Zottenreifungsstörungen der Plazenta beim Gestationsdiabetes - in Abhängigkeit von mütterlichen und fetalen Parametern des Glukosestoffwechsels

Schäfer, U.; Vogel, Markus; Unger, Manfred; Dupak, J; Vetter, K.

doi:10.1055/s-2007-1023077

Cited by 3 publications

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“…Despite the differences in the frequency of pathological placental changes in manifest diabetes mellitus, it is clear that disturbances in glucose metabolism in pregnancy result in an increase in disturbances of villous maturation of various types and forms [52,54,59,65,73,74]. Both with manifest and latent metabolic disturbances, the incidence and forms of maturation defects depend on the blood sugar levels of the mother during pregnancy [44,46].…”

Section: The Placenta In Gestational Diabetesmentioning

confidence: 99%

“…Only 48% of these placentas were almost fully matured. There was a highly significant correlation between the severity of the mother's glucose tolerance test, as diagnosed by means of OGTT, and the appearance of a disturbance in villi maturation in the placenta (p ϭ 0.02) [74]. Further, the disturbance of maturation showed a correlation with the concentration of insulin in the amniotic fluid and in the blood of the umbilical cord, as well as with the fetal parameters of glucose metabolism [77,78].…”

Section: The Placenta In Gestational Diabetesmentioning

confidence: 99%

“…The fetal insulin level in the amniotic fluid had a significant correlation with the placenta morphology (p ϭ 0.02), but the morphology did not correlate significantly with the level of insulin in the blood in the umbilical cord (p ϭ 0.09). Since 50% of the placentas of pregnant women with gestational diabetes demonstrated a disturbance in villous maturation and over one third of the placentas of mothers with borderline glucose tolerance also showed a disturbance of villous maturation, the possibility should be considered of monitoring pregnant women with IGT as closely as women with gestational diabetes, with respect to both the metabolism of the mother and the status of the fetus [74].…”

Section: The Placenta In Gestational Diabetesmentioning

confidence: 99%

“…Percent of placentas with disorders of villous maturation in pregnancies with normal, borderline (IGT) and pathological glucose tolerance (GDM) (n ϭ 325)[74] …”

mentioning

confidence: 99%

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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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Section: The Placenta In Gestational Diabetesmentioning

confidence: 99%

Section: The Placenta In Gestational Diabetesmentioning

confidence: 99%

Section: The Placenta In Gestational Diabetesmentioning

confidence: 99%

“…Percent of placentas with disorders of villous maturation in pregnancies with normal, borderline (IGT) and pathological glucose tolerance (GDM) (n ϭ 325)[74] …”

mentioning

confidence: 99%

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Morphological Findings in Infants and Placentas of Diabetic Mothers

Kos¹,

Vogel²

2005

Frontiers in Diabetes, 2005

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“…Als Ursache der fetalen Dystrophie und der damit verbundenen Problematik hinsichtlich der Mangelgeburtlichkeit sowie der assoziierten Komplikationen stellt sie nach wie vor ein erhebliches Problem dar [4]. Zwar existieren Daten zu den pathoanatomischen Grundlagen und Ursachen einer Plazentainsuffizienz [2,5,6,13] sowie den prädisponierenden Faktoren der Plazentainsuffizienz, wie etwa mütterliche Hypertonie, Diabetes mellitus, Nikotinabusus oder sozialer Status [1,7,8,11,12,14], die Frage des Wiederholungsrisikos dieser geburtshilflichen Risikosituation ist jedoch noch nicht hinreichend geklärt, wobei es speziell an Studien unter Einbeziehung histomorphologischer Parameter als möglichen prädiktiven Faktoren fehlt.…”

Section: Introductionunclassified

Wiederholungsrisiko der Plazentainsuffizienz aus klinischer und morphologischer Sicht

Steiner¹,

Hofmann²,

Weikel³

et al. 2001

Geburtsh u Frauenheilk

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ZusammenfassungFragestellung: Diese Studie untersucht die Wertigkeit der histomorphologischen Untersuchungsergebnisse als eigenständige prädiktive Faktoren für das wiederholte Auftreten einer Plazentainsuffizienz. Material und Methode: In der vorliegenden Auswertung von 15 863 Geburten an der Mainzer Universitätsfrauenklinik fanden wir 32 Wiederholungsfälle einer Wachstumsretardierung. Die klinischen Daten zur Anamnese, Schwangerschafts-und Geburtsverlauf sowie den Untersuchungsergebnissen der histomorphologischen Beurteilung der Plazenten wurden für drei Gruppen (eine Mangelgeburt, mehrere Mangelgeburten und eine Vergleichsgruppe ohne Mangelgeburt) erarbeitet und statistisch hinsichtlich ihrer eigenständigen Signifikanz hin ausgewertet. Ergebnisse: Die Auswertung der Daten zeigte, dass ± neben dem Alter der Mutter und ihrem sozialen Umfeld ± den histomorphologischen Plazentabefunden eine wichtige Bedeutung als prädiktiven Faktoren zukommt. Das Risikoprofil für ein wiederholtes Auftreten einer Wachstumsretardierung lässt sich nach unseren Daten wie folgt darstellen: In der mütterlichen Anamnese ist ein Alter von über 35 Jahren, ein fortgesetzter Nikotinabusus, ein bekannter Diabetes mellitus oder eine essenzielle Hypertonie mit einem erhöhten Risiko verbunden. Für die Daten aus den vorangegangenen Schwangerschaften ist neben der Information über stattgehabte Aborte oder intrauterine Fruchttode insbesondere der Nachweis einer Hypovaskularisation des Zottenbaumes mit einer erhöhten Wiederholungsrate verbunden. Aus dem Verlauf der aktuellen Schwangerschaft sind insbesondere Nachweis gestosetypischer Veränderungen sowie das Auftreten einer vorzeitigen Wehentätigkeit. SummaryObjective: We evaluated whether recurrence of intrauterine growth restriction (IUGR) in subsequent pregnancies can be predicted by histologic findings in the placenta. Methods: A total of 15,863 singleton deliveries were reviewed. A total of 32 cases of recurrent IUGR were identified. We reviewed the clinical data and the results of histomorphologic examination of the placentas in 61 mothers with 1 pregnancy complicated by IUGR, the 32 mothers with recurrent pregnancies complicated by IUGR, and 130 mothers with uncomplicated pregnancies. Maternal age > 35 years, coincidental social factors, and structural changes of the placental villi were analyzed as possible predictive factors. Results: Maternal age > 35 years, smoking, maternal diabetes or hypertension, and hypovascularization of the placenta (13 % in the mothers with one pregnancy with IUGR, 28% in the mothers with recurrent IUGR and none in the control group) were risk factors for the recurrence of IUGR. Conclusion: Hypovascularization of the placental villi is an independent risk factor for recurrent IUGR in a subsequent pregnancy.

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Pathologie der Plazenta: Spätschwangerschaft und fetoplazentare Einheit

Vogel

2012

Pathologie

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Zottenreifungsstörungen der Plazenta beim Gestationsdiabetes - in Abhängigkeit von mütterlichen und fetalen Parametern des Glukosestoffwechsels

Cited by 3 publications

References 0 publications

Morphological Findings in Infants and Placentas of Diabetic Mothers

Morphological Findings in Infants and Placentas of Diabetic Mothers

Wiederholungsrisiko der Plazentainsuffizienz aus klinischer und morphologischer Sicht

Pathologie der Plazenta: Spätschwangerschaft und fetoplazentare Einheit

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