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Clinical data in the 1980s showed a close relationship between the conceptional glycated hemoglobin and the occurrence of spontaneous early abortions and fetal malformations. Blood glucose level during pregnancy was similarly correlated with the risk of fetal macrosomia, due to significant links between birthweight, fetal hyperinsulinemia and mean maternal blood glucose. Tight blood glucose control from conception to term was shown to be able to lower the risk of fetal malformations and perinatal mortality to that of the offspring of a non diabetic mother. Prerequisites include: 1) contraception until tight blood glucose control, 2) close partnership between diabetologist and obstetrician, 3) assessment of diabetic complications. Seldom, coronary heart disease or advanced nephropathy contraindicate pregnancy. Uncontrolled proliferative or pre-proliferative retinopathy, or macular edema, are temporary contraindications to pregnancy. Laser photocoagulation must then be performed before tightening blood glucose control. A complete review of diabetes management is associated with therapeutic intensification. Blood glucose objectives allow as limits: 70 to 100 mg/dl before meals, up to 140 mg/dl one hour and 120 mg/dl two hours after meals. HbA1c allowing conception is close to 7%. Blood glucose monitoring requires 6-7 measurements per day. The most efficient insulin regimens include 3 to 4 shots per day. The distribution between regular and NPH or lente insulins is adapted individually. Lispro insulin, now appearing as safe, may be used to improve post-meal blood glucose control. Insulin pumps may be useful in case of late-night poor control or frequent hypoglycemic events. Patient acceptance of this option is unavoidable to obtain a benefit. Preconceptional insulin therapy must be maintained until pregnancy term. Follow-up must be intensified after twenty fourth week. Labor and delivery, cesarean section, fetal maturation by corticosteroids and use of i.v. betamimetic drugs require continuous i.v. insulin delivery. The continuation of intensive insulin management in post-partum is encouraged.
Diabetes Metab 2001 Sep
PMID:[Insulin therapy in type 1 diabetes for and during pregnancy: by which means and for which objectives?]. 1178 39

My brief is to discuss maternal diabetes and its implications for birth defects. The perinatal mortality in Britain has fallen in the last 70 years from 60 per 1000 live births to less than 10. For the baby of the diabetic mother there has been a more dramatic decrease from 249 per thousand live births reported by Peel and Oakley in 1949 to approximately 30 in the Swedish cohort in 1993. However even in countries such as Sweden with one of the lowest figures there is still a three fold higher perinatal mortality for the baby of the diabetic mother compared with the background population. There has been a much less dramatic decrease in the incidence of congenital malformations. Peel and Oakley reported an incidence of 6.9% in 1949, and Hanson from Sweden in 1993 reported only a marginally lower incidence of 6.1%. Recent observations indicate that gestational diabetes (GDM) may be associated with increased incidence of fetal malformation and perinatal mortality. The most frequent and significant morbidity is fetal macrosomia, which in turn is associated with increased risk of birth injuries and asphyxia, (Persson and Hanson. 1998). Detection and definition of congenital malformation vary but in spite of this and the much better maternal diabetic control, congenital malformation today forms a major cause of the perinatal morbidity and mortality.
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PMID:Maternal diabetes and its cell membrane abnormalities as they affect the foetus: implications for the mother and birth defects. 1200 91

In this study we report antepartum and obstetric findings in cases of persistent hyperinsulinemic hypoglycemia of infancy (PHHI). The study is retrospective and covers the years 1983 to 1994, when there were 9 infants treated for PHHI in the region of the University Hospital of Kuopio. One of the mothers had gestational diabetes mellitus and one had insulin-dependent diabetes mellitus (IDDM). There were signs of fetal distress in cardiotocography (CTG) in 3 of 9 cases prenatally and in 3 of 9 cases intrapartum (33%). There were 5 premature deliveries (56%) and 5 cesarean sections (56%) in this series. Five neonates (56%) were macrosomic and one delivery was complicated by shoulder dystocia. Three neonates (33%) had a 1-minute Apgar score of <6, but there were no cases at 5 minutes. In cases of fetal macrosomia without a maternal diabetic problem amniocentesis may be carried out after 34 weeks of gestation to assay amniotic fluid insulin, C-peptide and erythropoietin to reveal rare cases of PHHI where there may be problems of fetal hypoxemia similar to those in diabetic pregnancies.
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PMID:Antepartum findings and obstetric aspects in pregnancies followed by neonatal persistent hyperinsulinemic hypoglycemia. 1201 92

