Morphohistometric investigations in placentas of gestational diabetes

Stoz, F.; Schuhmann, R.; Barbara, Haas

doi:10.1515/jpme.1988.16.3.205

Cited by 18 publications

(9 citation statements)

References 9 publications

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“…An association between altered glucose tolerance during pregnancy and increased incidence of placental immaturity has been demonstrated, as well in pregnancies complicated by pre-existing diabetes [1,8,17,25] as in GDM [10,20]. We observed an increased incidence of severe placental immaturity in pregnancies with mild glucose intolerance or GDM compared to those with maternal normal OGTT.…”

Section: Commentsupporting

confidence: 47%

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: Commentsupporting

confidence: 47%

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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“…These would seem to include expanded villous surface areas and global intervillous volumes, reduced pore sizes and more clustered spatial associations. These predictors would seem to fit the structural and blood flow alterations reported previously Teasdale, 1981Teasdale, , 1983Teasdale, , 1985Nylund et al 1982 ;Bjo$ rk & Persson, 1984 ;Boyd et al 1986 ;Teasdale & JeanJacques, 1986 ;Stoz et al 1988) including the increase in cytotrophoblast hyperplasia (Jones & Fox, 1976). Provided there is no hypoxia-related impairment of cytotrophoblast fusion into syncytiotrophoblast (Alsat et al 1996), the natural differentiation within syncytium (Huppertz et al 1998 ;Mayhew et al 1999) might be expected to contribute to the expansion of villous surface area (Mayhew & Simpson, 1994).…”

Section: Discussionmentioning

confidence: 57%

“…Some of these problems might be mediated by changes in placental morphology but morphometric studies have been inconsistent about the nature and extent of such changes (Aherne & Dunnill, 1966 ;Jones & Fox, 1976 Singer et al 1981 ;Teasdale, 1981Teasdale, , 1983Teasdale, , 1985Bjo$ rk & Persson, 1984 ;Boyd et al 1986 ;Teasdale & Jean-Jacques, 1986 ;Stoz et al 1988). The inconsistencies might be attributable to various factors including arbitrary tissue sampling, model-based morphometry, failure to cater for various confounders (e.g.…”

Section: mentioning

confidence: 99%

Stereological comparison of 3D spatial relationships involving villi and intervillous pores in human placentas from control and diabetic pregnancies

Mayhew

Jairam

2000

Journal of Anatomy

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In human placenta, 3D spatial relationships between villi and the maternal vascular bed determine intervillous porosity and this, in turn, influences haemodynamics and transport. Recently-developed stereological methods were applied in order to examine and quantify these relationships. Placentas were collected after 37 wk from control pregnancies and those associated with maternal diabetes mellitus classified according to duration and severity (White classification scheme). Two principal questions were addressed : (1) are normal spatial arrangements maintained in well-controlled diabetes mellitus ? and (2) do arrangements vary between diabetic groups ? To answer these questions, tissue sections cut at random positions and orientations were generated by systematic sampling procedures. Volume densities of villi (terminaljintermediate), intervillous spaces and perivillous fibrin-type fibrinoid deposits were estimated by test point counting and converted to global volumes after multiplying by placental volumes. Design-based estimates of the sizes (volume-and surface-weighted volumes) of intervillous ' pores ' were obtained by measuring the lengths of point-and intersection-sampled intercepts. From these, theoretical numbers of pores were calculated. Model-based estimates (cylinder model) of the hydraulic diameters and lengths of pores were also made. Second-order stereology was used to examine spatial relationships within and between villi and pores and to test whether pair correlation functions deviated from the value expected for ' random ' arrangements. Estimated quantities did not differ significantly between diabetic groups but did display some departures from control values in non-insulin-dependent (type 2) diabetic placentas. These findings support earlier studies which indicate that essentially normal microscopical morphology is preserved in placentas from diabetic subjects with good glycaemic control. Therefore, it is likely that fetal hypoxia associated with maternal diabetes mellitus is due to metabolic disturbances rather than abnormalities in the quantities or arrangements of maternal vascular spaces.

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“…Les modifications placentaires n'ont pas été attribuées à la rétention en l'absence des autres signes histologiques caractéristiques, et ce, d'autant que les capillaires occupaient cette position particulière dans l'axe des villosités. Le diabète constitue un autre diagnostic différentiel, caractérisé histologiquement par des villosités hypovascularisées mais immatures, de grande taille, plus ou moins oedémateuses, dont les capillaires sont en position périphérique et non centrale ; il peut même exister, à l'inverse, une augmentation du nombre des capillaires, voire une chorioangiose placentaire [16]. L'hypothèse selon laquelle le retard de maturation villositaire serait un signe précoce d'un diabète maternel a été émise, sans que le suivi des patientes non diabétiques dans l'étude de Stallmach et al n'ait permis de l'étayer [4].…”

Section: Discussionunclassified

Dysfonction placentaire aiguë par retard de maturation villositaire et décès fœtal tardif

Paciencia

Dolley

Jeanne-Pasquier

et al. 2008

Journal de Gynécologie Obstétrique et Biologie de la Reproducti

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Morphohistometric investigations in placentas of gestational diabetes

Cited by 18 publications

References 9 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

Stereological comparison of 3D spatial relationships involving villi and intervillous pores in human placentas from control and diabetic pregnancies

Dysfonction placentaire aiguë par retard de maturation villositaire et décès fœtal tardif

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