Comparison of placental findings in type 1 and type 2 diabetic pregnancies

Starikov, Roman; Inman, Kyle; Chen, K.; Lopes, Vrishali; Coviello, Elizabeth; Pınar, Halit; He, Mai

doi:10.1016/j.placenta.2014.10.008

Cited by 39 publications

(35 citation statements)

References 23 publications

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“…Nonetheless, the maternal-placental and fetal-placental circulations exchange blood at the terminal villi. Maternal complications of pregnancy, such as maternal diabetes (2), and fetal morbidities, including stillbirth (3) and fetal growth abnormalities (3, 4), have been significantly associated with placental vascular abnormalities. However, the association of placental vascular abnormalities with various diabetes types has not been well elucidated; therefore, an enhanced understanding of the effect of maternal diabetes on placental pathology and, specifically, placental vasculature is warranted.…”

Section: Introductionmentioning

confidence: 99%

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Type 1, type 2 and gestational diabetes mellitus differentially impact placental pathologic characteristics of uteroplacental malperfusion

et al. 2015

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Introduction During a pregnancy complicated by diabetes, the placenta undergoes a number of functional and structural pathologic changes. However, differences across studies may reflect pathophysiologic differences of diabetes types under investigation. Methods We examined placental pathology from women ages 18–40 years with self-identified race/ethnicity; singleton, live births; and type 1 (T1DM; n=36), type 2 (T2DM; n=37), or gestational diabetes mellitus (GDM; n=126). Clinical data were abstracted from medical records. Placental diagnoses were independently re-reviewed by a perinatal pathologist. Multivariable analyses adjusting for race, gestational weight gain, gestational age, and systolic blood pressure were conducted. Results Women with T1DM compared with either T2DM or GDM had higher gestational weight gain (mean ± SD, T1DM vs. T2DM: 28.5 ± 12.4 vs. 20.5 ± 13.4 kg, p=0.03; or GDM: 21.3 ± 12.7 kg, p=0.009) and insulin use (T2DM: 100.0% vs. 85.3%, p=0.02; or GDM: 4.0%, p<0.001). Women with T1DM compared with either T2DM or GDM also had a similarly lower prevalence of placental infarcts in univariate analyses; however, these findings did not remain significant after multivariable adjustment. Also, placentas from women with T2DM compared to GDM had higher rates of decidual vasculopathy when excluding women with preeclampsia (10.3 vs. 1.6%, p=0.049) and diffuse chorangiosis (62.2 vs. 32.5%, p< 0.001) but a lower rate of villous immaturity (10.8 vs. 90.5%, p=0.007) after full adjustment. Discussion Placental vasculopathic abnormalities differ by maternal diabetes type, potentially reflecting underlying pathophysiologic mechanisms. Further research on placental pathology and metabolic derangements is warranted.

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Section: Introductionmentioning

confidence: 99%

“…These pathologies comprise uteroplacental malperfusion or underperfusion (7) and have been described in relation to maternal diabetes (2). Abnormalities in fetal-placental circulation are evidenced by fetal vascular lesions, including chorangiosis and fetal thrombotic vasculopathy (5).…”

Section: Introductionmentioning

confidence: 99%

Type 1, type 2 and gestational diabetes mellitus differentially impact placental pathologic characteristics of uteroplacental malperfusion

et al. 2015

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“…Nowadays, diabetes in pregnant women is widespread. It is estimated that pre-gestational diabetes complicates about 4% and gestational diabetes affects even 8% of pregnancies [14]. Depending on the type of diabetes, different complications may be expected.…”

Section: Discussionmentioning

confidence: 99%

Impact of experimental diabetes and chronic hypoxia on rat fetal body weight

et al. 2018

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Objectives: The aim of the study is to determine the impact of the experimental diabetes and the chronic hypoxia on pregnancy development and rat fetal body weight. Material and methods:The experiment was performed on female Wistar rats. Animals were divided into the experimental groups. I -Controls, II -Untreated diabetes, III -Insulin-treated diabetes, IV -No diabetes with chronic hypoxia, V -Untreated diabetes and chronic hypoxia, VI -Insulin-treated diabetes and chronic hypoxia. Diabetes was induced in groups II, III, V and VI with intraperitoneal injection of streptozocin (STZ) at a dose of 40 mg/kg. Chronic hypoxia was induced by placing dams (groups IV, V and VI) in conditions of 10.5% oxygen and 89.5%. Insulin was administered subcutaneously at the dose of 9 IU/kg. Starting from the 6 th day after STZ injection and chronic hypoxia conditions animals were caged together for 12 hours for 3 consecutive days to ensure fertilization. On day 21 of gestation the animals were decapitated, the fetuses were removed and weighted.Results: Mean fetal body weight in separate groups were: I -5.38 g, II -6.04g, III -5.32g, IV-5.56 g, V -3.45 g, VI -6.23 g. Conclusions:Pre-existing type 1 diabetes does not affect fetal body weight compared to healthy newborn control rats. Prolonged hypoxia does not impact on fetal body weight. Chronic hypoxia during pregnancy complicated with untreated type 1 diabetes mellitus leads to significant reduction of fetal body weight. Insulin treatment reversed the detrimental effect of chronic hypoxia on fetal development.

