Echocardiographic measurements in infants of diabetic mothers and macrosomic infants of nondiabetic mothers

AIM: To compare echocardiographic findings of infants of diabetic mothers (IDMs), macrosomic infants of nondiabetic mothers and healthy full term appropriate-for-gestational-age (AGA) infants. METHODS: Included in this study were 83 infants, admitted to our Neonatology Unit. Thirty-three IDMs, including both macrosomic and nonmacrosomic, comprised Group A, 25 macrosomic infants of nondiabetic mothers comprised group B, and 25 healthy full term AGA infants comprised group C. Echocardiographic measurements were performed in the first three days after birth and compared by using one-way ANOVA, Post Hoc Tukey HSD and Student's t tests. RESULTS: The left ventricular end-systolic/left ventricular end-diastolic diameter ratio of group A was significantly smaller than that of group C (P<0.05). The interventricular septum/posterior wall thickness ratios of groups A and B were greater than those of group C (P<0.05). The left ventricular mass index of group A was greater than those of groups B and C (P<0.05). The shortening fraction and ejection fraction of group A were increased in comparison to group C (P<0.05). When comparing the values of echocardiographic measurements of macrosomic IDMs (n=9) with nonmacrosomic ones (n=24), and infants of pregestational diabetic mothers (n=11) with those of gestational diabetes mothers (n=22), no statistical difference was found. CONCLUSION: The present study suggests that underlying mechanisms common to both macrosomic infants of nondiabetic mothers and IDMs lead to less cardiac alterations in the macrosomic infants of nondiabetic mothers than in IDMs.     

Hypertrophic cardiomyopathy in infants of diabetic mothers: an update

Infants of diabetic mothers (IDMs) are at known risk for developing a hypertrophic type of cardiomyopathy. The severity of IDM cardiomyopathy can vary from an incidental finding on echocardiography to an infant with severe symptoms of congestive heart failure. The purpose of this article is to review the pathophysiologic mechanisms involved in the development of cardiomyopathy in IDMs and to discuss the diagnostic tests utilized in making the diagnosis (especially echocardiography) and the potential mechanisms that may result in congestive heart failure. This report will conclude with a review of a 2 1/2 year prospective study of diabetic women who had carefully maintained diabetic control during pregnancy. Although the IDMs in this study continued to have mild evidence of generalized hypertrophy when compared with control newborn infants, none developed symptoms of congestive heart failure. These data support the contention that careful diabetic management in pregnancy reduces the severity of hypertrophic cardiomyopathy in IDMs.     

Umbilical cord androgens in infants of diabetic mothers

The aim was to measure umbilical cord testosterone and androstenedione and to explore possible relationships with fetal weight and insulin levels. Testosterone, androstenedione and insulin were measured at birth in venous umbilical blood in 12 infants of gestational diabetic mothers and in 12 control subjects. The mean concentrations of umbilical testosterone and androstenedione were not significantly different between the infants of the diabetic and control mothers. No significant correlation was found between maternal weight, fetal weight or insulin concentrations and androgen levels. Received: 15 October 1996 / Accepted: 31 October 1996     

Neonatal polycythemia in infants of insulin-dependent diabetic mothers

The rate of neonatal polycythemia was determined prospectively in 34 infants of diabetic mothers pair-matched to 34 infants of nondiabetic mothers (control group) for site of sampling, time of sampling, time of cord clamping, gestational age, mode of delivery, and one- and five-minute Apgar scores. Polycythemia (venous hematocrit greater than or equal to 65%) was present in 29.4% of infants of diabetic mothers and 5.9% of control subjects (P less than .03). Mean nucleated red blood cell counts were significantly higher in infants of diabetic mothers than in controls. Polycythemia did not correlate with higher maternal hemoglobin A1 concentration or with increased infant weight percentile, but did correlate with neonatal hypoglycemia. The authors speculate that increased erythropoiesis exists in infants of diabetic mothers and might be subsequent to fetal hypoxemia due to fetal hyperglycemia, hyperinsulinism, and hyperketonemia.     

Prothrombotic risk factors in infants of diabetic mothers.

BACKGROUND: Infants of diabetic mothers (IDMs) are at an increased risk for thromboembolic disease. The mechanism(s) to explain this association is unclear. We hypothesized that the pathophysiology of thrombosis in IDMs is multifactorial and likely involves interactions among genetic and acquired factors affecting the procoagulant, anticoagulant and fibrinolytic pathways. OBJECTIVE: To compare the prevalence of common prothrombotic risk factors in a cohort of IDMs to a matched control group. PATIENTS/METHODS: Full-term infants born to mothers with diet controlled (A1-IDM) (N=17), insulin requiring diabetes (ID-IDM) (N=20) and healthy term infants (controls) (N=20) matched for mode of delivery had cord blood collected at delivery. Samples were analyzed for the following: factor V Leiden (FVL), prothrombin 20210A (P20210A), methylenetetrahydrofolate reductase C677 T (MTHFR), Factor VIII (FVIII), Protein C (PC), Lipoprotein(a) (Lp(a)) and plasminogen activator inhibitor-1 (PAI-1). RESULTS: None of the infants had a clinically apparent thrombotic event. IDM mothers and their infants were clinically similar to controls except for a higher prevalence of hypoglycemia (30 vs 0%; p=0.005). There was no significant difference in the prevalence of the common genetic risk factors (FVL, P20210A, MTHFR) FVIII, or PAI-1 levels. Elevated Lp(a) levels were seen more frequently in IDMs than Controls (40 vs 20%) but this difference was not statistically significant. The PC activity (%) was significantly decreased in the IDM group compared to controls, 35+/-12 vs 44+/-9 (p<0.005). A1-IDM had lower PC activity compared to ID-IDM (p=0.05) and controls (p=0.001). CONCLUSIONS: PC deficiency is likely one mechanism to explain thrombosis in IDMs.     

