with the latter. In AF, most proteins of the coagulation and fibrinolysis system, known as plasma constituents, have been identified based on the activity and/or presence of antigen. The AF levels of most of these proteins are low (< 2 to 5% of the respective maternal plasma levels). However, there are some exceptions: tissue factor (TF), urokinase plasminogen activator (uPA) and its receptor (uPAR), as well as plasminogen activator inhibitors. The AF level of fetal fibrinogen is trace, which is a particular exception. The key enzymes of coagulation and fibrinolysis, thrombin and plasmin, are generated in AF. Thrombin generation is four- to fivefold higher than in maternal plasma as measured by the concentration of the prothrombin fragments 1 + 2 (F 1 + 2) and thrombin-antithrombin complexes, whereas plasmin generation is relatively low as measured by the plasmin-α-2-antiplasmin complexes. Phosphatidylserine, a phospholipid, and thrombin-activatable fibrinolysis inhibitor (TAFI) are novel components of AF. Phosphatidylserine contributes to DIC in AF embolism; TAFI is considered a link between coagulation and fibrinolysis. uPA and uPAR are the factors contributing to PROM via plasmin-dependent proteolysis. Intriguing is the assumption that TF and its inhibitor can be risk factors for PROM through thrombin-dependent activation of matrix prometalloproteinases in the decidua and fetal membranes. It is unknown whether the amniotic pool of hemostatic components is involved in pre-eclampsia pathogenesis. Topics: Amniotic Fluid; Blood Coagulation; Embolism, Amniotic Fluid; Female; Fetal Membranes, Premature Rupture; Fibrinolysin; Fibrinolysis; Humans; Phosphatidylserines; Pre-Eclampsia; Pregnancy; Thrombin; Thromboplastin | 2011 |
Is preeclampsia an autoimmune disease?
Preeclampsia is a life-threatening hypertensive disease of pregnancy. The condition is characterized by the presence of autoantibodies that activate the major angiotensin receptor, AT(1). Research conducted during the past decade has shown that these autoantibodies activate AT(1) receptors on a variety of cell types and provoke biological responses that are relevant to the pathophysiology of preeclampsia. The introduction of these autoantibodies into pregnant mice results in hypertension, proteinuria and a variety of other features of preeclampsia including small fetuses and placentas. These findings demonstrate the pathophysiological role of these autoantibodies in preeclampsia. The biological properties of these autoantibodies can be blocked by a 7-amino acid peptide that corresponds to a specific sequence associated with the second extracellular loop of the AT(1) receptor. The fact that autoantibodies from different individuals are directed to a common epitope provides obvious diagnostic and therapeutic opportunities. Research reviewed here raises the intriguing possibility that preeclampsia may be a pregnancy-induced autoimmune condition characterized by the presence of disease-causing angiotensin receptor activating autoantibodies. Topics: Adoptive Transfer; Angiogenesis Inducing Agents; Animals; Autoantibodies; Autoimmune Diseases; Female; Humans; Pre-Eclampsia; Pregnancy; Reactive Oxygen Species; Receptor, Angiotensin, Type 1; Thrombophilia; Thromboplastin | 2009 |
The functional role of the renin-angiotensin system in pregnancy and preeclampsia.
During normal pregnancy, the renin-angiotensin system (RAS) plays a vitally important role in salt balance and subsequent well-being of mother and fetus. In this balance, one must consider not only the classical renal RAS but also that of the uteroplacental unit, where both maternal and fetal tissues contribute to the signaling cascade. Many studies have shown that in normal pregnancy there is an increase in almost all of the components of the RAS. In derangements of pregnancy this delicate equilibrium can become unbalanced. Preeclampsia is one such case. It is a disorder of pregnancy characterized by hypertension, proteinuria and placental abnormalities associated with shallow trophoblast invasion and impaired spiral artery remodeling. Despite being a leading cause of maternal death and a major contributor to maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of preeclampsia are poorly understood. Immunological mechanisms and the RAS have been long considered to be involved in the development of preeclampsia. Numerous recent studies demonstrate the presence of the angiotensin II type I receptor agonistic autoantibody (AT1-AA). This autoantibody can induce many key features of the disorder and upregulate molecules involved in the pathogenesis of preeclampsia. Here we review the functional role of the RAS during pregnancy and the impact of AT1-AA on preeclampsia. Topics: Angiotensin II; Animals; Autoantibodies; Calcium; Disease Models, Animal; Female; Humans; Peptidyl-Dipeptidase A; Placenta; Placenta Diseases; Plasminogen Activator Inhibitor 1; Pre-Eclampsia; Pregnancy; Reactive Oxygen Species; Renin-Angiotensin System; Thromboplastin; Vascular Endothelial Growth Factor Receptor-1 | 2008 |
Decidual cell-expressed tissue factor in human pregnancy and its involvement in hemostasis and preeclampsia-related angiogenesis.
During extravascular trophoblast (EVT) invasion of the decidua, thrombin generated from decidual cell-expressed tissue factor (TF) forms a "hemostatic envelope" that protects against hemorrhage during the initial breaching of capillaries by EVTs and subsequent invasion and remodeling of the spiral arteries and arterioles. Preeclampsia, the world's leading cause of fetal and maternal morbidity and mortality, stems from shallow trophoblast invasion leading to incomplete vascular remodeling that impairs uteroplacental blood flow. A considerable subset of cases of preeclampsia is associated with decidual hemorrhage and maternal thrombophilias, which form excess thrombin from decidual cell-expressed TF. Thrombin affects several cell functions by binding to protease-activated receptors. In first-trimester decidual cells, thrombin enhances expression of sFlt-1, which can block the angiogenic effects of vascular endothelial growth factor (VEGF) and placental growth factor. By contrast, thrombin does not affect decidual cell VEGF expression. Thrombin-enhanced sFlt-1 expression by decidual cells, the predominant cell type encountered by invading cytotrophoblasts, could promote preeclampsia by interfering with angiogenesis-dependent vascular remodeling to reduce uteroplacental blood flow. Topics: Animals; Decidua; Female; Hemostasis; Humans; Mice; Models, Biological; Neovascularization, Pathologic; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Thrombin; Thromboplastin; Vascular Endothelial Growth Factor A | 2008 |
Blood clotting abnormalitis in relation to pre-eclampsia: a review.
Topics: Abruptio Placentae; Adrenal Glands; Aminocaproates; Animals; Basement Membrane; Biopsy; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Platelets; Brain; Female; Fibrin; Fibrinogen; Fibrinolysis; Fluorescent Antibody Technique; Hemorrhage; Hemorrhagic Disorders; Heparin; Humans; Hypertension, Malignant; Kidney Cortex Necrosis; Kidney Failure, Chronic; Kidney Glomerulus; Liver; Maternal Mortality; Microscopy, Electron; Myocardium; Placental Extracts; Pre-Eclampsia; Pregnancy; Rabbits; Shwartzman Phenomenon; Thromboplastin; Thrombosis | 1969 |
Trials
1 trial(s) available for thromboplastin and Pre-Eclampsia
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Preeclampsia: the role of tissue factor and tissue factor pathway inhibitor.
Preeclampsia (PE) is a multi-system disorder of human pregnancy, whose etiology remains poorly understood. Preeclamptic women are known to have an increased hypercoagulable state that result in excess fibrin deposition in several organs, which compromises their function. Tissue factor (TF) is the main physiological initiator of blood coagulation and its activity is regulated by a specific inhibitor known as Tissue factor pathway inhibitor (TFPI). Based on the important role of TF and TFPI in hemostasis, we hypothesize that their levels may change in the severe PE contributing to exacerbate hypercoagulable state. Some studies have assessed the balance between TF and TFPI in preeclamptic women, but results are inconsistent. Therefore, the aim of this study was to examine these inconsistencies and to assess TF and TFPI plasma levels in three groups of age matched women; pregnant with severe PE (n = 60), normotensive pregnant (n = 50) and normotensive non-pregnant women (n = 50). There was not significantly different among the three groups for TF plasma levels; severe PE women: 338.4 pg/mL (248.1-457.6), normotensive pregnant women: 301.5 pg/mL (216.4-442.9) and normotensive non-pregnant women 393 pg/mL (310.3-522.9). TFPI plasma levels were higher in severe PE comparing to normotensive pregnant women and normotensive non-pregnant women, 115.8 ng/mL (75-149.8); 80.3 ng/mL (59.6-99.7) and 74.5 ng/mL (47.1-98.0), respectively No difference was found between normotensive pregnant women and normotensive non-pregnant women. As for gestational age, a significant difference in TFPI levels was found between severe PE and normotensive pregnant women up to the 33rd week of pregnancy (p = 0.001), and severe PE and non-pregnant women up to the 34th (p = 0.01). In summary, our results indicated that TF plasma levels did not vary in the studied groups, while TFPI plasma levels were significantly increased in severe PE compared to normotensive pregnant and normotensive non-pregnant women. So, our data do not explain the exacerbated hypercoagulability state observed in severe PE. Further studies evaluating genes expression, TF activity and antigen, total and free TFPI and TFPI-2, both in plasma and obstetric tissues, throughout the pregnancy in PE (mild and severe forms) are required. Topics: Adolescent; Adult; Case-Control Studies; Female; Humans; Lipoproteins; Pre-Eclampsia; Pregnancy; Pregnancy Trimester, Third; Severity of Illness Index; Thromboplastin | 2012 |
Other Studies
47 other study(ies) available for thromboplastin and Pre-Eclampsia
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The procoagulant phospholipid dependent clotting time and the initiation phase of thrombin generation test are mandatory for the evaluation of the risk for severe early onset preeclampsia.
