The placental vascular component in early and late intrauterine fetal death

Bar, Jacob; Schreiber, Letizia; Ben-Haroush, Avi; Ahmed, Hamza; Golan, Abraham; Kovo, Michal

doi:10.1016/j.thromres.2012.09.013

Cited by 16 publications

(8 citation statements)

References 29 publications

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“…The findings therefore support the hypothesis that late‐onset preeclampsia is usually a mild maternal disorder, and early onset preeclampsia is a placental disease . It is interesting that in this material, fetal growth restriction clustered only with oligohydramnios in the second trimester (Figures a, a), being a component of the early onset oligohydramnios sequence with a small placenta at term, but not with histological placental phenotypes as suggested by some authors who linked it to fetal vascular lesions in late fetal death , or with maternal vascular supply lesions in early onset fetal growth restriction .…”

Section: Discussionsupporting

confidence: 86%

Clinicoplacental phenotypes vary with gestational age: an analysis by classical and clustering methods

Stanek

Biesiada

Trzeszcz

2014

Acta Obstet Gynecol Scand

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The applied statistical analyses made it possible to simultaneously compare the strength of clinicoplacental associations separately in three pregnancy intervals. Placental clinicopathological associations are strongest for the second trimester, i.e. severe preeclampsia and preterm ascending infection-related conditions, but were not significant for other pregnancy complications such as mild preeclampsia, chronic hypertension, diabetes mellitus, or umbilical cord compromise.

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Section: Discussionsupporting

confidence: 86%

Clinicoplacental phenotypes vary with gestational age: an analysis by classical and clustering methods

Stanek

Biesiada

Trzeszcz

2014

Acta Obstet Gynecol Scand

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“…Placental vascular lesions are divided into maternal or fetal vascular origin ( Figs. 4 and 5 ) ( Redline et al, 2005 ; Bar et al, 2012 ). Lesions of the maternal vascular compartment include placental marginal and retro-placental hemorrhages, lesions related to maternal underperfusion (acute atherosis and mural hypertrophy, increased syncytial knots, villous agglutination, increased intervillous fibrin deposition, villous infarcts) ( Redline et al, 2005 ).…”

Section: What Are the Changes In The Hemostatic System Associated Witmentioning

confidence: 99%

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

Mastrolia

Mazor

Loverro

et al. 2014

PeerJ

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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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“…The frequency of the specific vascular placental lesions varies among these obstetrical syndromes 105 . Placental vascular lesions are divided into maternal or fetal vascular origin ( figure 1-2) 106,107 .…”

Section: Placental Pathology In the Great Obstetrical Syndromesmentioning

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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The placental vascular component in early and late intrauterine fetal death

Cited by 16 publications

References 29 publications

Clinicoplacental phenotypes vary with gestational age: an analysis by classical and clustering methods

Clinicoplacental phenotypes vary with gestational age: an analysis by classical and clustering methods

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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