Fetal macrosomia may occur even in adequately controlled diabetic mothers. This may reflect the problem of using maternal glycemia as an indicator of fetal glycemia, because the placenta interposed between both compartments has its own glucose metabolism. Here, we propose a model by which the placenta protects the fetus at moderate levels of maternal hyperglycemia. One characteristic feature of the human placenta in diabetes is the increased deposition of glycogen. Neither hyperglycemia nor hyperinsulinemia increase the glycogen content in the trophoblast. Since the glycogen increments in diabetes are predominantly located around fetoplacental vessels, it is tempting to assume a fetal origin of glucose making up the glycogen deposits. In fact, glucose can be transported back from the fetus into the placenta and this reflux is increased in diabetes. Therefore, in conditions of fetal glucose levels exceeding the demand for sustaining fetal growth and metabolism, glucose can be stored in the liver and other fetal tissues. Once these stores are saturated, glucose is extracted from the fetal circulation by the glucose transporters GLUT1 and GLUT3 on cells surrounding the fetoplacental vasculature and stored therein, again in the form of glycogen. These processes might be under the control of fetal insulin, because insulin injected into the fetal circulation increases placental glycogen stores. Fetal macrosomia would then occur only when fetal hyperglycemia exceeds the placental capacity to store excess fetal glucose. Thus, the placental failure to protect the fetus would cause the 'unexplained' phenotypic changes occasionally found in fetuses born to well-controlled diabetic women.
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PMID:Is fetal macrosomia in adequately controlled diabetic women the result of a placental defect?--a hypothesis. 1237 81

Shoulder dystocia is an unpredictable obstetric complication with the incidence of 0.15% to 2%. An increase in the incidence of shoulder dystocia has been recorded over the last 20 years, probably just because it has now been regularly registered at maternity wards as an obstetric complication. The risk factors for shoulder dystocia include fetal macrosomia, fetal malformations and tumors, maternal adiposity, excessive weight gain during pregnancy, diabetes mellitus, pathologic pelvis, multiparity, short maternal stature, advanced maternal age, postterm pregnancy, so-called midforceps delivery or vacuum extraction, prolonged delivery stage II, oxytocin labor induction, premature fetal expression according to Kristeller, and previous shoulder dystocia in macrosomatic children. The sequels of shoulder dystocia and obstetric maneuvers for incarcerated shoulder release include clavicular fracture, brachial plexus lesions, sternocleidomastoid muscle distension with or without hematoma, diaphragmatic paralysis, Horner's syndrome, peripartal asphyxia and consequential cerebral lesions (cerebral palsy), and peripartal death. Maternal complications due to shoulder dystocia are postpartal hemorrhage, cervical and vaginal lacerations, frequent infections during the puerperium, symphysiolysis and rupture of the uterus, and secondary cesarean section with related complications due to unsuccessful obstetric procedures or as continuation of Zavanelli's maneuver. McRoberts' maneuver (or Gaskin maneuver) is recommended as the initial procedure for shoulder release in case of shoulder dystocia. If it fails, other obstetric procedures such as Resnik's suprapubic pressure and Woods' grip with posteriorly placed arm release should be used, always with gross lateral episiotomy. The performance of all these obstetric procedures requires skilfull and highly experienced obstetrician and obstetric team as a whole.
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PMID:Fetal shoulder dystocia. 1259 26

The concept of a metabolic disorder of carbohydrate tolerance that progresses with age is examined. It is considered that acute exacerbations may occur at the time of puberty or during pregnancy or the menopause, leading to the development of manifest clinical diabetes.Pregnancy offers a unique opportunity for early diagnosis of potential diabetes in the mother. Existing screening tests are not satisfactory or reliable in uncovering this inborn error of metabolism that may lead to stillbirth or a grossly overweight baby, the onset of clinical diabetes in the mother occurring only many years later.Evidence is presented concerning four conditions that may cause maternal and fetal hyperinsulinism (the primary cause of fetal macrosomia). Also reported is the finding that approximately 50% of apparently normal women over the age of 50 show impaired glucose tolerance.
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PMID:DIABETES AND THE GYNECOLOGIST. 1429 85

Fetal development is dependent on maternal supply of fuels and building blocks. Disturbed maternal metabolism or inappropriate maternal nutrition confronts the fetus with an unfavourable intra-uterine milieu. Structural and functional adaptations occur during development and maturation of organs. Consequences of these fetal alterations persist postnatally and may result in metabolic alterations throughout life. Gestational diabetes can occur in these offspring and transmit the effect to the next generation. These alterations in fetal development can be associated with fetal macrosomia (maternal diabetes) or fetal growth-restriction (maternal/fetal malnutrition). The relation between birth weight and later metabolic disease therefore is U-shaped. Adult metabolic condition is thus to a considerable extent programmed in utero, fetal and neonatal weight being symptoms of disturbed fetal development. This concept of intra-uterine programming of disease is illustrated with a review of epidemiological human studies and experimental animal studies.
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PMID:Intra-uterine transmission of disease. 1458 Mar 72