Topics: Blood Coagulation Tests; Female; Humans; Phospholipids; Pre-Eclampsia; Pregnancy; Thrombin; Thromboplastin | 2022 |
Soluble syndecan-1 and glycosaminoglycans in preeclamptic and normotensive pregnancies.
Preeclampsia, an important cause of maternal and fetal morbidity and mortality, is associated with increased sFLT1 levels and with structural and functional damage to the glycocalyx contributing to endothelial dysfunction. We investigated glycocalyx components in relation to preeclampsia in human samples. While soluble syndecan-1 and heparan sulphate were similar in plasma of preeclamptic and normotensive pregnant women, dermatan sulphate was increased and keratan sulphate decreased in preeclamptic women. Dermatan sulphate was correlated with soluble syndecan-1, and inversely correlated with blood pressure and activated partial thromboplastin time. To determine if syndecan-1 was a prerequisite for the sFlt1 induced increase in blood pressure in mice we studied the effect of sFlt1 on blood pressure and vascular contractile responses in syndecan-1 deficient and wild type male mice. The classical sFlt1 induced rise in blood pressure was absent in syndecan-1 deficient mice indicating that syndecan-1 is a prerequisite for sFlt1 induced increase in blood pressure central to preeclampsia. The results show that an interplay between syndecan-1 and dermatan sulphate contributes to sFlt1 induced blood pressure elevation in pre-eclampsia. Topics: Adult; Animals; Blood Pressure; Dermatan Sulfate; Female; Glycocalyx; Heparitin Sulfate; Humans; Keratan Sulfate; Mice; Mice, Inbred C57BL; Pre-Eclampsia; Pregnancy; Syndecan-1; Thromboplastin; Vascular Endothelial Growth Factor Receptor-1; Vasoconstriction | 2021 |
Expression of tissue factor and thrombomodulin in the placentas of pregnancies affected by early-onset and late-onset preeclampsia.
To analyze the differential genetic expression and protein localization of thrombomodulin (THBD) and tissue factor (F3) in the placentas of pregnancies affected by preeclampsia.. We assessed the expression of THBD and F3 by immunohistochemistry and real-time polymerase chain reaction (PCR) in placentas from 20 PE cases: 10 early-onset PE placentas, 10 late-onset PE placentas, and 10 control cases (normal pregnancies).. In cases, we found higher THBD and F3 RNA levels in placental tissue. Protein expression in controls differed from that in late-onset PE placentas, which had lower THBD levels in syncytiotrophoblasts and amniotic cells. Likewise, late-onset PE placentas exhibited comparatively lower F3 expression in the perivillous fibrin. In contrast, early-onset PE had high F3 expression in the subdecidual fibrin. We found no significant differences in the F3/THBD ratio between the groups.. Our study supports evidence that shows the involvement of F3 and THBD in placental disorders. Furthermore, this finding contributes to a better understanding of the physio-pathological role that these molecules may play in the development of this heterogeneous disease. Topics: Case-Control Studies; Female; Humans; Placenta; Pre-Eclampsia; Pregnancy; Thrombomodulin; Thromboplastin; Trophoblasts | 2021 |
Tissue factor activity in women with preeclampsia or SGA: a potential explanation for the excessive thrombin generation in these syndromes.
The aim of this study was to determine whether the activity of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in the plasma of women with preeclampsia (PE) and small for gestational age (SGA) neonate differ from that of normal pregnant women and whether they are related to specific placental lesions.. This cross-sectional study included the following groups: (1) normal pregnancy (n = 68); (2) PE (n= 128); and (3) SGA (n = 56). Maternal plasma TF and TFPI activity was determined with chromogenic assays.. (1) The median maternal plasma TF activity, but not TFPI activity, differed among the study groups (p < .0001 and p = .4, respectively); (2) patients with PE had a higher median maternal plasma TF activity than women with normal pregnancies (p < .0001) and mothers with SGA fetuses (p = .002); (3) among patients with PE, those with distal villous hypoplasia had a higher median maternal TF activity than those without these placental lesions (p = .018); and (4) following adjustment for confounding variables, maternal plasma TF and TFPI activity were not associated with an SGA neonate.. Plasma TF activity is higher in women with PE than in those with SGA or normal pregnancies. We propose that these changes may be responsible, at least in part, for the increased in-vivo thrombin generation observed in this obstetrical syndrome. Topics: Adult; Cross-Sectional Studies; Female; Humans; Infant, Small for Gestational Age; Lipoproteins; Placenta; Pre-Eclampsia; Pregnancy; Thrombin; Thromboplastin; Young Adult | 2018 |
Elevated plasma TFPI activity causes attenuated TF-dependent thrombin generation in early onset preeclampsia.
Early onset preeclampsia (EOP) is a pregnancy-specific proinflammatory disorder that is characterised by competing thrombotic and bleeding risks. It was the aim of this study to characterise thrombin generation, a major determinant of thrombotic and bleeding risk, in order to better understand the haemostatic balance in patients with EOP. Patients with EOP were recruited at the Rotunda Hospital, Dublin. Twenty-six cases of EOP were recruited over a 21-month period, out of 15,299 deliveries at the Rotunda. Blood samples were collected into sodium citrate plus corn trypsin inhibitor anticoagulated vacutainers, platelet-poor plasma was prepared, and calibrated automated thrombography was used to assess thrombin generation. Results were compared to age and sex-matched non-pregnant controls (n=13) and age- and gestation-matched pregnant controls (n=20). The rate and extent of thrombin generation triggered by low-dose tissue factor (TF) was significantly reduced in patients with EOP compared to pregnant controls, most significantly in cases of severe EOP. EOP patients displayed a trend towards an increased response to endogenous activated protein C and thrombomodulin relative to pregnant controls. Plasma tissue factor pathway inhibitor (TFPI) activity was increased in EOP patients. Inhibition of TFPI abolished the attenuation of thrombin generation stimulated by low-dose TF. In conclusion, patients with EOP are characterised by an attenuated coagulation response characterised by reduced thrombin generation stimulated by low-dose TF and elevated plasma TFPI activity. These changes in coagulation may modulate thrombotic risk and bleeding risk in patients with EOP. Topics: Adult; Biomarkers; Blood Coagulation; Blood Coagulation Tests; Carboxypeptidase B2; Case-Control Studies; Female; Gestational Age; Hemorrhage; Humans; Ireland; Pre-Eclampsia; Pregnancy; Prognosis; Protein C; Protein S; Risk Factors; Thrombin; Thrombomodulin; Thromboplastin; Thrombosis; Up-Regulation | 2017 |
Increased tissue factor expression and promoter hypomethylation in preeclampsia placentas in a Chinese population.
