Foetal Defects Following Insulin Coma Therapy in Early Pregnancy

Wickes, Ian G.

doi:10.1136/bmj.2.4895.1029

Cited by 37 publications

(9 citation statements)

References 4 publications

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“…Horii and his colleagues (1966) have shown that treatment with insulin prevents the occurrence of an increased incidence of malformation in the foetuses of alloxandiabetic mice, which suggests that in these animals the teratogenic effect of diabetes in pregnancy is directly due to metabolic abnormalities in the foetal environment arising from the maternal diabetes. However, other workers have shown that insulin itself can be teratogenic (Duraiswami, 1950;Wickes, 1954)" perhaps when its administration causes severe hypoglycaemia early in pregnancy. However, other workers have shown that insulin itself can be teratogenic (Duraiswami, 1950;Wickes, 1954)" perhaps when its administration causes severe hypoglycaemia early in pregnancy.…”

Section: Congenital Abnormalitiesmentioning

confidence: 99%

Some Aspects of Carbohydrate Metabolism in Pregnancy With Special Reference to the Energy Metabolism and Hormonal Status of the Infant of the Diabetic Woman and the Diabetogenic Effect of Pregnancy

Baird¹

1969

Journal of Endocrinology

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Section: Congenital Abnormalitiesmentioning

confidence: 99%

Some Aspects of Carbohydrate Metabolism in Pregnancy With Special Reference to the Energy Metabolism and Hormonal Status of the Infant of the Diabetic Woman and the Diabetogenic Effect of Pregnancy

Baird¹

1969

Journal of Endocrinology

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“…There is some evidence (Kim et al 1960;Van Assche 1975) that the fetal rat responds to maternal diabetes by hyperplasia of beta cells in pancreatic islets. Hypoglycemia has also been associated with an increased frequency of congenital malformations (Wickes 1954). Such studies support the hypothesis that hypoglycemia may induce changes in the metabolism ofprecartilage and cartilage precursors.…”

Section: Discussionmentioning

confidence: 88%

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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“…Compared to other metabolic alterations of diabetes, hypoglycemia has only recently received serious attention as a potential teratogenic factor. Early reports suggested an association between hypoglycemic coma induced by insulin shock therapy and fetal malformations and mortality (40)(41)(42), but the number of cases reported was small. In one study of nineteen pregnant women receiving insulin shock therapy, six cases of "fetal damage" resulted, including four deaths and two malformed infants.…”

Section: Teratogenicity Of Hypoglycemiamentioning

confidence: 99%

Hypoglycemia and embryonic heart development

Smoak

2002

Front Biosci

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Abnormal embryonic development is a complication of the diabetic pregnancy, and heart defects are among the most common and detrimental congenital malformations of the diabetic embryopathy. Hypoglycemia is a common side effect of diabetes therapy and is a potential teratogen. An association between hypoglycemia and congenital defects has been difficult to demonstrate in humans, but in vivo and in vitro animal studies have illustrated the importance of glucose as a substrate for normal development. Hypoglycemia alters embryonic heart morphology, producing abnormal looping and chamber expansion, decreased myocardial thickness, disorganized layers, and decreased overall size. Hypoglycemia decreases embryonic heart rate and vascularity, and it alters embryonic heart metabolism by increasing glucose uptake and glycolysis. Hypoglycemia also affects protein expression in the embryonic heart, increasing the expression of glucose regulated proteins, hexokinase, and glucose transport protein. Thus, hypoglycemia interferes with normal cardiogenesis and alters morphology, function, metabolism, and expression of certain proteins in the developing heart. It is likely that these factors contribute to heart defects observed in the diabetic embryopathy, but the definitive link has yet to be made. Future studies are expected to further elucidate mechanisms mediating hypoglycemia-induced cardiac dysmorphogenesis.

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Foetal Defects Following Insulin Coma Therapy in Early Pregnancy

Cited by 37 publications

References 4 publications

Some Aspects of Carbohydrate Metabolism in Pregnancy With Special Reference to the Energy Metabolism and Hormonal Status of the Infant of the Diabetic Woman and the Diabetogenic Effect of Pregnancy

Some Aspects of Carbohydrate Metabolism in Pregnancy With Special Reference to the Energy Metabolism and Hormonal Status of the Infant of the Diabetic Woman and the Diabetogenic Effect of Pregnancy

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

Hypoglycemia and embryonic heart development

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