Congenital Malformations in Newborn Infants of Diabetic Women Correlation With Maternal Diabetic Vascular Complications

Pedersen, Lars; Tygstrup, Inge; Pedersen, Julie Steen

doi:10.1016/s0140-6736(64)91805-7

Cited by 322 publications

(25 citation statements)

References 11 publications

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“…Clinical studies reporting on the potential effects of maternal hypoglycemia on the developing fetus are summarized in Table 2 [13,[15][16][17][78][79][80][81][82]. None of them suggest an increase in the incidence of congenital malformations in relation to maternal hypoglycemia.…”

Section: Studies In Humansmentioning

confidence: 99%

Maternal hypoglycemia during pregnancy in type 1 diabetes: maternal and fetal consequences

Braak

Evers

Erkelens

et al. 2002

Diabetes Metabolism Res

141

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There is strong evidence that the avoidance of hyperglycemia is essential inoptimizing pregnancy outcome in type 1 diabetes. The price to pay is a striking increase in severe hypoglycemia (SH), defined as episodes requiring help from another person. During type 1 diabetic pregnancy, occurrence rates of SH up to 15 times higher as in the intensively treated group of the Diabetes Control and Complications Trial (DCCT) are reported. Blood glucose (BG) treatment targets differ considerably between clinics; some authors advocate lower limits as low as 3.3 mmol/l. Improved glycemic control and/or recurrent hypoglycemia (i.e. BG <3.9 mmol/l) may result in impairment of glucose counterregulatory responses. Also, glucose counterregulation may be altered by pregnancy itself. Short-acting insulin analogs may help reduce hypoglycemia with preservation of good glycemic control, but their use during pregnancy has yet to be proven safe.Several clinical studies did not establish an association between maternal hypoglycemia and diabetic embryopathy. However, animal studies clearly indicate that hypoglycemia is potentially teratogenic during organogenesis. Increased rates of macrosomia continue to be observed despite near normal HbA(1c) levels. This may, at least in part, be the result of rebound hyperglycemia elicited by hypoglycemia. Exposure to hypoglycemia in utero may have long-term effects on offspring including neuropsychological defects. It is yet unclear to what extent the benefits of tight glycemic control balance with the increased risk of (severe) hypoglycemia during type 1 diabetic pregnancy. Efforts must be made to avoid low BG, i.e. <3.9 mmol/l, when tightening glycemic control.

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Section: Studies In Humansmentioning

confidence: 99%

Maternal hypoglycemia during pregnancy in type 1 diabetes: maternal and fetal consequences

Braak

Evers

Erkelens

et al. 2002

Diabetes Metabolism Res

141

View full text Add to dashboard Cite

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“…Thus, the expected incidence for congenital malformation may be five to six times higher in diabetic compared to nondiabetic pregnancy (see Eriksson et al, 2003 and references therein). Given the magnitude of the problem, it is not surprising that embryonic and foetal development in diabetic pregnancy has been studied extensively in both clinical (Mølsted-Pedersen et al, 1964;Ray et al, 2001) and experimental (Lazarow et al, 1960;Wentzel et al, 2001) studies. In brief, there is conclusive evidence that hyperglycaemia per se acts as primary teratogen (Styrud et al, 1995;Moley et al, 1998aMoley et al, , 1998b, but that other factors, such as inositol depletion (Baker et al, 1990), alterations of arachidonic acid (Goldman et al, 1985), and oxidative stress (Baynes, 1991) are also causative in abnormal embryonic and foetal development.…”

Section: Introductionmentioning

confidence: 99%

Influence of murine maternal diabetes on placental morphology, gene expression, and function

Singh

Wei

et al. 2008

Archives of Physiology and Biochemistry

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Maternal diabetes causes placental and foetal abnormalities in both rat and humans; however, its effect is less well documented in the mouse. We used a standard approach to induce manifest diabetes in pregnant mice and assessed morphology, function and gene expression in the placentas isolated from these females. We found that diabetic placentas exhibit a consistent abnormal phenotype characterized by increased junctional zone cross sectional area. Lipid profiling of diabetic foetuses and placentas showed that the placental phenotypes do not compromise the lipid transport function of this organ. In a genomewide survey of mRNA expression by using cDNA micro-arrays, we identified 118 ESTs, corresponding to 59 annotated genes, with differential expression in the diabetic placentas. A significant proportion of these known is involved in metabolism, immunity and defence, and signal transduction. In addition, we found two imprinted genes, Igf2 and Gatm, which exhibited altered expression. The expression of other imprinted genes, Peg1, Gtl2, Peg3, Igf2r and Grb10, was determined by quantitative RT-PCR. For all of these genes, slight changes in gene expression were observed between diabetic placentas and control placentas. Our study thus provides the basis for future work that will address gene action in the diabetic mouse placenta.

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“…Of the several anomalies observed in this case, only "caudal regression" (Lenz and Maier 1964;Rusnak and Driscoll 1965;Stern et al 1965;Passarge and Lenz 1966;Fields et al 1968;Ku~era 1971;Assemany et al 1972), gross skeletal malformations (Molsted-Pedersen et al 1964;Ku~era 1971) and congenital heart defects (Ku~era 1971; Rowland et al 1973) appear frequently in the offspring of diabetic mothers.…”

Section: Discussionmentioning

confidence: 71%

A fetus with upper limb amelia, “caudal regression” and Dandy-Walker defect with an insulin-depedent diabetic mother

et al. 1980

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We describe the fetus delivered to an insulin-dependent diabetic woman who had had a previous large, stillborn, non-malformed male infant and a normal female infant. The present fetus had a most unusual combination of malformations which to date had not been described in diabetic embryopathy. The anomalies include: upper limb amelia, "caudal regression" with bilateral absence of the fibulae, unilateral absence of a femur and ipsilateral oligodactyly; undescended testes; atrial septal defect; multiple vertebral and rib anomalies with cervical scoliosis and right webbed neck; left cleft lip and cleft palate; severe micrognathia; left microtia with atresia of the ear canal; and central nervous system defects including hydrocephalus with the Dandy-Walker malformation, asymmetry of the lateral ventricles, abnormal frontal gyral formation, and ependymal and ganglion cell heterotopias of the spinal cord. The pathogenesis of diabetic embryopathy is discussed.

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Congenital Malformations in Newborn Infants of Diabetic Women Correlation With Maternal Diabetic Vascular Complications

Cited by 322 publications

References 11 publications

Maternal hypoglycemia during pregnancy in type 1 diabetes: maternal and fetal consequences

Maternal hypoglycemia during pregnancy in type 1 diabetes: maternal and fetal consequences

Influence of murine maternal diabetes on placental morphology, gene expression, and function

A fetus with upper limb amelia, “caudal regression” and Dandy-Walker defect with an insulin-depedent diabetic mother

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