To explore the relationship between expression of tissue factor and its methylation levels in the placentas of preeclampsia among Chinese Han population.. In this study, we explored gene manifestation or expression of tissue factor, and evaluated methylation levels of tissue factor promoter areas in 16 clinical preeclampsia placentas as well as 16 paired normal pregnancy placentas from the Chinese Han population. Real-time PCR, immunohistochemistry, Western blotting, and methylation-specific PCR were conducted.. Expression of tissue factor protein in the preeclampsia group was 0.857±0.043, which was considerably elevated over that in the control group (0.248±0.035) (P<0.05). Expression of tissue factor was elevated in mRNA as well as in protein quantities in preeclampsia placentas, compared with the control group (1.45±0.42vs. 0.25±0.28, P<0.05). Immunohistochemical staining for tissue factor showed positive within syncytio-cytotrophoblast layers, and there was additional scattered staining in the preeclampsia group. Methylation-specific PCR showed that methylation levels of tissue factor promoter were considerably reduced in preeclamptic placentas (0.928±0.148), in comparison with control group (0.187±0.112, P<0.05).. Tissue factor is expected to participate in preeclampsia etiology through methylation regulation. Topics: Adult; Asian People; Case-Control Studies; China; DNA Methylation; Female; Humans; Immunohistochemistry; Placenta; Polymerase Chain Reaction; Pre-Eclampsia; Pregnancy; Promoter Regions, Genetic; RNA, Messenger; Thromboplastin | 2017 |
Tissue factor-dependent pathway in severe preeclampsia revisited: a Brazilian cohort study.
Previously we investigated the tissue factor (TF)-dependent coagulation pathway and key haemostatic cofactors in white women with preeclampsia (P-EC) and suggested that plasma factor VII (FVII) levels can differentiate women with P-EC from healthy nonpregnant women or normal pregnant women, at the same trimester, with high sensitivity, specificity, positive and negative predictive values. Here we re-examine the TF-dependent pathway in a large cohort of Brazilian women. A total of 240 women were studied. These included healthy nonpregnant women (n = 79), normotensive pregnant women (n = 80) and women with severe P-EC (n = 81). Commercially available enzyme-linked immunosorbent assays were used to measure plasma FVII, activated factor VII (FVIIa), TF and tissue factor pathway inhibitor (TFPI). All study participants were matched for age. Pregnant women (with/without P-EC) were matched for gestational age and parity. Plasma levels of FVII, FVIIa and TFPI were significantly increased in women with severe P-EC compared with healthy nonpregnant women (P < 0.01) or normotensive pregnant women (P < 0.01). FVIIa was also higher in normotensive pregnant women compared with nonpregnant women (P < 0.01). However, no such significant trends were observed for plasma TF levels (P = 0.074). In conclusion, circulating FVII, FVIIa and TFPI were significantly elevated in women with severe P-EC in the absence of comparable changes in plasma TF levels. The present work is in agreement with our previous report on FVII levels in white women with P-EC. Thus, this lends further support to the notion that plasma FVII levels are potentially valuable diagnostic marker for P-EC, irrespective of ethnicity. Topics: Adult; Blood Coagulation; Blood Pressure; Brazil; Case-Control Studies; Cohort Studies; Factor VII; Factor VIIa; Female; Gene Expression; Humans; Lipoproteins; Pre-Eclampsia; Pregnancy; Severity of Illness Index; Thromboplastin | 2016 |
Increased tissue factor and thrombomodulin expression and histopathological changes in placentas of pregnancies with preeclampsia.
Preeclampsia has a global frequency of 2-8% and a frequency of 10% in developing countries. In Colombia, preeclampsia causes 42% of maternal mortality. Alterations in placental homeostasis have been proposed to be involved in its pathophysiology. The aim of this study was to compare mRNA and protein levels of tissue factor (F3) and thrombomodulin (THBD) and the histopathological findings of placentas.. We studied 16 placentas from patients with preeclampsia and 19 term placentas with uncomplicated pregnancy. An expert pathologist, who was masked to the group assignment, conducted an evaluation to determine specific histological changes. Assessments of mRNA and protein levels of F3 and THBD were performed using real-time PCR and ELISA, respectively.. Cases and controls differed in the frequency of decidual arteriopathy (p = 0.027), acute infarction (p = 0.001) and hyperplasia of the syncytiotrophoblast (p = 0.0017). Cases had increased levels of F3 mRNA (p = 0.0124) and protein (p < 0.0001) and THBD mRNA (p < 0.0001) and protein (p < 0.0001).. In placenta of patients with preeclampsia, we detected abnormal expression of F3 and THBD with increased protein and mRNA levels. The role of these molecules in the pathogenesis of this disease and in alterations of hemostatic and histopathological aspects of placentas need further studying. Topics: Adult; Case-Control Studies; Female; Humans; Placenta; Pre-Eclampsia; Pregnancy; RNA, Messenger; Thrombomodulin; Thromboplastin | 2016 |
Changing the guard.
Topics: Antithrombins; Blood Coagulation; Female; Humans; Neoplasms; Pre-Eclampsia; Pregnancy; Thromboplastin; Thrombosis | 2016 |
Possibility of Coagulation System Activation Determination with Tissue Factor in Pregnancy Complications.
In this part of the study, where we determined the causes of preeclampsia and other obstetric complications, we focused on the role of tissue factor (TF) in the activation of these pathophysiological processes. Recent findings attribute a significant part of the activation of coagulation creation of autoantibodies. Once this mechanism is activated, the antibodies induce expression of tissue factor (TF, CD142) on monocytes and vascular endothelial cells.. We have proposed a monitor activation model of the coagulation system in preeclampsia and other pregnancy complications using TF expression on monocytes by flow cytometry and simultaneous determination the TF-induced thrombin generation in plasma. To determine expression of tissue factor (CD142) on monocytes, we proposed a method of multicolor flow cytometry using anti CD45 PerCP, anti CD14 APC, anti CD16b FITC, and anti CD142 PE antibodies and the corresponding isotype controls.. We verified the model on patients with severe antiphospholipid syndrome, which is a high expression of antibodies, in particular against beta-2GPI.. We demonstrated complete inhibition of TF expression on monocytes and a significant reduction of thrombin generation in plasma. Topics: Adult; Antiphospholipid Syndrome; Blood Coagulation; Female; Flow Cytometry; Humans; Monocytes; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Thromboplastin | 2016 |
Tissue factor and tissue factor pathway inhibitor in women with a past history of preeclampsia: implication for a hypercoagulable state postpregnancy.
Preeclampsia (P-EC) is a multisystem disorder of pregnancy whose cause and pathogenesis remain poorly understood. However, abnormal haemostasis and endothelial dysfunction are thought to be implicated. Women with a past medical history of P-EC have a baseline hypercoagulable state postpregnancy. The aim of this study is to examine the relationship between tissue factor (TF) and TF pathway inhibitor (TFPI) in women who have had P-EC within the last 3 years (more than 6 months postpartum) and their normal counterparts. Blood specimens were collected from women known to have had P-EC within the last 3 years (n = 26) and aged-matched healthy women without past history of P-EC in previous pregnancy (n = 26). Plasma TF and TFPI levels were measured using ELISAs. Women who have had P-EC showed increased TF levels compared with their normal counterparts, whereas TFPI levels were reduced. Neither parameter differed significantly when the groups were tested against each other. Interestingly, the TF/TFPI ratio was significantly increased (P = 0.024) when the two groups were compared. In summary, there was a trend towards increased TF and reduced TFPI levels in the P-EC group. Such a tendency was not statistically significant. However, the TF/TFPI ratio was significantly increased when the groups were compared. Our findings suggest an imbalance between TF/TFPI levels in women with past history of P-EC postpregnancy. This may contribute to the development of maternal hypercoagulable states and may predispose women with a history of P-EC to cardiovascular risks later in life. Topics: Adult; Case-Control Studies; Female; Humans; Lipoproteins; Middle Aged; Pre-Eclampsia; Pregnancy; Thrombophilia; Thromboplastin; Young Adult | 2014 |
Preeclampsia: integrated network model of platelet biomarkers interaction as a tool to evaluate the hemostatic/immunological interface.
