Stereology of the placenta in type 1 and type 2 diabetes

Higgins, Mary; Felle, Patrick; Mooney, Eoghan E.; Bannigan, John; McAuliffe, Fionnuala M.

doi:10.1016/j.placenta.2011.04.015

Cited by 72 publications

(56 citation statements)

References 19 publications

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“…73 Diabetes mellitus is a state of chronic oxidative stress, 74 and glycemia appears to have an affect on the capillary, but not the stromal component, of chorionic villi. 75 Placental angiogenesis is stimulated by insulin via ephrin-B2 expression, a signaling molecule implicated in sprouting. 76 Therefore, this subtype of PR chronic hypoxic pattern appears to include the PU component because of fetal hyperinsulinemia.…”

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confidence: 99%

Hypoxic Patterns of Placental Injury: A Review

Stanek

2013

Archives of Pathology &Amp; Laboratory Medicine

124

126

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Context.—In utero hypoxia is an important cause of perinatal morbidity and mortality and can be evaluated retrospectively to explain perinatal outcomes, to assess recurrence risk in subsequent pregnancies, and to investigate for medicolegal purposes by identification of many hypoxic placental lesions. Definitions of some placental hypoxic lesions have been applied relatively liberally, and many of them are frequently underreported. Objectives.—To present a comprehensive assessment of the criteria for diagnosing acute and chronic histologic features, patterns, and lesions of placental and fetal hypoxia and to discuss clinicopathologic associations and limitations of the use thereof. The significance of lesions that have been described relatively recently and are not yet widely used, such as laminar necrosis; excessive, extravillous trophoblasts; decidual multinucleate extravillous trophoblasts; and, most important, the patterns of diffuse chronic hypoxic preuterine, uterine, and postuterine placental injury and placental maturation defect, will be discussed. Data Sources.—Literature review. Conclusions.—The placenta does not respond in a single way to hypoxia, and various placental hypoxic features should be explained within a clinical context. Because the placenta has a large reserve capacity, hypoxic lesions may not result in poor fetal condition or outcome. On the other hand, very acute, in utero, hypoxic events, followed by prompt delivery, may not be associated with placental pathology, and many poor perinatal outcomes can be explained by an etiology other than hypoxia. Nevertheless, assessment of placental hypoxic lesions is helpful for retrospective explanations of complications in pregnancy and in medicolegal investigation.

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confidence: 99%

Hypoxic Patterns of Placental Injury: A Review

Stanek

2013

Archives of Pathology &Amp; Laboratory Medicine

124

126

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“…Despite currently available treatment, maternal diabetes comprises unfit conditions for embryonic and fetoplacental development. The pregnancies with type 1 or type 2 diabetes have an increased risk of miscarriage, stillbirth, congenital malformations, placental abnormalities, and intrauterine malprogramming (2). However, reports on the pathology of placenta are usually incompatible with diabetes mellitus.…”

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confidence: 99%

Histopathological, Ultrastructural and Apoptotic Changes in Diabetic Rat Placenta

Gül¹,

Bayat²,

Çetin³

et al. 2015

Balkan Med J

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Background:The exchange of substances between mother and fetus via the placenta plays a vital role during development. A number of developmental disorders in the fetus and placenta are observed during diabetic pregnancies. Diabetes, together with placental apoptosis, can lead to developmental and functional disorders. Aims: Histological, ultrastructural and apoptotic changes were investigated in the placenta of streptozotocin (STZ) induced diabetic rats. Study Design: Animal experimentation. Methods: In this study, a total of 12 female Wistar Albino rats (control (n=6) and diabetic (n=6)) were used. Rats in the diabetic group, following the administration of a single dose of STZ, showed blood glucose levels higher than 200 mg/dL after 72 hours. When pregnancy was detected after the rats were bred, two pieces of placenta and the fetuses were collected on the 20 th day of pregnancy by cesarean incision under ketamine/ xylazine anesthesia from in four rats from the control and diabetic groups. Placenta tissues were processed for light microscopy and transmission electron microscopy (TEM). Hematoxylin-eosin (HE) and periodic acid Schiff-diastase (PAS-D) staining for light microscopic and caspase-3 staining for immunohistochemical investigations were performed for each placenta. Electron microscopy was performed on thin sections contrasted with uranyl acetate and lead nitrate. Results: Weight gain in the placenta and fetuses of diabetic rats and thinning of the decidual layer, thickening of the hemal membrane, apoptotic bodies, congestion in intervillous spaces, increased PAS-D staining in decidual cells and caspase-3 immunoreactivity were observed in the diabetic group. After the ultrastructural examination, the apoptotic appearance of the nuclei of trophoblastic cells, edema and intracytoplasmic vacuolization, glycogen accumulation, dilation of the endoplasmic reticulum and myelin figures were observed. In addition, capillary basement membrane thickening, capillary endothelial cells chromatin condensation in the nucleus and corrugation of the nucleus were found. Conclusion: Diabetes causes histomorphometric, ultrastructural and apoptotic changes in rat placenta.

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“…The placental volume does not correspond notably to uteroplacental flow, which is also demonstrated earlier in normal pregnancies (11) and even in diabetic pregnancies (9). It is noteworthy, that our sample is collected based on the new principles of criteria of diabetes, whereas there has not been reported any reports on placenta ratio according to the new guidelines.…”

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confidence: 57%

“…Inclusion and exclusion (e.g. preeclampsia, assisted reproductive technology) criteria, diagnostic requirements for diabetes, determination of gestational age, fetal biometry and Doppler artery flowmetry in uterine and umbilical arteries were described in our previous article (9). After standard 2-D measurements were taken, a 3-D sweep was performed through the placenta by a The angle of volume acquisition varied between 45º and 70º according to placental size.…”

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confidence: 99%

Placental volume relative to fetal weight estimated by sonography in diabetic pregnancies

Surányi

Kozinszky

Molnár

et al. 2015

The Journal of Maternal-Fetal & Neonatal Medicine

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Our purpose was to analyze the placental volume and fetal weight ratio in diabetic pregnancies during mid-pregnancy. Fifty-four diabetic pregnancies (27 gestational diabetes mellitus (GDM) and 27 diabetes mellitus (DM) type I with good glycemic control) and three-hundred and sixteen healthy cases were analyzed by threedimensional sonographic volumetry of the placenta, while fetal weight was estimated by two-dimensional technique. The gestational age-specific estimated fetal weight and placental volume-to-fetal weight ratio was significantly higher in GDM pregnancies, whereas placental volume in GDM was similar compared to control data. DM with good glycemic control did not predispose to any changes in sonographic volumetric differences compared to control values. The disproportional placental growth correlated to fetal growth takes place in the second trimester in GDM, whereas DM with good glycemic control does not pose a significant risk of unequal feto-placental development in mid-pregnancy.

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Stereology of the placenta in type 1 and type 2 diabetes

Cited by 72 publications

References 19 publications

Hypoxic Patterns of Placental Injury: A Review

Hypoxic Patterns of Placental Injury: A Review

Histopathological, Ultrastructural and Apoptotic Changes in Diabetic Rat Placenta

Placental volume relative to fetal weight estimated by sonography in diabetic pregnancies

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