Increased fetoplacental angiogenesis during first trimester in anaemic women

Kadyrov, Named; Kosanke, G.; Kingdom, John; Kaufmann, Peter

doi:10.1016/s0140-6736(98)02069-8

Cited by 130 publications

(57 citation statements)

References 16 publications

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“…The capillary:villus length ratio in control subjects was about 3.7 (0.12) km/km, equivalent to roughly two capillary loops per villus. In diabetic patients, the growth in length of capillaries tended to exceed the linear growth of villi and ratios [20,40]. In fact, capillary volumes and lengths are reduced [20].…”

Section: Resultsmentioning

confidence: 98%

Enhanced fetoplacental angiogenesis in pre-gestational diabetes mellitus: the extra growth is exclusively longitudinal and not accompanied by microvascular remodelling

Mayhew

2002

Diabetologia

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Aims/hypothesis. Morphometric studies on pregnancies complicated by gestational diabetes mellitus have found no evidence of increased fetoplacental angiogenesis. Here, placentas from control subjects and patients with pre-gestational Type I (insulin-dependent) diabetes mellitus were used to test for differences in measures of angiogenesis and vascular remodelling. Methods. Term placentas were collected from non-diabetic subjects and well-controlled diabetic patients grouped according to duration and severity into White classes B, C, D and F/R. Tissues were obtained by uniform random sampling for position and orientation. Volumes, surface areas and lengths of peripheral villi and their capillaries were estimated stereologically. Comparisons were drawn by analysis of variance and used to interpret mechanisms of growth, villous capillarization and vessel remodelling. Results. Placentas associated with all classes of diabetes contained greater (19-45%) volumes of fetal capillaries attributable solely to increases in the combined length of capillaries (12-47%) and not to alteration of vessel cross-sectional area or perimeter. Longitudinal growth tended to increase capillarization (capillary:villus length ratios up to 19% larger) but changes were inconsistent between diabetic classes. There was no evidence of altered vascular remodelling (cross-sectional shape factors, perimeter 2 /area, were preserved). Conclusions/interpretations. In well-controlled pre-gestational diabetes, fetoplacental angiogenesis is enhanced and occurs exclusively by longitudinal growth. Differences may involve hypoxic or other metabolic effects on endothelial cells, perivascular cells and angiogenic factors. The findings differ from those previously reported in gestational diabetes. No differences were associated exclusively with the presence of diabetic complications.

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Section: Resultsmentioning

confidence: 98%

Enhanced fetoplacental angiogenesis in pre-gestational diabetes mellitus: the extra growth is exclusively longitudinal and not accompanied by microvascular remodelling

Mayhew

2002

Diabetologia

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“…36 Contrary to what has been suggested by some authors, 7,37 based on the current correlation with the clinical outcomes, the author is inclined to agree with the opinion that pathogenesis of diffuse chorangiosis is due not to poor uteroplacental perfusion, but to preuterine factors preconditioning the placenta by increasing resistance to ischemiareperfusion injury during labor, 16,38,39 and, unlike in the uterine hypoxia, it may be associated with deep placental invasion. 13 Villous hypervascularity may then be an adaptive change, as in pregnancy at high altitudes and fetal growth restriction. 5,18,19,39 Some authors conclude that vascular dilatation rather than proliferation is an adaptive change to chronic hypoxia.…”

Section: Resultsmentioning

confidence: 99%

“…6,41 It has also to be stressed that two types of chronic hypoxic placental injury 6 represented by groups 1 and 2 are developmental and therefore start early in pregnancy. 13,15 It takes at least several weeks for chorangiosis to occur, 20 but chorangiosis seems to increase placental resistance to more acute hypoxic events (group 1), unlike the uterine pattern, which renders the placenta more vulnerable because of the sequelae of vascular structural lesions (shallow placentation, decidual arteriolopathy). The cause of chorangiosis in group 3 is less clear; may be secondary to the same clinical factors as in group 1 but either subclinical or only mildly manifested and therefore underreported.…”

Section: Resultsmentioning

confidence: 99%

“…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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“…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

125

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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Increased fetoplacental angiogenesis during first trimester in anaemic women

Cited by 130 publications

References 16 publications

Enhanced fetoplacental angiogenesis in pre-gestational diabetes mellitus: the extra growth is exclusively longitudinal and not accompanied by microvascular remodelling

Enhanced fetoplacental angiogenesis in pre-gestational diabetes mellitus: the extra growth is exclusively longitudinal and not accompanied by microvascular remodelling

Chorangiosis of Chorionic Villi: What Does It Really Mean?

Hypoxic Patterns of Placental Injury: A Review

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