Morphohistometric investigations of placentas of diabetic patients in correlation to the metabolic adjustment of the disease

Stoz, F.; Schuhmann, R.; Schultz, Regina

doi:10.1515/jpme.1988.16.3.211

Cited by 11 publications

(3 citation statements)

References 19 publications

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“…Thus the impressing higher rate of severe placental immaturity in pregnancies with one abnormal value in the maternal OGTT is unlikely to be the consequence of the earlier delivery of these pregnancies compared to the normal group. The incidence and degree of placental immaturity seems to be less dependent on the duration of diabetes, expressed by the White classification, than on the glycemic control during pregnancy [18,21]. Disorders of placental maturation may have an adverse effect on the function of the placenta and therefore on the fetal outcome, especially when a wide area of the placenta is affected by severe immaturity [24].…”

Section: Commentmentioning

confidence: 99%

Hyperinsulinism, neonatal obesity and placental immaturity in infants born to women with one abnormal glucose tolerance test value

Schäfer‐Graf¹,

Dupak²,

Vogel³

et al. 1998

Jpme

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Several groups have reported a risk of fetal macrosomia in pregnancies with maternal glucose intolerance which is intermediate between gestational diabetes (GDM) and normal glucose tolerance. The present study was designed to determine whether these pregnancies are also at risk for fetal obesity, hyperinsulinism and placental villous immaturity. 325 women with risk factors for GDM underwent a 75 g OGTT interpreted according to the O'Sullivan criteria. All women who met the criteria for GDM were managed with diet therapy. Insulin therapy was added for women with a mean serum glucose value > 100 mg/dl on a 24 hour glucose profile. Patients not meeting the GDM criteria were managed without special intervention. Primary outcome variables were measures of neonatal weight and skinfold thickness, fetal and neonatal insulin and glucose concentration, and placental villous maturation. Outcome parameters were compared among three groups: pregnancies with normal OGTT (control, n = 95), 1 abnormal value in the OGTT (1 abnl, n = 76) and GDM (n = 154). The outcome of pregnancies with 1 abnormal value in the OGTT was different from those with normal OGTT. Regarding fetal growth, rates of LGA were approximately twice as high in groups with one abnormal value and GDM (21% and 24%) compared to women with normal OGTTs (11%: p < 0.05 vs GDM and p = 0.07 vs 1 abnormal value). The percent of infants with skinfold thickness > 90th percentile was also greater in the 1 abnormal value and GDM groups (31.1 and 31.6% respectively) compared to controls (19.2%; p < 0.05 for GDM vs control only). Regarding fetal hyperinsulinism, AFI concentrations were similar in control and GDM groups (3.1 +/- 0.4 and 3.4 +/- 0.8 microU/ml, respectively), but were higher in the group with one abnormal OGTT value (4.3 +/- 1.2 microU/ml, p < 0.05 vs controls). Cord blood insulin: glucose ratios were elevated in both the 1 abnormal value and GDM groups (0.22 +/- 0.05 and 0.20 +/- 0.02 microU/ml per mg/dl), compared to controls (0.12 +/- 0.01 microU/ml per mg/dl, p < 0.05 vs 1 abnormal value). Neonatal glycemia < 30 mg/dl was significantly more common in the one abnormal value than in the control group (49% vs 34% of infants) and intermediate in the GDM group (40%). Severe placental villous immaturity was more than twice as frequent in the 1 abnormal value group compared to controls (24% vs 9%, p < 0.05) and the most frequent in the GDM group (33%; p < 0.001 vs controls). Pregnancies with glucose intolerance below the thresholds for diagnosis of GDM have an increased risk for fetal obesity, hyperinsulinism, postpartum hypoglycemia and placental immaturity. These findings indicate the continuum of risk for fetal morbidity associated with increasing maternal glucose intolerance in pregnancy.