Preeclampsia (PE) is associated with platelet activation, which may be involved in its pathogenesis promoting coagulation and mediating inflammation. We investigated whether the platelet activation status together with the frequency of platelet-leukocyte aggregates/PLA and monocyte tissue factor/TF expression could be used as laboratorial biomarkers for PE diagnosis and prognosis.. Ninety-seven women were evaluated including severe PE/sPE (N=15), mild PE/mPE (N=20), normotensive pregnant/NP (N=31) and non-pregnant women/nonP (N=31). Platelet markers were analyzed by flow cytometry.. Platelet counts and CD41a expression by platelets were lower in NP and sPE vs nonP. The expression of CD61 was lower during pregnancy. Altered balance of platelet marker expression was also observed in NP and sPE vs nonP. No significant differences in the PLA and TF expression by monocytes were observed among the groups. There are several correlations between platelet activation markers, especially in sPE, which suggest a relevant role of the hemostatic/immunological cross-talk in this disease.. PE is not associated with increased platelet activation markers. It cannot rule out a role of platelet activation in the PE pathophysiology. Despite those correlations, we did not find a putative laboratorial biomarker that could be useful by itself for PE diagnosis and prognosis. Topics: Adult; Biomarkers; Blood Platelets; Female; Gene Expression Regulation; Hemostasis; Humans; Models, Biological; Monocytes; Platelet Activation; Platelet Aggregation; Pre-Eclampsia; Pregnancy; Prognosis; Thromboplastin | 2014 |
Plasma factor VII: a potential marker of pre-eclampsia.
Normal pregnancy is associated with a local hypercoagulable state that becomes more profound in certain obstetric complications such pre-eclampsia (P-EC). Current literature on the levels of individual haemostatic factors in women with P-EC is limited and results are inconsistent. In this study we provide detailed investigation on the tissue factor (TF)-dependent pathway in women with P-EC.. Enzyme-linked immunosorbent assays (ELISA) were used to measure plasma factor (F) FVII, FVIIa, TF and tissue factor pathway inhibitor (TFPI) in healthy non-pregnant women (n = 22), normal pregnant women (n = 15), and women with P-EC (n = 20). All subjects were age matched. In addition, pregnant women were matched for gestational age, parity and were all at the third trimester.. Plasma FVII levels were significantly higher in women with P-EC compared to the healthy non-pregnant (P<0.001) or the normal pregnant groups (P<0.001). No such significant trends were observed for plasma FVIIa, TF or TFPI levels. Plasma FVII levels can distinguish women with P-EC from healthy non-pregnant women or normal pregnant women at the third trimester, with high sensitivity (90%), specificity (80%), positive and negative predictive values (86%).. Plasma FVII levels are significantly elevated in women with P-EC, in the absence of comparable changes in other TF-dependent pathway factors (FVIIa, TF and TFPI). We propose the use of plasma FVII as a marker for P-EC. Topics: Adult; Biomarkers; Case-Control Studies; England; Enzyme-Linked Immunosorbent Assay; Factor VII; Factor VIIa; Female; Humans; Lipoproteins; Pre-Eclampsia; Predictive Value of Tests; Pregnancy; Pregnancy Trimester, Third; Reproducibility of Results; Sensitivity and Specificity; Thromboplastin; Up-Regulation; Young Adult | 2011 |
Alternations of maternal and cord plasma hemostasis in preeclampsia before and after delivery.
The aim of this study was to investigate the role of hemostatic factors in the pathogenesis of preeclampsia.. Maternal and cord plasma concentrations of tissue factor (TF), tissue factor pathway inhibitor (TFPI), von willebrand factor (vWF), soluble P-selectin (sP-selectin), fibrinopeptide A (FPA), D-dimer, and antithrombin III (AT-III) were measured by enzyme-linked immunosorbent assay (ELISA) in 46 women with preeclampsia and 40 normotensive pregnant women before and after delivery.. The maternal plasma concentrations of TF, vWF, and sP-selectin were higher, but lower concentrations of TFPI, AT-III, and D-dimer were observed in women with preeclampsia compared to normotensive pregnant women before and after delivery. Compared with maternal plasma, fetal plasma concentrations of TF concentrations were increased significantly in both groups, whereas vWF, FPA, TFPI, AT-III, and D-dimer were decreased. Compared with normotensive pregnancy, fetal plasma concentrations of TF were markedly increased in preeclampsia, accompanied with a higher vWF and a lower sP-selectin and D-dimer levels. Furthermore, fetal plasma TF concentrations were more significantly increased in women with high blood pressure and severe proteinuria.. Imbalance in the coagulation/fibrinolysis equilibrium, especially alterations in the extrinsic pathway of coagulation and anticoagulation, may play an important role in the pathogenesis of preeclampsia. In addition, fetal alteration of TF may be involved in the pathogenesis of fetal complications of preeclampsia. Topics: Adult; Delivery, Obstetric; Female; Fibrin Fibrinogen Degradation Products; Hemostasis; Humans; P-Selectin; Pre-Eclampsia; Pregnancy; Thrombomodulin; Thromboplastin; Tissue Plasminogen Activator; Umbilical Cord; von Willebrand Factor | 2011 |
Role of tissue factor in pregnancy complications: crosstalk between coagulation and inflammation.
Bad pregnancy outcomes have been associated with increased activation of the coagulation cascade and inflammation, in particular the activation of the complement cascade. Recent studies have suggested that inflammatory processes modulate thrombogenic pathways and vice versa. We studied the cross-talk between the coagulation and the complement cascade in the pathogenesis of recurrent miscarriages and preeclampsia in mice. We identified tissue factor (TF) as a crucial mediator of fetal and placental damage in mouse models of recurrent miscarriages and preeclampsia. Increased TF expression increases the release of reactive oxygen species and antiangiogenic molecules from inflammatory cells inducing trophoblast damage and bad pregnancy outcomes. We also demonstrated that pravastatin, by downregulating TF expression, prevents miscarriages and the onset of preeclampsia in mice. Topics: Abortion, Habitual; Animals; Anticholesteremic Agents; Blood Coagulation; Complement Activation; Complement System Proteins; Female; Humans; Inflammation; Mice; Pravastatin; Pre-Eclampsia; Pregnancy; Thromboplastin | 2011 |
Decidual hemostasis, inflammation, and angiogenesis in pre-eclampsia.
Invasion of the decidua by extravillous trophoblasts (EVTs) is accompanied by thrombin generation from decidual cell (DC)-expressed tissue factor (TF). This TF protects against hemorrhage as EVTs breach capillaries and subsequently invade and remodel spiral arteries and arterioles. Pre-eclampsia (P-EC) is the world's leading cause of fetal and maternal morbidity and mortality. It is associated with decidual hemorrhage and maternal thrombophilias, which form excess thrombin from DCs, and with maternal infections and other inflammatory conditions that are associated with excess expression of the proinflammatory cytokines interleukin (IL)-1 β and tumor necrosis factor (TNF) α. In human first-trimester leukocyte-free DCs, (1) thrombin enhances expression of soluble fms-like tyrosine kinase-1 (sFlt-1), a potent inhibitor of angiogenesis; (2) thrombin, IL-1β and TNF-α increase monocyte-recruiting chemokine expression leading to a macrophage excess in the pre-eclamptic decidua. The pathogenesis of P-EC likely stems from shallow EVT invasion leading to impaired decidual vascular remodeling. The resulting reduced uteroplacental blood flow is associated with a hypoxic placenta, which appears to secrete excess sFlt-1 into the maternal plasma. A regulatory role for DCs in vascular remodeling is indicated because impaired decidual vascular remodeling could stem from an aberrant local antiangiogenic milieu elicited by excess sFlt-1 and/or macrophage-inhibited EVT decidual invasion. Topics: Decidua; Female; Hemostasis; Humans; Interleukin-1beta; Neovascularization, Pathologic; Pre-Eclampsia; Pregnancy; Thrombin; Thromboplastin; Trophoblasts; Tumor Necrosis Factor-alpha; Vascular Endothelial Growth Factor Receptor-1 | 2011 |
Syncytiotrophoblast microvesicles released from pre-eclampsia placentae exhibit increased tissue factor activity.
Pre-eclampsia is a complication of pregnancy associated with activation of coagulation. It is caused by the placenta, which sheds increased amounts of syncytiotrophoblast microvesicles (STBM) into the maternal circulation. We hypothesized that STBM could contribute to the haemostatic activation observed in pre-eclampsia.. STBM were collected by perfusion of the maternal side of placentae from healthy pregnant women and women with pre-eclampsia at caesarean section. Calibrated automated thrombography was used to assess thrombin generation triggered by STBM-borne tissue factor in platelet poor plasma (PPP). No thrombin was detected in PPP alone but the addition of STBM initiated thrombin generation in 14/16 cases. Pre-eclampsia STBM significantly shortened the lag time (LagT, P = 0.01) and time to peak thrombin generation (TTP, P = 0.005) when compared to normal STBM. Blockade of tissue factor eliminated thrombin generation, while inhibition of tissue factor pathway inhibitor significantly shortened LagT (p = 0.01) and TTP (P<0.0001), with a concomitant increase in endogenous thrombin potential.. STBM triggered thrombin generation in normal plasma in a tissue factor dependent manner, indicating that TF activity is expressed by STBM. This is more pronounced in STBM shed from pre-eclampsia placentae. As more STBM are shed in pre-eclampsia these observations give insight into the disordered haemostasis observed in this condition. Topics: Adult; Female; Humans; Pre-Eclampsia; Pregnancy; Recombinant Proteins; Thrombin; Thromboplastin; Trophoblasts | 2011 |
The relationship between plasma and placental tissue factor, and tissue factor pathway inhibitors in severe pre-eclampsia patients.
