Trophoblast basement membrane haemosiderosis in the placental lesion of fetal artery thrombosis: A marker for disturbance of maternofetal transfer?

McDermott, Mary McGrae; Gillan, John

doi:10.1016/0143-4004(95)90006-3

Cited by 26 publications

(6 citation statements)

References 6 publications

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“…The consequent fetoplacental ischaemia is the primary event in many placentae from pregnancies complicated with growth retardation and/or preeclampsia (12,16,23). The uteroplacental and fetoplacental circulation regulate each other, with disturbances on the one side leading to disturbances on the other (18). It is generally assumed that destruction of 20% of the placental parenchyma may result in fetal death (4).…”

Section: Discussionmentioning

confidence: 99%

“…In most cases of chronic villitis, no infection is observed and chronic villitis has been related to conditions of low uteroplacental circulation (23), but in the present material, chronic villitis was not specific in the autopsy group with growth retardation. In the further examination of placenta on suspicion of vascular insufficiency, other lesions not included in this study such as fetal erythroblastosis (2,25), iron deposition in villi (17,18,24), trophoblast volume (2,16) and occurrence of endovascular trophoblast in decidual arteries (14) might contribute to the diagnosis. The listed lesions of uteroplacental vascular insufficiency are associated with preeclampsia, maternal hypertension and growth retardation, and for some of the lesions a risk of recurrence in future pregnancies (1 5).…”

Section: Discussionmentioning

confidence: 99%

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Morphological findings and value of placental examination at fetal and perinatal autopsy

Larsen

Græm

1999

APMIS

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The purpose of this study was to report on the morphological findings in placentae from abortions, stillbirths and perinatal deaths, and to assess the value of the results of the placental examinations. The material included 341 placentae and their matched autopsies. Fifty placentae came from abortions induced for medical reasons, 194 from spontaneous abortions, 84 from stillbirths, and 13 from livebirths. Histological slides from all placentae were reviewed and the placental diagnoses were related to the autopsy diagnoses. Frequently observed placental lesions were inflammation of the membranes and/or umbilical cord, placental edema, vascular lesions, single umbilical artery, and degenerative lesions. The placental examination in pregnancies terminating with fetal or perinatal death was of value in half the cases. Some placental lesions provide us with clues when assessing the cause of fetal death, but such lesions are rare. Two important groups of lesions, acute inflammation of the membranes and/or umbilical cord and lesions consistent with uteroplacental vascular insufficiency, seen mainly as infarction and decidual arteriopathy, were observed. Gross examination is informative, though microscopic examination is often necessary.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Morphological findings and value of placental examination at fetal and perinatal autopsy

Larsen

Græm

1999

APMIS

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“…Placental tissue was immersed in Perl solution for 20 minutes to detect early infarcted tissue. 7 Standard avidin-biotin-peroxidase complex immunohistochemical staining, using 3,3'-diaminobenzidine as a chromogen, was conducted with antibodies to a smooth muscle actin (monoclonal, 1A4 clone, dilution 1:2; DakoCytomation, Carpinteria, CA), desmin (monoclonal, D33 clone, dilution 1:100; DakoCytomation), Ki-67 antigen (monoclonal, MIB-1 clone, dilution 1:50; DakoCytomation), and the vascular endothelial growth factor (VEGF) receptor, Flk-1 (monoclonal, A-3 clone, dilution 1:300; Santa Cruz Biotechnology, Santa Cruz, CA) in 4 cases (3, 5, 6, and 8) with appropriate control samples. Samples from a normal placenta at 36 weeks' gestation also were stained for comparison.…”

Section: Methodsmentioning

confidence: 99%

Placental Mesenchymal Dysplasia Is Associated With High Rates of Intrauterine Growth Restriction and Fetal Demise: A Report of 11 New Cases and a Review of the Literature

Pham

Steele

Stayboldt

et al. 2006

American Journal of Clinical Pathology

119

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Placental mesenchymal dysplasia (PMD) is a rare condition of placentomegaly and abnormal chorionic villi often clinically mistakenly as partial hydatidiform mole. However, it is clinicopathologically distinct with high incidence of intrauterine growth restriction (IUGR) and fetal death. This study presents 11 new PMD cases and provides a meta-analysis of the associated IUGR and fetal death rates. The cases were identified between 1971 and 2005, mostly from consultation files. To our knowledge, 71 PMD cases have previously been reported; 15 of these were associated with Beckwith-Wiedemann syndrome (BWS). With the addition of our new results, among all cases without BWS, 50% had IUGR and 43% had intrauterine fetal demise (IUFD) or neonatal death. Females represented 82% of cases. Thus, PMD is associated with high IUGR and IUFD/neonatal death rates and disproportionally affects females. The cause and pathogenesis are yet unknown. The current understanding and hypotheses involving PMD are discussed.

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“…Both are considered indicative of segmental as opposed to global FVM. Additional findings in intermediate to large foci of AV include (i) an increase in syncytial knots, ascribed to cytotrophoblast necrosis (M. Parast, personal communication and unpublished SPP abstract 2015), and (ii) iron deposition in the trophoblast basement membrane, which may reflect either lack of egress due to lack of fetal vessels or remnants of fetal red blood cells from preceding VSK . It should be noted that because villous trees interdigitate within the placenta there may be some mixing of viable and nonviable villi within lesions.…”

Section: Findings Consistent With Segmental Complete Fvmmentioning

confidence: 99%

Fetal vascular malperfusion, an update

Redline

Ravishankar

2018

APMIS

153

104

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Fetal vascular malperfusion is the most recent term applied to a group of placental lesions indicating reduced or absent perfusion of the villous parenchyma by the fetus. The most common etiology of malperfusion is umbilical cord obstruction leading to stasis, ischemia, and in some cases thrombosis. Other contributing factors may include maternal diabetes, fetal cardiac insufficiency or hyperviscosity, and inherited or acquired thrombophilias. Severe or high grade fetal vascular malperfusion is an important risk factor for adverse pregnancy outcomes including fetal growth restriction, fetal CNS injury, and stillbirth. Overall recurrence risk for subsequent pregnancies is low.

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Trophoblast basement membrane haemosiderosis in the placental lesion of fetal artery thrombosis: A marker for disturbance of maternofetal transfer?

Cited by 26 publications

References 6 publications

Morphological findings and value of placental examination at fetal and perinatal autopsy

Morphological findings and value of placental examination at fetal and perinatal autopsy

Placental Mesenchymal Dysplasia Is Associated With High Rates of Intrauterine Growth Restriction and Fetal Demise: A Report of 11 New Cases and a Review of the Literature

Fetal vascular malperfusion, an update

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