The prevalence of obstetric, perinatal and neonatal complications associated with fetal macrosomia at Holberton Hospital in Antigua and Barbuda was assessed by a retrospective, case-control study. All babies of birthweight (BW) greater than 4.5 kg born between July 1991 and January 1997 and all babies with BW greater than 4.0 kg born between July 1991 and January 1995, were included. Control babies, were selected from those born on the same day as the index case. Babies of BW > 4.0 kg and babies of BW > 4.5 kg were 5.7% and 1% of births respectively Records were complete for 157 large babies (40 with BW > 4.5 kg) and 157 control babies < 4.0 kg. Mothers of large babies were significantly older, more parous, more likely to have diabetes mellitus, hypertension, and deliver after 40 weeks gestation. At delivery, mothers of large babies were more likely to bleed. Large babies had lower one minute and five minute Apgar score, were more likely to be meconium stained, have respiratory distress, have birth trauma or dystocia and to be admitted to Special Care Nursery. There was no difference in Caesarean section rate, hospital days, neonatal jaundice or mortality. Babies with BW > 4.5 kg had mortality of 7.5% versus 1.8% for those < 4.5 kg. Fetal macrosomia remains a difficult obstetrical problem associated with significant maternal, perinatal and neonatal consequences. Morbidity and mortality are still significant in developed and developing countries alike.
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PMID:A case control study of the prevalence of perinatal complications associated with fetal macrosomia in Antigua and Barbuda. 1464 6

The present study was aimed to investigate pregnancy outcome among obese women and specifically the correlation between maternal obesity and incidence of caesarean section (CS) while controlling for the potential confounding effects of other variables associated with obesity. A population-based study was performed comparing all pregnancies of obese (maternal pre-pregnancy body mass index (BMI) of 30 kg/m2 or more) and non-obese patients, between the years 1988 and 2002. Patients with hypertensive disorders and diabetes mellitus as well as patients lacking prenatal care were excluded from the analysis. Stratified analyses, using the Mantel-Haenszel technique, and a multiple logistic regression model were performed to control for confounders. During the study period there were 126,080 deliveries meeting the inclusion criteria, of which 1769 (1.4%) occurred in obese patients. Using a multivariable analysis, the following conditions were significantly associated with maternal obesity: failure to progress during the first stage (odds ratio (OR) = 3.1; 95% confidence interval [CI] 2.5, 3.8; P < 0.001), fertility treatments (OR = 2.0; [95% CI 1.6, 2.5]; P < 0.001), previous CS (OR = 1.7; [95% CI 1.5, 1.9]; P < 0.001), malpresentations (OR = 1.4; [95% CI 1.2, 1.6]; P < 0.001), recurrent miscarriages (OR = 1.4; [95% CI 1.2, 1.7]; P < 0.001) and fetal macrosomia (OR = 1.4; [95% CI 1.2, 1.7]; P < 0.001). Higher rates of caesarean deliveries were found among obese parturients (27.8% vs. 10.8%; OR = 3.2; [95% CI 2.9, 3.5]; P < 0.001). When controlling for possible confounders, using the Mantel-Haenszel technique, the association between maternal obesity and CS remained significant. No significant differences were noted between the groups regarding perinatal complications such as perinatal mortality, congenital malformations, shoulder dystocia and low Apgar scores. In conclusion, a significant association was found between obesity and CS even after the exclusion of hypertensive disorders and diabetes mellitus. Importantly, obesity alone was not associated with adverse perinatal outcome. Obstetricians should be encouraged to allow obese patients not suffering from diabetes or hypertensive disorders an adequate trial of labour.
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PMID:Maternal obesity as an independent risk factor for caesarean delivery. 1513 Jan 59

Gestational diabetes mellitus has been associated with adverse maternal and infant outcomes, including preeclampsia and fetal macrosomia. Although cigarette smoking has been associated with increased insulin resistance, its effect on gestational diabetes mellitus risk is uncertain. The authors evaluated the effects of smoking on glucose tolerance in a cohort of pregnant women who participated in the Calcium for Preeclampsia Prevention trial, a randomized study of nulliparous women conducted in five US medical centers from 1992 to 1995. Results of screening and diagnostic testing for gestational diabetes mellitus were analyzed. For 3,774 of the 4,589 women enrolled, plasma glucose concentration 1 hour after a 50-g oral glucose challenge and complete information on pregnancy outcome were available; for 3,602 of the women, gestational diabetes mellitus status was known. Adjusted mean 1-hour plasma glucose concentration (mg/dl) was elevated in women who smoked at study enrollment (112.6, 95% confidence interval: 110.0, 115.3) compared with women who had never smoked (108.3, 95% confidence interval: 106.7, 109.8; p < 0.01). Women who smoked were at increased risk of gestational diabetes mellitus when criteria proposed by the National Diabetes Data Group were used (adjusted odds ratio = 1.9, 95% confidence interval: 1.0, 3.6). These findings support an association between smoking and gestational diabetes mellitus.
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PMID:Glucose tolerance and risk of gestational diabetes mellitus in nulliparous women who smoke during pregnancy. 1558 73


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