To investigate the mechanism underlying the hypercoagulable state in severe pre-eclampsia.. Plasma tissue factor (TF) and tissue factor pathway inhibitor (TFPI) expression from pre-eclampsia patients and healthy pregnant controls were determined by ELISA. Placental TF and TFPI gene and protein expression were detected by quantitative RT-PCR, immunohistochemistry, and Western analysis.. The plasma TF level in the pre-eclampsia group was significantly higher than the control group (p<0.01), and surprisingly, the plasma TFPI-1 and TFPI-2 in the pre-eclampsia group were significantly lower (p<0.01). Placental TF gene and protein expression levels in the pre-eclampsia group was significantly higher than the control group, while TFPI-1 and TFPI-2 levels were significantly lower (p<0.05). Lastly, a significant correlation was found between plasma and placental TF protein levels in the pre-eclampsia group (p<0.01).. Higher expression and/or release of TF from the placenta may contribute towards a pathological hypercoagulable state in pre-eclampsia patients. Topics: Case-Control Studies; Enzyme-Linked Immunosorbent Assay; Female; Glycoproteins; Humans; Immunohistochemistry; Lipoproteins; Placenta; Pre-Eclampsia; Pregnancy; Retrospective Studies; Reverse Transcriptase Polymerase Chain Reaction; Thromboplastin; Treatment Outcome | 2010 |
Coagulation and fibrinolysis related cytokine imbalance in preeclampsia: the role of placental trophoblasts.
Cytokine imbalance might have a pivotal role in hypercoagulability seen in preeclampsia. Our objective was to determine the relationship of blood coagulation related factors in placental tissue and peripheral blood in preeclamptic and normal pregnancies.. We compared mRNA and protein levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), and tissue factor (TF) in the placenta of normal and preeclamptic pregnancies. Placental and peripheral blood t-PA and PAI-1 levels were examined. Trophoblasts were used to study the effects of hypoxia, hypoxia-reperfusion, and inflammatory cytokines on t-PA, PAI-1, tissue factor pathway inhibitor (TFPI), and TF.. PAI-1 and TF mRNA and protein levels were higher in placental tissue of preeclamptic pregnancies and in the peripheral blood of patients with preeclampsia. mRNA and protein secretion of TF, TFPI, PAI-1, but not t-PA, was increased in trophoblast cell culture under hypoxia and hypoxia-reoxygenation. Cell cultures with high levels of tumor necrosis factor-alpha (TNF-alpha) exhibited increased expression and secretion of TF and PAI-1, decreased TFPI, and no significant change of t-PA.. Imbalanced synthesis of t-PA, PAI-1, TFPI, and TF in trophoblasts may contribute to hypercoagulability in patients with preeclampsia. Topics: Adult; Cells, Cultured; Cytokines; Female; Fibrinolysis; Humans; Hypoxia; Lipoproteins; Placenta; Plasminogen Activator Inhibitor 1; Pre-Eclampsia; Pregnancy; RNA, Messenger; Thromboplastin; Tissue Plasminogen Activator; Trophoblasts; Young Adult | 2009 |
Elevated circulating soluble thrombomodulin activity, tissue factor activity and circulating procoagulant phospholipids: new and useful markers for pre-eclampsia?
One of the most frequently proposed mechanisms for pre-eclampsia refers to uteroplacental thrombosis. However, the contribution of classical thrombotic risk factors remains questionable. The aims of this study were to investigate the activities of thrombomodulin, tissue factor and procoagulant phospholipids to assess endothelial cell injury in pregnant women with pre-eclampsia and to compare them with other classical markers of vascular injury and thrombotic risk.. Using three new functional assays we studied the plasma levels of these new markers in 35 healthy women, 30 healthy pregnant women, and 35 women with pre-eclampsia.. We found that plasma levels of thrombomodulin activity, tissue factor activity and procoagulant phospholipids were significantly elevated in women with pre-eclampsia versus normal pregnant and non-pregnant women.. It is thus suggested that elevated levels of these parameters in pre-eclampsia may reflect vascular endothelium damage, and may be a more valuable biomarker than antigen for the assessment of endothelial damage in pre-eclampsia. The high increased levels of procoagulant phospholipids and tissue factor activities in pre-eclampsia could suggest that the procoagulant potential may be implicated in this complication and makes these markers very promising for the understanding, follow-up and therapeutic handling of complicated pregnancy. Topics: Biomarkers; Blood Coagulation Factors; Case-Control Studies; Female; Humans; Phospholipids; Pre-Eclampsia; Pregnancy; Thrombomodulin; Thromboplastin; Young Adult | 2009 |
Evidence of maternal platelet activation, excessive thrombin generation, and high amniotic fluid tissue factor immunoreactivity and functional activity in patients with fetal death.
Fetal death can lead to disseminated intravascular coagulation or fetal death syndrome. However, currently it is not clear what are the changes in the coagulation system in patients with a fetal death without the fetal death syndrome. This study was undertaken to determine: (1) whether fetal death in the absence of fetal death syndrome is associated with changes in hemostatic markers in maternal plasma and amniotic fluid; and (2) whether maternal hypertension or placental abruption are associated with further changes in the hemostatic profile of these patients.. A cross-sectional study included the following: (1) determination of changes in markers of coagulation and platelet activation in patients with a normal pregnancy (n = 71) and patients with fetal demise (FD) without disseminated intravascular coagulation (n = 65); (2) determination of the amniotic fluid (AF)-tissue factor concentration and activity, as well as the concentrations of thrombin-antithrombin III (TAT) complexes in patients with a normal pregnancy (n = 25) and those with a FD (n = 36) who underwent amniocentesis. Plasma and AF concentrations of TAT complexes and TF (an index of thrombin generation), as well as maternal plasma concentrations of sCD40L (a marker of platelet activation), tissue factor pathway inhibitor (TFPI) and prothrombin fragments (PF) 1 + 2 (also an indicator of in vivo thrombin generation) were measured by ELISA. TF and TFPI activity were measured using chromogenic assays.. (1) patients with FD without hypertension had a higher median maternal plasma sCD40L concentration than normal pregnant women (P < 0.001); (2) patients with FD had a higher median maternal plasma TAT III complexes than women with a normal pregnancy (P < 0.001); (3) the median AF-TF concentration and activity were higher in the FD group than in the normal pregnancy group (P < 0.001 for both); (4) patients with preeclampsia and FD had a higher median maternal plasma immunoreactive TF concentration than both normotensive patients with FD and women with normal pregnancies (P < 0.001 and P = 0.001, respectively); (5) the median plasma TF activity was higher in patients with preeclampsia and FD than that of women with normal pregnancies (P = 0.003); (6) among patients with a FD, those with placental abruption had a higher median AF-TAT complexes concentration than those without abruption (P = 0.0004).. Our findings indicate that: (1) mothers with a FD have evidence of increased in vivo thrombin generation and platelet activation than women with normal pregnancies; (2) patients with a FD and hypertension had a higher degree of TF activation than those with fetal death but without hypertension; (3) the AF of women with a FD had a higher median TF concentration and activity than that of normal pregnant women. AF can be a potential source for tissue factor and it participates in the development of fetal death syndrome in patients with a retained dead fetus. Topics: Adult; Amniotic Fluid; Antithrombin III; CD40 Ligand; Cross-Sectional Studies; Female; Fetal Death; Humans; Lipoproteins; Peptide Fragments; Peptide Hydrolases; Platelet Activation; Pre-Eclampsia; Pregnancy; Protein Precursors; Prothrombin; Thrombin; Thromboplastin | 2009 |
Tissue factor and its natural inhibitor in pre-eclampsia and SGA.
