Placental pathology in women with gestational diabetes

Daskalakis, G.; Marinopoulos, Spyridon S; Krielesi, Vasiliki; Papapanagiotou, Angeliki; Papantoniou, Nikolaos; Mesogitis, S.; Antsaklis, Aris

doi:10.1080/00016340801908783

Cited by 166 publications

(118 citation statements)

References 14 publications

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“…We also confirmed that chorangiosis has been associated with normoblastemia of fetal blood. 9 Interestingly, frequencies of maternal diabetes mellitus were similar in all 3 groups, which confirms not only that chorangiosis is common in diabetic placentas, 1,11,40 but also that the various degrees of control of diabetes mellitus and/ or superimposed preeclampsia may have an impact on placental morphology that would lead to inclusion into either group 1, group 2 or group 3. Poorly controlled cases of maternal diabetes mellitus were most likely to fall in group 1, those complicated by hypertensive diseases into group 2, and those apparently well controlled and without complications into group 3.…”

Section: Resultssupporting

confidence: 49%

“…7,8 It has been related to several chronic obstetric complications and outcomes, 4 to mention only perinatal deaths, maternal diabetes mellitus, chronic infection, in utero asphyxia, umbilical cord problems, congenital anomalies, fetal vascular thrombosis, maternal anemia, smoking, air pollution, and multiple pregnancy. 7,[9][10][11][12][13][14][15][16][17][18][19][20] The incidence of chorangiosis is low in the second trimester and increases in the third trimester, 21 in which it is lower in preterm than in term pregnancies. 22 Chorangiosis has statistically nonsignificantly clustered with preuterine hypoxia, multiple pregnancy, and normoblasts in fetal circulation.…”

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confidence: 99%

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Chorangiosis of Chorionic Villi: What Does It Really Mean?

Stanek

2016

Archives of Pathology &Amp; Laboratory Medicine

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Chorangiosis has been regarded as a result of low-grade placental hypoxia associated with pregnancy risk factors and abnormal outcomes. It is unknown whether these are a consequence of chorangiosis itself or of associated other placental pathology.Context.— To prove that chorangiosis itself does not portend an increased risk for pregnancy unless associated with other placental pathology.Objective.— This retrospective statistical study analyzes 1231 consecutive placentas with diffuse or focal hypervascularity of chorionic villi: 328 with preuterine pattern of chronic hypoxic placental injury (group 1), 297 with uterine type of chronic hypoxic placental injury (group 2), and 606 cases with chorangiosis (group 3) not fulfilling the inclusion criteria for groups 1 or 2.Design.— Group 2, with 33 cases of chorangiosis (11.1%), featured 10 and 11 statistically significant highest percentages of abnormal clinical and placental variables, respectively; group 3 featured the highest percentages of multiple pregnancy, the heaviest placentas, and the most common acute chorioamnionitis, fetal inflammatory response; and group 1 had the highest proportion of mild erythroblastosis of fetal blood. When comparing groups 1 and 3, 21 of 29 clinical risk factors/outcomes (72.4%) and 30 of 41 placental variables (73.2%) were more common in group 1.Results.— Presence of diffuse hypoxic patterns of placental injury adds prognostically negative significance to increased vascularity of chorionic villi. Chorangiosis without those patterns portends minimal risk for the pregnancy, and is associated with significantly fewer pregnancy risk factors, abnormal outcomes, and other placental abnormalities.Conclusions.—

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Section: Resultssupporting

confidence: 49%

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confidence: 99%

Chorangiosis of Chorionic Villi: What Does It Really Mean?

Stanek

2016

Archives of Pathology &Amp; Laboratory Medicine

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“…21,39 The pattern is evoked by maternal hypoxemia secondary to decreased oxygen pressure in the environment (pregnancies at high altitudes), decreased oxygen binding capacity of the maternal blood (maternal anemia), air pollution and maternal smoking, increased distension of the uterus (multiple pregnancy), and maternal diabetes mellitus (abnormal oxygen-hemoglobin dissociation curve). 21,[38][39][40][41][42][43][44] Clusters of multinucleate giant cells in the decidua basalis and excessive numbers of extravillous trophoblasts are less commonly seen in this than in other patterns of diffuse hypoxic placental injury, 21 most likely because of the association of PR with deep trophoblastic, myometrial invasion, which was proven, at least in maternal anemia. 45 This pattern has a better prognosis than other types of chronic hypoxic injury, 21 probably because of hypoxic preconditioning and resistance to ischemia-reperfusion injury during labor, as was proven in pregnancies at high altitudes 46 and multiple pregnancies.…”

Section: Patterns Of Chronic Hypoxic Placental Injurymentioning

confidence: 99%

Hypoxic Patterns of Placental Injury: A Review

Stanek

2013

Archives of Pathology &Amp; Laboratory Medicine

121

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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“…Impaired reproductive performance is a well-known result of the diabetic syndrome in many mammalian species, including humans (Chieri et al 1969;Kirchick et al 1978;Vomachka and Johnson 1982;Garris et al 1986). Placental dysfunction contributes to an increased frequency of fetal complications in diabetic pregnancies (Daskalakis et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Heat shock protein production and immunity and altered fetal development in diabetic pregnant rats

Saito

Damasceno

Dallaqua

et al. 2013

Cell Stress and Chaperones

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We evaluated associations between the concentrations of heat shock proteins (hsp60 and hsp70) and their respective antibodies, alterations in maternal reproductive performance, and fetal malformations in pregnant rats with hyperglycemia. Mild diabetes (MD) or severe diabetes (SD) was induced in Sprague-Dawley rats prior to mating; nontreated non-diabetic rats (ND) served as controls. On day 21 of pregnancy, maternal blood was analyzed for hsp60 and hsp70 and their antibodies; and fetuses were weighed and analyzed for congenital malformations. Hsp and anti-hsp levels were correlated with blood glucose levels during gestation. There was a positive correlation between hsp60 and hsp70 levels and the total number of malformations (R0 0.5908, P00.0024; R00.4877, P00.0134, respectively) and the number of malformations per fetus (R 00.6103, P0 0.0015; R 00.4875, P 00.0134, respectively). The antihsp60 IgG concentration was correlated with the number of malformations per fetus (R00.3887, P00.0451) and the anti-hsp70 IgG level correlated with the total number of malformations (R00.3999, P00.0387). Moreover, both hsp and anti-hsp antibodies showed negative correlations with fetal weight. The results suggest that there is a relationship between hsp60 and hsp70 levels and their respective antibodies and alterations in maternal reproductive performance and impaired fetal development and growth in pregnancies associated with diabetes.

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Placental pathology in women with gestational diabetes

Abstract: Histological abnormalities were observed more frequently in the diabetic placentas compared to the controls. These findings support the hypothesis that impaired placental function is one of the main reasons for the increased frequency of fetal complications in diabetic pregnancies.

Cited by 166 publications

References 14 publications

Chorangiosis of Chorionic Villi: What Does It Really Mean?

Chorangiosis of Chorionic Villi: What Does It Really Mean?

Hypoxic Patterns of Placental Injury: A Review

Heat shock protein production and immunity and altered fetal development in diabetic pregnant rats

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