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Section: Commentmentioning

confidence: 99%

Hyperinsulinism, neonatal obesity and placental immaturity in infants born to women with one abnormal glucose tolerance test value

Schäfer‐Graf¹,

Dupak²,

Vogel³

et al. 1998

Jpme

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“…The results of histometric investigations give no uniform figure. Stolz et al [61] found evidence of a delayed maturation of the villi, above all in the placentas of women with diabetes mellitus of the White stage D. Boyd et al [62] and Teasdale [42] determined an increase in the villi surface. Teasdale also determined an increase in the villi vessel surface in the placentas of mothers with diabetes of the White stages B and C [41,42].…”

Section: The Placenta In Overt Diabetes Mellitusmentioning

confidence: 98%

Morphological Findings in Infants and Placentas of Diabetic Mothers

Kos¹,

Vogel²

2005

Frontiers in Diabetes, 2005

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Infants of diabetic mothers have many problems, usually called diabetic embryopathy, i.e. fetopathy. Congenital malformations together with spontaneous abortions are usually summarized under the term diabetic embryopathy, while the term diabetic fetopathy encompasses increased incidence of perinatal death, increased somatic size (macrosomia) and hypertrophy of the islets of Langerhans with B cell hyperplasia and hyperinsulinaemia. Before the discovery of insulin and its widespread use in every day practice, many infants, but their mothers as well, have died during pregnancy complicated with diabetes. Close surveillance of diabetic pregnancy has resulted in a decrease of overall perinatal mortality to 2.8%, and even to less than 2% [1-3]. These figures are still 2-to 3-fold greater than in uncomplicated pregnancies. The risk of a lethal outcome for the infant depends upon the duration and intensity of the mother's diabetes and also upon the degree of blood vessel damage it has caused. Increased perinatal mortality is the result of both increased intrauterine and neonatal mortality. Thirty years ago the main causes of neonatal death in infants from diabetic pregnancies were extreme prematurity, hyaline membrane disease, pulmonary changes unrelated to hyaline membranes, congenital malformations, infections (lung infections excluded) and changes due to asphyxia [3]. Despite many advances in the last 30 years, the rate of early and late fetal death and of neonatal mortality still remains higher than in uncomplicated pregnancies [2, 4-9]. The increased risk of fetal death begins during the third trimester, increasing gradually between 30 and 40 weeks' gestation. The autopsy of stillborn infants often fails to reveal the cause of death [10]. Experiments have shown that hyperglycaemia in lambs causes hyperinsulinaemia, increased basal metabolism and hypoxaemia. We can assume that a similar reaction in human Downloaded by: Univ. of California San Diego 198.143.33.65 -8/19/2015 12:47:14 PM Kos/Vogel 128fetuses leads to an increase in cardiac output and an abundant norepinephrine excretion together with a decrease in glucagon secretion. This pathophysiological mechanism may in humans also be the cause of unexplained intrauterine deaths in diabetic pregnancies [11]. However, strict control of maternal glycaemia has significantly reduced the stillbirth rate. In diabetic pregnancies there exists an increased risk of most congenital malformations, and the term 'diabetic embryopathy and fetopathy' has been long known in medicine [12]. In a large retrospective study carried out in Washington State, USA, the prevalence of congenital malformations was compared in infants of mothers with established pre-existing diabetes, gestational diabetes and the non-diabetic control group. In infants of mothers with pre-existing diabetes the prevalence of congenital malformations was 7.2%, in those of mothers with gestational diabetes 2.8%, while it was 2.1% in infants of healthy mothers [5]. These results differ from the results of studies in ...

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“…It is known that DM pregnancies are associated with increased placental weight and birth weight and an increased birth weight/placental weight-ratio [6]. Current knowledge on the fetoplacental vasculature in DM pregnancies is based on macroscopic examinations [7], histomorphometry [3,[8][9][10][11][12][13][14][15][16], stereology [4,[17][18][19][20], x-ray angiograms [21], and measurements of the placental residual blood volume after birth [22]. In T1DM pregnancies conflicting results are demonstrated as some studies describe an increased fetoplacental vascular volume, surface area, and capillary length compared to normal [3,4,8,9,[17][18][19]22], while others describe decreased vessel diameter and number of vessels [7,[10][11][12][13][14][15]21].…”

Section: Introductionmentioning

confidence: 99%

Postpartum placental CT angiography in normal pregnancies and in those complicated by diabetes mellitus

et al. 2018

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Morphohistometric investigations of placentas of diabetic patients in correlation to the metabolic adjustment of the disease

Cited by 11 publications

References 19 publications

Hyperinsulinism, neonatal obesity and placental immaturity in infants born to women with one abnormal glucose tolerance test value

Hyperinsulinism, neonatal obesity and placental immaturity in infants born to women with one abnormal glucose tolerance test value

Morphological Findings in Infants and Placentas of Diabetic Mothers

Postpartum placental CT angiography in normal pregnancies and in those complicated by diabetes mellitus

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