Tissue factor (TF), the major activator of the extrinsic pathway of coagulation, is abundant in the placenta and decidua. The aim of this study was to determine the maternal plasma concentrations of TF and its primary inhibitor, tissue factor pathway inhibitor (TFPI), in women who delivered small for gestational age (SGA) neonates, and in pre-eclampsia.. A cross-sectional study included the following groups: 1) women with normal pregnancies (n = 86); 2) patients who delivered SGA neonates (n = 61) and 3) women with pre-eclampsia (n = 133). Maternal plasma concentrations of TF and TFPI were measured by a sensitive immunoassay. Non-parametric statistics were used for analysis.. 1) Women with pre-eclampsia had a significantly higher median plasma concentration of TF than patients with a normal pregnancy (median: 1187 pg/mL; range: 69-11675 vs. median: 291.5 pg/mL; range: 6.3-2662.2; p < 0.0001, respectively); 2) Similarly, TFPI concentrations were higher in pre-eclampsia than in normal pregnancy (median: 87.5 ng/mL; range 25.4-165.1 vs. median: 66.1 ng/mL; range: 14.3-86.5; p < 0.0001, respectively); 3) Surprisingly, mothers with SGA neonates had a lower median maternal plasma concentration of TF (median: 112.2 pg/mL; range: 25.6-1225.3) than women with a normal pregnancy (p < 0.0001).. 1) Maternal plasma concentrations of TF in patients with pre-eclampsia, but not in those who delivered an SGA neonate, were higher than in women with normal pregnancies; 2) Although the role of immunoreactive plasma TF in coagulation remains controversial, our observations suggest that changes are present in the context of complications of pregnancy. Topics: Adult; Cross-Sectional Studies; Female; Fetal Growth Retardation; Humans; Infant, Newborn; Infant, Small for Gestational Age; Lipoproteins; Placenta; Pre-Eclampsia; Pregnancy; Thromboplastin; Young Adult | 2008 |
Absence of enhanced systemic inflammatory response at 18 weeks of gestation in women with subsequent pre-eclampsia.
To compare indicators of systemic inflammatory response in the second trimester in women who developed pre-eclampsia with normal pregnancies.. Prospective nested case control study derived from a cohort of 2190 pregnant women. Blood samples were obtained at 18 weeks of gestation. The following inflammatory parameters were measured: tumour necrosis factor-alpha (TNF-alpha), plasminogen activator inhibitor-1 (PAI-1), interleukin-1beta (IL-1beta), IL-6, IL-10, microCRP and tissue factor (TF).. Institute of Medical Genetics, University of Oslo, and Department of Medical Genetics, Ullevål University Hospital and Departments of Obstetrics and Gynecology, Aker University Hospital, Oslo, Norway.. The cases were 71 women who subsequently developed pre-eclampsia. The controls were 71 healthy, pregnant women matched for age, parity and first trimester body mass index (BMI).. Venous blood was drawn from fasting subjects into 5 mL test tubes containing EDTA. Samples were analysed for inflammatory parameters: IL-1-beta, IL-6, IL-10, TNF-alpha, PAI-1, TF (ELISA-technique) and CRP (latex-enhanced immunonephelometric assay), strictly according to the manufacturer's recommendation.. The matched case and control subjects were compared by the paired two-tailed Wilcoxon signed rank test. All P values were two-tailed and P < 0.05 was deemed statistically significant.. We found no differences in plasma concentrations of PAI-1, IL-1beta, IL-6,IL-10, microCRP, TNF-alpha or TF at 18 weeks of gestation between women who subsequently developed pre-eclampsia and matched control women.. In contrast to findings from women with overt pre-eclampsia, the present study indicates that there are no indications of intensified systemic inflammatory response at 18 weeks of gestation in women who later develop pre-eclampsia. Topics: C-Reactive Protein; Case-Control Studies; Cohort Studies; Female; Humans; Interleukins; Plasminogen Activator Inhibitor 1; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Infectious; Prospective Studies; Systemic Inflammatory Response Syndrome; Thromboplastin; Tumor Necrosis Factor-alpha | 2002 |
Activation of the novel prothrombinase, fg12, as a basis for the pregnancy complications spontaneous abortion and pre-eclampsia.
Impaired trophoblast invasion during the first trimester of pregnancy is linked to spontaneous abortion, and defective invasion in the second trimester to hypertension + proteinuria (pre-eclampsia). Hypertension developing during the third trimester of human pregnancy represents, in part, a corrective response in the mother to provide adequate placental perfusion for fetal growth when trophoblast has not to invaded and converted the myometrial porprtion of maternal spiral arteries into to low resistance-high capacitance conduits. Deportation of vesicles from hypoxemic trophoblast is thought to cause hypertension plus proteinuria, vascular damage and a systemic coagulopathy. Trophoblast invasion may be inhibited by local cytokines, such as TGF-betas but Thl-type cytokines associated with pre-eclapmsia and spontaneous abortions (e.g., IL-1, TNF-alpha, IFN-gamma) are not known to inhibit migration at in situ concentrations. Trophoblast invasion is also inhibited by the binding of surface integrins to fibronectin and fibrin, and fibrin production is stimulated by these Th1 cytokines via up-regulation of prothrombinases(s) such as fg12 which directly and via TNF-alpha-facilitated inflamation compromise trophoblast cell integrity. We, therefore, asked if fg12 expression and TNF-alpha are increased in first trimester human miscarriage and in third trimester pre-eclampsia.. fg12 mRNA was detected using in situ hybridization and fg12 protein by immunohistochemistry. TNF-alpha mRNA and protein were similarly tested. The techniques were validated using uterine sections from day 8.5 of CBA x DBA/2 pregnancies, and then were applied to sections of placentae from normal and pre-eclamptic pregnancies with and without intrauterine fetal growth restriction (IUGR). Fibrin was detectectd by immunohistochemistry.. Expression of fg12 protein correlated with fg12 mRNA expression in mouse uteri and in placentae from normal human pregnancies. Increased expression of fg12 and TNF-alpha mRNA and protein, and increased fibrin deposition was detected in placental trophoblast.. Activation of fg12 prothrombinase by Th1-type cytokines in pregnancy may lead to spontaneous abortion, or in ongoing pregnancy, to pre-eclampsia and/or IUGR. Topics: Abortion, Spontaneous; Animals; Enzyme Activation; Female; Humans; In Situ Hybridization; Male; Mice; Mice, Inbred BALB C; Mice, Inbred CBA; Mice, Inbred DBA; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Trimester, First; Pregnancy Trimester, Third; RNA, Messenger; Thromboplastin; Tumor Necrosis Factor-alpha | 2001 |
AT(1) receptor agonistic antibodies from preeclamptic patients cause vascular cells to express tissue factor.
We recently described autoantibodies (angiotensin-1 receptor autoantibodies, AT(1)-AA) directed at the AT(1) receptor in the serum of preeclamptic patients, whose placentas are commonly infarcted and express tissue factor (TF). Mechanisms of how AT(1)-AA might contribute to preeclampsia are unknown. We tested the hypothesis that AT(1)-AA cause vascular smooth muscle cells (VSMC) to express TF.. IgG from preeclamptic patients containing AT(1)-AA was purified with anti-human IgG columns. AT(1)-AA were separated from the IgG by ammonium sulfate precipitation. We transfected Chinese hamster ovary cells overexpressing the AT(1) receptor with TF promoter constructs coupled to a luciferase reporter gene. VSMC were obtained from human coronary arteries. Extracellular signal-related kinase activation was detected by an in-gel kinase assay. AP-1 activation was determined by electromobility shift assay. TF was measured by ELISA and detected by immunohistochemistry. Placentas from preeclamptic women stained strongly for TF, whereas control placentas showed far less staining. We proved AT(1)-AA specificity by coimmunoprecipitating the AT(1) receptor with AT(1)-AA but not with nonspecific IgG. Angiotensin (Ang) II and AT(1)-AA both activated extracellular signal-related kinase, AP-1, and the TF promoter transfected VSMC and Chinese hamster ovary cells, but only when the AP-1 binding site was present. We then demonstrated TF expression in VSMC exposed to either Ang II or AT(1)-AA. All these effects were blocked by losartan. Nonspecific IgG or IgG from nonpreeclamptic pregnant women had a negligible effect.. We conclude that AT(1)-AA and Ang II both stimulate the AT(1) receptor and initiate a signaling cascade resulting in TF expression. These results show an action of AT(1)-AA on human cells that could contribute to the pathogenesis of preeclampsia. Topics: Angiotensin II; Angiotensin Receptor Antagonists; Animals; Antibodies; Cells, Cultured; CHO Cells; Coronary Vessels; Cricetinae; Enzyme Activation; Female; Humans; Losartan; Mitogen-Activated Protein Kinases; Muscle, Smooth, Vascular; Placenta; Pre-Eclampsia; Pregnancy; Receptor, Angiotensin, Type 1; Receptor, Angiotensin, Type 2; Receptors, Angiotensin; Reference Values; Thromboplastin; Transcription Factor AP-1; Transfection | 2000 |
Tissue factor levels and high ratio of fibrinopeptide A:D-dimer as a measure of endothelial procoagulant disorder in pre-eclampsia.
