Elevated Maternal Hemoglobin A1c in Early Pregnancy and Major Congenital Anomalies in Infants of Diabetic Mothers

Miller, Edith; Hare, John; Cloherty, John P.; Dunn, Peter J.; Gleason, Ray E.; Soeldner, J S; Kitzmiller, John L.

doi:10.1097/00006254-198202000-00020

Cited by 115 publications

(146 citation statements)

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“…Major congenital malformations were those responsible for death, those causing a significant future disability, or those requiring major surgery for correction (11). Serious adverse fetal outcome represented was major congenital malformations or perinatal death.…”

Section: Methodsmentioning

confidence: 99%

Poor Pregnancy Outcome in Women With Type 2 Diabetes

et al. 2005

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OBJECTIVE -To evaluate the perinatal outcome and the frequency of maternal complications in pregnancies of women with type 2 diabetes during 1996 -2001.RESEARCH DESIGN AND METHODS -Medical records of 61 consecutive singleton pregnancies in women with type 2 diabetes from 1996 to 2001 were studied. Pregnancy outcome was compared with that of pregnant women with type 1 diabetes during 1996 -2000, the background population, and pregnant women with type 2 diabetes during 1980 -1992 from the same department.RESULTS -The perinatal mortality in pregnancies complicated by type 2 diabetes (4/61, 6.6%) was increased four-and ninefold, respectively, and the rate of major congenital malformations (4/60, 6.7%) was more than doubled, although not statistically significant, compared with type 1 diabetic pregnancies and the background population. The glycemic control was similar or better in women with type 2 diabetes compared with women with type 1 diabetes. Multivariate logistic regression analysis in the pooled group of pregnancies with pregestational diabetes from 1996 to 2001 showed that high HbA 1c at admission and type 2 diabetes were independently associated with a serious adverse fetal outcome (perinatal mortality and/or major congenital malformations). The perinatal mortality and the rate of major congenital malformations in type 2 diabetic pregnancies have increased during the last decade.CONCLUSIONS -The perinatal outcome of pregnancies in women with type 2 diabetes during 1996 -2001 is poor. It is worse than the outcome of pregnancies in women with type 1 diabetes and the background population in the same period, as well as in women with type 2 diabetes studied during 1982-1990. Diabetes Care 28:323-328, 2005T he prevalence of type 2 diabetes is increasing rapidly in all age-groups. In line with this, it is a general clinical observation that the number of pregnant women with pregestational type 2 diabetes has become more frequent in the recent years; however, little knowledge exists concerning the prevalence and outcome of these pregnancies (1,2).A study from Birmingham, U.K., showed a similar perinatal mortality but a higher frequency of congenital malformations, preterm delivery, large-forgestational-age infants, and fetal loss before 24 weeks' gestation in 57 pregnancies in women with type 2 diabetes compared with pregnancies in women with type 1 diabetes (3,4). In 182 pregnancies in women with type 2 diabetes compared with the general population, there was a 2.5-fold greater risk of perinatal mortality and an 11-fold greater risk of a congenital malformation (5). A study from New Zealand reported a threefold increased perinatal mortality rate in pregnancies related to type 2 diabetes compared with pregnancies related to type 1 diabetes. In addition, the study indicated that the outcome was poorer if type 2 diabetes was diagnosed during pregnancy compared with before pregnancy (6). The prevalence of type 2 diabetes in pregnancy was the highest in non-Caucasian women, who had a nonsignificantly higher HbA 1c dur...

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Section: Methodsmentioning

confidence: 99%

Poor Pregnancy Outcome in Women With Type 2 Diabetes

et al. 2005

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“…Miller et al 36 found no major anomalies if the HbA1C was less than 6.9%, and significantly lower incidence if HbA1C was less than 8.5%. Greene et al 37 observed a 3% risk of major malformation with HbA1C of less than 9.3%, and 40% with HbA1C of more than 14.4%.…”

Section: Discussionmentioning

confidence: 96%

Caudal Regression Syndrome in Twin Pregnancy With Type II Diabetes

Zaw

Stone

2002

J Perinatol

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“…The metabolic profiles of type 1 and type 2 diabetes are different, except for episodic hyperglycaemia. Numerous studies have shown that the incidences of early miscarriage and congenital malformations are associated with poor glycaemic control [8][9][10]. These observations suggest that excess glucose, or a metabolic process activated by high glucose concentration in both type 1 and type 2 diabetes, is responsible for the teratogenic effect of diabetic pregnancy.…”

Section: Introductionmentioning

confidence: 99%

Expression of the gene encoding the high-K m glucose transporter 2 by the early postimplantation mouse embryo is essential for neural tube defects associated with diabetic embryopathy

Thorens

Loeken

2007

Diabetologia

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Aims/hypothesis Excess glucose transport to embryos during diabetic pregnancy causes congenital malformations. The early postimplantation embryo expresses the gene encoding the high-K m GLUT2 (also known as SLC2A2) glucose transporter. The hypothesis tested here is that high-K m glucose transport by GLUT2 causes malformations resulting from maternal hyperglycaemia during diabetic pregnancy. Materials and methods Glut2 mRNA was assayed by RT-PCR. The K m of embryo glucose transport was determined by measuring 0.5-20 mmol/l 2-deoxy[ 3 H]glucose transport. To test whether the GLUT2 transporter is required for neural tube defects resulting from maternal hyperglycaemia, Glut2 +/− mice were crossed and transient hyperglycaemia was induced by glucose injection on day 7.5 of pregnancy. Embryos were recovered on day 10.5, and the incidence of neural tube defects in wild-type, Glut2 +/− and Glut2 −/− embryos was scored. Results Early postimplantation embryos expressed Glut2, and expression was unaffected by maternal diabetes. Moreover, glucose transport by these embryos showed Michaelis-Menten kinetics of 16.19 mmol/l, consistent with transport mediated by GLUT2. In pregnancies made hyperglycaemic on day 7.5, neural tube defects were significantly increased in wild-type embryos, but Glut2 +/− embryos were partially protected from neural tube defects, and Glut2 −/− embryos were completely protected from these defects. The frequency of occurrence of wild-type, Glut2 +/− and Glut2 −/− embryos suggests that the presence of Glut2 alleles confers a survival advantage in embryos before day 10.5. Conclusions/interpretations High-K m glucose transport by the GLUT2 glucose transporter during organogenesis is responsible for the embryopathic effects of maternal diabetes.

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Elevated Maternal Hemoglobin A1c in Early Pregnancy and Major Congenital Anomalies in Infants of Diabetic Mothers

Cited by 115 publications

References 0 publications

Poor Pregnancy Outcome in Women With Type 2 Diabetes

Poor Pregnancy Outcome in Women With Type 2 Diabetes

Caudal Regression Syndrome in Twin Pregnancy With Type II Diabetes

Expression of the gene encoding the high-K m glucose transporter 2 by the early postimplantation mouse embryo is essential for neural tube defects associated with diabetic embryopathy

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