Amnioplastin: New Reagent for Coagulation Tests

Creter, D

doi:10.1016/s0140-6736(77)92871-9

Cited by 9 publications

(11 citation statements)

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“…In humans, a substantial increase in decidual and myometrial TF expression and concentrations was reported during the luteal phase of the menstrual cycle [15,16,50,51], as well as during early and late stages of pregnancy [15,16,50-52]. Similarly, high TF concentrations have been detected in the fetal membranes (mainly the amnion) and amniotic fluid [23,53-55]. In contrast, the maternal plasma TF concentrations do not change significantly during normal pregnancy in comparison to non-pregnant women [56,57], though women in labor at term have significantly higher maternal plasma TF concentrations than non-pregnant women [23].…”

Section: Commentsmentioning

confidence: 99%

A link between a hemostatic disorder and preterm PROM: a role for tissue factor and tissue factor pathway inhibitor

Erez

Espinoza

Chaiworapongsa

et al. 2008

The Journal of Maternal-Fetal & Neonatal Medicine

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Objective-Vaginal bleeding is a risk factor for preterm PROM (PPROM). A disorder of decidual hemostasis has been implicated in the genesis of PROM. Indeed, excessive thrombin generation has been demonstrated in PPROM both before and at the time of diagnosis. Decidua is a potent source of tissue factor (TF), the most powerful natural pro-coagulant. A decidual hemostatic disorder may link vaginal bleeding, PPROM, and placental abruption. This study was conducted to determine the behavior of maternal TF and its natural inhibitor, the tissue factor pathway inhibitor (TFPI) in PPROM.Methods-This cross-sectional study included women with PPROM (n=123) and women with normal pregnancies (n=86). Plasma concentrations of TF and TFPI were measured by a sensitive immunoassay. Non-parametric statistics were used for analysis. Results-1)The median maternal plasma TF concentration was significantly higher in patients with PPROM than in women with normal pregnancies (median: 369.5 pg/ml; range: 3.27-2551 pg/ ml vs. median: 291.5 pg/ml; range: 6.3-2662.2 pg/ml, respectively; p=0.001,); 2) the median maternal TFPI plasma concentration was significantly lower in patients with PPROM than in women with a normal pregnancies (median: 58.7 ng/ml; range: 26.3-116 ng/ml vs. median: 66.1 ng/ml; range: 14.3-86.5 ng/ml, respectively; p=0.019); 3) there was no correlation between the plasma concentration of TF and TFPI and the gestational age at sample collection; and 4) among patients with PPROM there was no association between the presence of intra-amniotic infection or inflammation and median plasma concentrations of TF and TFPI. Conclusions-1) Patients with PPROM have a higher median plasma concentration of TF and a lower median plasma concentration of TFPI than women with normal pregnancies. 2) These findings suggest that PPROM is associated with specific changes in the hemostatic/coagulation system. NIH Public Access

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Section: Commentsmentioning

confidence: 99%

A link between a hemostatic disorder and preterm PROM: a role for tissue factor and tissue factor pathway inhibitor

Erez

Espinoza

Chaiworapongsa

et al. 2008

The Journal of Maternal-Fetal & Neonatal Medicine

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“…The principal anticoagulant mechanism inhibiting TF activation pathway is tissue factor pathway inhibitor (TFPI), which mRNA is highly expressed in the macrophages in the villi in term placenta 19 . Similarly, high TF concentrations have been detected in the fetal membranes (mainly the amnion) and amniotic fluid 7,[20][21][22][23] . TFPI has been found in amniotic fluid as well 20 , but it is not clear if the presence of TF and its natural inhibitor is related to coagulation per se or is somehow connected with embryonic development 24 .…”

Section: What Are the Changes In The Coagulation System During Normalmentioning

confidence: 96%

“…During normal pregnancy, there is an increase in the amniotic fluid TF concentration 7,[20][21][22][23] . In .…”

Section: Hemostatic Changes In the Amniotic Fluid Of Women With Obstementioning

confidence: 99%

Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromes

Mastrolia

Mazor

Loverro

et al. 2014

Preprint

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View the peer-reviewed version (peerj.com/articles/653), which is the preferred citable publication unless you specifically need to cite this preprint. Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromesObstetrical complications including preeclampsia, fetal growth restriction, preterm labor, preterm prelabor rupture of membranes and fetal demise are all the clinical endpoint of several underlying mechanisms (i.e. infection inflammation, thrombosis, endocrine disorder, immunologic rejection, genetic, and environmental), therefore, they may be regarded as syndromes. Placental vascular pathology and increased thrombin generation were reported in all of these obstetrical syndromes. Moreover, elevated concentrations of thrombin-antithrombin III complexes and changes in the coagulation as well as anticoagulation factors can be detected in the maternal circulation prior to the clinical development of the disease in some of these syndromes. In this review, we will assess the changes in the hemostatic system during normal and complicated pregnancy in maternal blood, maternal-fetal interface and amniotic fluid, and describe the contribution of thrombosis and vascular pathology to the development of the great obstetrical syndromes.PeerJ PrePrints | http://dx.doi.org/10.7287/peerj.preprints.487v1 | CC-BY 4.0 Open Access |

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Section: Preprintsmentioning

confidence: 99%

“…During normal pregnancy, there is an increase in the amniotic fluid TF concentration 7,[20][21][22][23] . In Patients with a fetal demise had higher median amniotic fluid-TF concentration and activity than those with normal pregnancies.…”

Section: Hemostatic Changes In the Amniotic Fluid Of Women With Obstementioning

confidence: 99%

Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromes

Mastrolia

Mazor

Loverro

et al. 2014

Preprint

View full text Add to dashboard Cite

Obstetrical complications including preeclampsia, fetal growth restriction, preterm labor, preterm prelabor rupture of membranes and fetal demise are all the clinical endpoint of several underlying mechanisms (i.e. infection inflammation, thrombosis, endocrine disorder, immunologic rejection, genetic, and environmental), therefore, they may be regarded as syndromes. Placental vascular pathology and increased thrombin generation were reported in all of these obstetrical syndromes. Moreover, elevated concentrations of thrombin-anti-thrombin III complexes and changes in the coagulation as well as anticoagulation factors can be detected in the maternal circulation prior to the clinical development of the disease in some of these syndromes. In this review, we will assess the changes in the hemostatic system during normal and complicated pregnancy in maternal blood, maternal-fetal interface and amniotic fluid, and describe the contribution of thrombosis and vascular pathology to the development of the great obstetrical syndromes.

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Amnioplastin: New Reagent for Coagulation Tests

Cited by 9 publications

References 0 publications

A link between a hemostatic disorder and preterm PROM: a role for tissue factor and tissue factor pathway inhibitor

A link between a hemostatic disorder and preterm PROM: a role for tissue factor and tissue factor pathway inhibitor

Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromes

Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromes

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