To assess coagulation activation and endothelial cell injury in normotensive and pre-eclamptic pregnant women, a comparison was made of plasma levels of tissue factor, fibronectin, fibrinopeptide A and D-dimer. Samples were taken from 50 nonpregnant women, 40 normotensive pregnant women in the third trimester and 27 women with pre-eclampsia after diagnosis and before treatment. High levels of fibrinopeptide A and D-dimer were found in pre-eclamptic women. Moreover, the ratio fibrinopeptide A:D-dimer was much greater in the pre-eclampsia group than in normotensive pregnant women. The levels of fibronectin and tissue factor were also higher in the pre-eclampsia group. The increase of tissue factor levels suggests an alteration of the extrinsic coagulation pathway in pre-eclampsia. The increase of fibrinopeptide A:D-dimer ratio shows that the activation of coagulation is associated with a relative hypofibrinolysis in pre-eclampsia. Topics: Adult; Antifibrinolytic Agents; Blood Coagulation Disorders; Female; Fibrin Fibrinogen Degradation Products; Fibrinopeptide A; Gestational Age; Humans; Pre-Eclampsia; Pregnancy; Thromboplastin | 1999 |
Abnormal expression of type 1 plasminogen activator inhibitor and tissue factor in severe preeclampsia.
Preeclampsia is a multisystemic obstetric disease of unknown etiology that is commonly associated with fibrin deposition, occlusive lesions in placental vasculature, and intrauterine fetal growth retardation. We previously reported that type 1 plasminogen activator inhibitor (PAI-1) levels are significantly increased in plasma and placenta from pregnant women with preeclampsia compared to normal pregnant women. In the present report we localize the expression of placental PAI-1 in greater detail and compare it with that of tissue factor (TF), a procoagulant molecule, and vitronectin (Vn), a PAI-1 cofactor. We also examine the expression of two cytokines, tumor necrosis factor alpha (TNFalpha) and interleukin-1 (IL-1), in order to begin to define the underlying mechanisms responsible for the elevated levels of PAI-1 and fibrin deposits observed in placenta from preeclampsia. We demonstrate a significant increase in PAI-1, TF and TNFalpha antigen and PAI-1 and TF mRNA in placentas from preeclamptic patients. PAI-1 mRNA was increased not only in syncytiotrophoblast and infarction areas, but also in fibroblasts and in some endothelial cells of fetal vessels in placentas from preeclamptic patients. However, there was no colocalization between PAI-1, TF, Vn and TNFalpha in placental villi. The elevated TNFalpha in the placenta may induce PAI-1 and TF, and thus promote the thrombotic alterations associated with preeclampsia. Topics: Female; Humans; Immunohistochemistry; In Situ Hybridization; Interleukin-1; Placenta; Plasminogen Activator Inhibitor 1; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; RNA, Messenger; Thromboplastin; Tumor Necrosis Factor-alpha; Vitronectin | 1998 |
Antithrombin III prevents renal dysfunction and hypertension induced by enhanced intravascular coagulation in pregnant rats: pharmacological confirmation of the benefits of treatment with antithrombin III in preeclampsia.
We tested the hypothesis that enhanced intravascular coagulation in pregnancy could produce clinical symptoms similar to those of preeclampsia, such as hypertension, proteinuria, and edema. Having confirmed this, we then examined whether the pathological changes caused by intravascular coagulation could be suppressed by administration of antithrombin III (AT III), an endogenous inhibitor active to thrombin and factor X a. Intravascular coagulation was induced in Wistar rats on day 16-20 of pregnancy by 1-h arterial infusion of tissue thromboplastin (TP) through the left ventricle of the heart. One hour after the end of the infusion period, organ blood flows were measured by the radioactive ((57)Co-labeled) microsphere method, and fibrin deposition in organs was measured by radiolabeling with [(125)I] fibrinogen injected before TP infusion. Infusion of TP produced fibrin deposition in the kidney, lung, and liver, but not in the myometrium and placenta, as well as an 80% decrease in renal blood flow (RBF), with oliguria and proteinuria. TP also caused an increase in blood pressure (BP) accompanied by an increase in plasma renin activity (PRA), both of which were suppressed by bilateral nephrectomy before TP infusion. The prophylactic administration of AT III concentrates (60 or 300 U/kg intravenously (i.v.), followed by infusion of 30 or 150 U/kg/2 h, respectively) prevented all pathological changes in a dose-dependent manner. AT III increased placental blood flow regardless of the state of coagulation. These findings suggest that intravascular coagulation plays a significant part in the pathophysiology of preeclampsia and that AT III concentrates may have therapeutic potential in the treatment of this condition. Topics: Animals; Antithrombin III; Blood Coagulation; Female; Fibrin; Hypertension; Kidney; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Proteinuria; Rats; Rats, Wistar; Regional Blood Flow; Renin; Serum Albumin; Thromboplastin | 1996 |
Selective effects of preeclamptic sera on human endothelial cell procoagulant protein expression.
Current concepts of preeclampsia suggest that dysfunction of maternal vascular endothelium in vivo is a central pathogenetic feature of this syndrome. This hypothesis is suggested by the activation of the coagulation cascade associated with preeclampsia and evidence for a role of endothelium in maintaining thromboresistance. Previous in vitro studies with monolayers of human umbilical vein endothelial cells demonstrated direct cytotoxic effects of sera from preeclamptic parturients. In the current studies, we have examined the in vitro expression of three procoagulant protein activities regulated by endothelial cells: cellular fibronectin, an important mediator of platelet aggregation known to be elevated in preeclamptic women in vivo; tissue factor, the most potent endogenous procoagulant activity; and von Willebrand factor, a major component of coagulation factor VIII. Monolayer cultures of human umbilical vein endothelial cells were incubated with pregnancy sera for 24 hours before these proteins and activities were quantified. Exposure of identical endothelial cell cultures to predelivery preeclamptic sera caused significantly greater release of cellular fibronectin than postdelivery preeclamptic or predelivery or postdelivery normal pregnancy sera (p less than 0.05). However, neither tissue factor activity nor von Willebrand factor expression appeared to be increased preferentially by preeclamptic sera. The data indicate that sera from women with preeclampsia induce a selective, but not a generalized, activation of endothelial cell procoagulant protein production. Topics: Adult; Endothelium, Vascular; Female; Fibronectins; Humans; Pre-Eclampsia; Pregnancy; Thromboplastin; von Willebrand Factor | 1991 |
Extrinsic coagulation pathway inhibitor and heparin cofactor II during normal and hypertensive pregnancy.
Topics: Adult; Factor VII; Female; Gestational Age; Heparin Cofactor II; Humans; Hypertension; Lipoproteins; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Thromboplastin | 1989 |
Increased sensitivity to thromboplastin synthesis in blood monocytes from pre-eclamptic patients.
The thromboplastin activity in blood monocytes was investigated in third-trimester pregnancies comprising 11 patients with severe pre-eclampsia, 10 with essential hypertension and 18 normal pregnancies. Thromboplastin activity in unstimulated monocytes from the severe pre-eclamptic group was on average three times that found in the normal pregnant group, but variation was wide and the differences were not statistically significant. Thromboplastin activity in endotoxin-stimulated monocytes was significantly higher in the severe pre-eclamptic group than in the other two groups (normal and chronic hypertensive). In the severe pre-eclamptic group, there was a significant negative linear correlation between thromboplastin activity of the endotoxin-stimulated monocytes and factor VII. Fibrinogen, factor VII and alpha 2-antiplasmin were significantly lower in the severe pre-eclamptic group than in the normal pregnant group, whereas no differences were observed in factors V, VIII, AT-III and prekallikrein. Topics: Adult; Endotoxins; Factor V; Factor VII; Factor VIII; Female; Humans; Hypertension; Monocytes; Postpartum Period; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Thromboplastin | 1985 |
Thromboplastin activity in amniotic fluid.