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“…Au cours de la grossesse diabétique, seule l'insulinothérapie est à ce jour utilisée. Des études ont montré que, malgré un contrôle adapté de la glycémie, le risque de complications foetales au cours de la grossesse (malformations congénitales et mortalité périnatale) est légèrement augmenté chez les patientes présentant un DT2 par rapport aux patientes ayant un DT1 [25]. Le diabète gestationnel est, quant à lui, associé à une insulinorésistance, une hyperglycémie et une hyperinsulinémie.…”

Section: Effets Du Diabète Maternel Sur La Fonction Placentaireunclassified

“…En revanche, chez 13 % des mères ayant un DT2, mais 5 % des mères présentant un DT1, il existe une insuffisance placentaire. Des anomalies villositaires sont également plus fréquentes chez les premières [25], de même que des anomalies de remaniement des artères spiralées, une nécrose fibrinoïde ou une thrombose en lien avec une augmentation de la circulation utéroplacentaire. Chez 17 % des patientes atteintes de diabète (DT1 et DT2), les placentas présentent des zones d'infarctus.…”

Section: Modifications Structurales Du Placentaunclassified

Impact de l’obésité et du diabète maternels sur la fonction placentaire

et al. 2016

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> Situé à l'interface foeto-maternelle, le placenta exerce des fonctions d'échanges, endocrines et immunitaires qui influencent le développement foetal. En contact direct avec l'environnement maternel, cet organe est sensible aux désordres métaboliques comme la surnutrition, l'obésité ou le diabète. L'altération des paramètres sanguins associée à ces conditions affecte l'histologie, la vascularisation et les transferts des nutriments placentaires et induit, en fonction du trouble métabolique, une inflammation locale ou une hypoxie. Ces modifications placentaires perturbent le développement et la croissance foetale, ce qui augmente le risque de pathologies à l'âge adulte chez la descendance. Le placenta est donc un acteur incontournable de la programmation foetale. < cet environnement afin d'optimiser le transport des nutriments et des gaz et ainsi promouvoir la survie foetale. Les modifications phénotypiques du placenta ayant des effets sur le phénotype de l'individu, le placenta représente donc un acteur crucial de la programmation foetale ou DOHaD (developmental origins of health and disease), concept développé dans ce numéro thématique de médecine/sciences qui lui est consacré [4]. Dans cette synthèse, nous présenterons notamment l'impact des désordres métaboliques maternels, tels que l'obésité et le diabète, sur la fonction placentaire en nous appuyant sur des données obtenues chez l'homme et à partir de modèles animaux. Effets de l'obésité sur la fonction placentaireLa prévalence de l'obésité ne cesse d'augmenter dans le monde. En France, d'après l'enquête ObEpi-Roche publiée en 2012 1 , une femme sur cinq en âge de procréer est en surpoids, et environ 15 % des femmes présentent une obésité (index de masse corporelle, IMC ≥ 30 kg/m 2 ). Cette obésité pré-gestationnelle favorise, au cours de la grossesse, les anomalies de la croissance foetale, le développement d'un diabète gestationnel, le retard de croissance intra-utérin (RCIU) ou la macrosomie, la pré-éclampsie et la mortalité foetale (➜).1

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Comparison of placental findings in type 1 and type 2 diabetic pregnancies

Cited by 39 publications

References 23 publications

Type 1, type 2 and gestational diabetes mellitus differentially impact placental pathologic characteristics of uteroplacental malperfusion

Type 1, type 2 and gestational diabetes mellitus differentially impact placental pathologic characteristics of uteroplacental malperfusion

Impact of experimental diabetes and chronic hypoxia on rat fetal body weight

Impact de l’obésité et du diabète maternels sur la fonction placentaire

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