Thromboplastin activity in amniotic fluid from 39 patients pregnant in weeks 14-40 has been studied. Amniotic fluid was obtained by amniocentesis. All fluids were fractionated and the activity studied in both supernatant and sediment in a highly specific and sensitive test system. All samples tested showed a very high thromboplastin activity. No correlation to gestational age was found. Amniotic samples from 19 of the patients were incubated with endotoxin. Endotoxin did not further increase the procoagulant activity. Topics: Amniotic Fluid; Blood Coagulation; Endotoxins; Female; Humans; Pre-Eclampsia; Pregnancy; Thromboplastin | 1985 |
[Disseminated intravascular coagulation in pregnancy toxemias].
Topics: Blood Platelets; Disseminated Intravascular Coagulation; Factor V; Factor VIII; Female; Fibrin Fibrinogen Degradation Products; Humans; Pre-Eclampsia; Pregnancy; Protamines; Prothrombin; Thrombin; Thromboplastin | 1978 |
Abnormal coagulation and fibrinolysis in eclampsia. A clinical and laboratory correlation study.
This study evaluated the existence of abnormally increased coagulation and fibrinolysis in 33 severely toxemic and eclamptic women by means of a combined hemotologic profile with clinical and morphologic correlations. The dominant findings were: different degrees of thrombocytopenia, abnormal levels of blood fibrinogen, prolonged thrombin time, and positive protamine sulfate test. Altered activated partial thromboplastin time and positive ethanol gelation test were slightly less frequent, and only few cases showed prolonged prothrombin time or early lysis of euglobulins. These abnormalities seemed to be more numerous and more pronounced in the worst cases of the series and their severity seemed to be associated with the age of the patient and the presence of previous underlying disease. These variously handicapped pregnant women exhibited worse hematologic hematologic abnormalities, and provided most of the fatal cases in the series. Finally, the main findings were discussed and commented upon. Topics: Adolescent; Adult; Blood Coagulation Disorders; Blood Coagulation Tests; Blood Platelets; Eclampsia; Ethanol; Female; Fibrinogen; Fibrinolysis; Humans; Pre-Eclampsia; Pregnancy; Protamines; Prothrombin Time; Thrombin; Thromboplastin | 1976 |
Maternal serum sialomucins during pregnancy and postpartum in patients with pre-eclampsia.
The seromucoid fraction of maternal serum glycoproteins is increased in pre-eclampsia and the rise, which is proportional to the severity of the disease, may reflect progressive placental deterioration with increasing trophoblast fragmentation and deportation. The pulmonary lysis of deported trophoblast effects the local release of fetal antigens and thromboplastin in the lungs. The former, which are immunologically inert because they are complexed with maternal serum seromucoid, are released into the peripheral circulation, while the local coagulation hazard presented by the latter is countered by intensified fibrinolytic activity, the products of which are also released into the peripheral circulation. In severe pre-eclampsia the peripheral circulation contains a considerable excess of physically similar proteins derived from the seromucoid fraction and fibrin degradation products, and the conditions which then obtain in the renal glomerulus favour the physical process of coacervation. In that event the mechanism of the origin and development of the renal lesion can be described in purely physical terms. Topics: Antigens; Female; Fibrin Fibrinogen Degradation Products; Glycoproteins; Humans; Immune Tolerance; Orosomucoid; Placenta; Postpartum Period; Pre-Eclampsia; Pregnancy; Pregnancy Trimester, Third; Sialic Acids; Thromboplastin; Trophoblasts | 1975 |
The relevance of intravascular coagulation to pre-eclampsia.
Topics: 5-Hydroxytryptophan; Abruptio Placentae; Animals; Blood Coagulation Factors; Desoxycorticosterone; Disease Models, Animal; Disseminated Intravascular Coagulation; Female; Fibrinogen; Fibrinolysis; Humans; Hypertension; Platelet Adhesiveness; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Hematologic; Pulmonary Circulation; Rabbits; Rats; Thrombocytopenia; Thromboplastin | 1973 |
[Pseudofibrinolysis in the thrombelastogram, factor XIII and fibrinogen split products in the 2nd half of normal pregnancy, during labor, and puerperium (author's transl)].
Topics: Factor V; Factor XIII; Female; Fibrinogen; Fibrinolysis; Humans; Labor, Obstetric; Postpartum Period; Pre-Eclampsia; Pregnancy; Thrombelastography; Thromboplastin; Time Factors | 1973 |
Intravascular coagulation and plasma fibrinogen in pregnancy.
Topics: Animals; Disease Models, Animal; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Humans; Placenta; Pre-Eclampsia; Pregnancy; Rabbits; Thromboplastin | 1973 |
Coagulation studies in the hypertensive toxemias of pregnancy.
Topics: Adult; Age Factors; Blood Cell Count; Blood Coagulation Tests; Blood Platelets; Disseminated Intravascular Coagulation; Factor V; Female; Fibrinogen; Fibrinolysin; Gestational Age; Humans; Hypertension; Parity; Plasminogen; Pre-Eclampsia; Pregnancy; Prothrombin Time; Thrombin; Thromboplastin | 1972 |
Coagulation, fibrinolysis and platelet function in pre-eclampsia, essential hypertension and placental insufficiency.
Topics: Adenosine Diphosphate; Adult; Antithrombins; Blood Cell Count; Blood Coagulation; Blood Coagulation Tests; Blood Platelets; Cold Temperature; Factor V; Factor VIII; Female; Fibrin; Fibrinogen; Fibrinolysis; Fibrinolytic Agents; Humans; Hypertension; Placenta; Placenta Diseases; Plasminogen; Platelet Adhesiveness; Postpartum Period; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Thromboplastin | 1971 |
[Morphogenetic and functional changes in EPH pregnancy toxemias. I].
Topics: Animals; Blood Platelets; Edema; Female; Humans; Hypertension, Renal; Immune Sera; Kidney Glomerulus; Kidney Tubules; Microscopy, Electron; Placenta; Pre-Eclampsia; Pregnancy; Proteinuria; Rabbits; Regional Blood Flow; Thromboplastin | 1970 |
False elevation of partial thromboplastin time and prothrombin time.
Topics: Adult; Blood Coagulation Tests; Diagnostic Errors; Female; Hematology; Hemorrhagic Disorders; Humans; Pre-Eclampsia; Pregnancy; Prothrombin Time; Thromboplastin | 1970 |
Coagulation and fibrinolysis in prematurely delivered mothers and their premature infants.
Topics: Abruptio Placentae; Blood Coagulation; Blood Coagulation Factors; Blood Coagulation Tests; Female; Fibrinolysis; Gestational Age; Hematocrit; Humans; Infant, Newborn; Infant, Premature; Obstetric Labor, Premature; Pre-Eclampsia; Pregnancy; Rh-Hr Blood-Group System; Thromboplastin | 1969 |
Influence of pre-eclampsia upon coagulation and fibrinolysis in women and their newborn infants immediately after delivery.
Topics: Blood Coagulation; Blood Coagulation Factors; Delivery, Obstetric; Female; Fibrinolysis; Hematocrit; Humans; Infant, Newborn; Infant, Premature; Pre-Eclampsia; Pregnancy; Thromboplastin | 1969 |
PRODUCTION OF ULTRA-STRUCTURAL GLOMERULAR LESIONS RESEMBLING THOSE OF TOXAEMIA OF PREGNANCY BY THROMBOPLASTIN INFUSION IN RABBITS.
Topics: Animals; Electrons; Female; Fibrin; Glomerulonephritis; Humans; Kidney Diseases; Kidney Glomerulus; Microscopy; Microscopy, Electron; Pathology; Phagocytosis; Pre-Eclampsia; Pregnancy; Rabbits; Research; Sepsis; Thromboplastin | 1963 |
[Thromboplastin and fibrinolysin in etiology and pathogenesis of gestoses].
Topics: Female; Fibrinolysin; Humans; Pre-Eclampsia; Pregnancy; Thromboplastin | 1953 |
[Thromboplastin activity of the chorion and dicumarol; experimental research].
Topics: Chorion; Dicumarol; Female; Humans; Pre-Eclampsia; Pregnancy; Thromboplastin; Toxemia | 1950 |