Asymmetrical septal hypertrophy in newborn infants of diabetic mothers

The objective of this paper is to determine the frequency and outcome of asymmetrical septal hypertrophy (ASH) in large-for-gestational-age infants (LGA) born to diabetic (DM) and nondiabetic mothers (NDM), and to establish the relationship between ASH and maternal diabetes control. A comparative study was design to assess ASH in infants born to DM and NDM. The study was conducted in the Departments of Neonatology and Pediatric Cardiology of the "Hospital de Gineco-Pediatria 48", Instituto Mexicano del Seguro Social from January to December 1997. Eighty-five full-term infants of DM (group A) and 85 LGA infants of NDM (group B) were included. As a control group (group C), we studied 85 healthy, full-term infants. In all cases a Doppler echocardiogram was obtained in the first 48 h after birth, and for the ASH infants, at 2 and 4 months. Chest X ray, electrocardiogram, and laboratory tests were performed as complementary studies. ASH was present in 38.8% of LGA infants of DM and in 7.1% of NDM. The difference was significant (p < 0.01). Interventricular septum (IVS) and IVS/ posterior wall of left ventricle ratio were significantly different between groups A and B with C. There was no correlation between Hb A1 level and the presence of ASH in group A. ASH is a common finding in infants of DM. We could not find a relationship between the degree of metabolic control during pregnancy and the incidence and severity of ASH.     

Decreased bone mineral content in infants of diabetic mothers

The present study was conducted to test the hypothesis that infants of diabetic mothers (IDMs) have decreased bone mineral content at birth, and whether or not decreased infant bone mineral content in IDMs correlates with poor control of diabetes during pregnancy, maternal bone mineral content, and the development of neonatal hypocalcemia. Forty-five pregnant diabetic women and their infants were enrolled in a prospective trial. In addition, 55 normal newborn infants of nondiabetic mothers were used as controls. Bone mineral content was measured before delivery in all diabetic pregnant patients and at birth in all infants by photon absorptiometry. Bone mineral content was significantly decreased in infants of diabetic mothers compared with control infants and correlated inversely with mean first trimester maternal capillary blood glucose; it did not correlate with cord serum 1,25-dihydroxyvitamin D concentrations. By stepwise multiple regression analysis, in infants of diabetic mothers, bone mineral content correlated inversely with mean first trimester capillary blood glucose and maternal bone mineral content, but did not correlate with maternal blood glycosylated hemoglobin, infant gestational age, infant birthweight or weight percentile, or development of neonatal hypocalcemia.     

Anthropometric differences in macrosomic infants of diabetic and nondiabetic mothers

The objective was to investigate the hypothesis that anthropometric and body composition differences exist between macrosomic infants of diabetic and nondiabetic mothers. Sixteen infants of mothers with diabetes, along with 58 control infants, were studied within 24 hours of delivery. The following measurements were obtained: birthweight, birth length and extremity length; circumferences of the head, chest, shoulders, and extremities; and triceps, subscapular, flank, and thigh skinfolds. Estimation of fat mass and calculation of percent body fat was performed according to the Dauncey method. Macrosomic infants of diabetic mothers were characterized by larger shoulder and extremity circumferences, a decreased head-to-shoulder ratio, significantly higher body fat, and thicker upper extremity skinfolds compared with nondiabetic control infants of similar birthweight and birth length. Differences in body composition and weight distribution may explain the propensity for shoulder dystocia in the diabetic population.     

Umbilical artery intima-media and wall thickness in infants of diabetic mothers

Background: Large for gestational age (LAG) neonates who had been exposed to an intrauterine environment of either diabetes or maternal obesity are at increased risk of developing the metabolic syndrome. This can be explained by exposure to high glucose and insulin levels in utero which alter fetal adaptation and programming. Objectives: The aim of the study was to evaluate the onset of preclinical atherosclerosis in utero. Methods: We measured umbilical artery wall thickness (ruWT) in the third trimester by obstetric ultrasound and umbilical artery intima-media thickness (uIMT) in pathologic specimens of umbilical cords obtained shortly after delivery and investigated the relation between these measurements and serum insulin level and C-peptide level in cord blood and assessed insulin resistance with the homeostasis model assessment of insulin resistance (HOMA-IR) in infants of diabetic mothers (IDMs), i.e. the study group, which was divided into a large for gestational age group (LGA)-IDM group and an appropriate for gestational age group (AGA)-IDM group and compared with a control group. Results: The LGA-IDM group had significantly higher insulin (p < 0.001), C-peptide (p = 0.018) and HOMA-IR levels (p < 0.001) compared with the AGA-IDM and control groups. The LGA-IDM group had significantly larger ruWT (p = 0.013) and uIMT (p < 0.001) compared with the AGA-IDM and the control groups. The LGA-IDM group had increased uIMT and ruWT that correlated with the severity of maternal hyperglycemia. Conclusions: Measurement of ruWT in the third trimester is feasible, reproducible and strongly correlated with pathological serum insulin, C-peptide in cord blood and HOMA-IR levels.     

Early neonatal predictors of neonatal hypocalcemia in infants of diabetic mothers: an epidemiologic study

Prematurity, neonatal asphyxia, hypomagnesemia, and advanced maternal diabetes are traditional risk factors for hypocalcemia in infants of diabetic mothers (IDMs). The aim of this study was to determine the relative contribution of these factors separately and combined in a cohort of diabetic pregnancies managed prospectively in the recent 9 years and to find accurate predictors of neonatal hypocalcemia in infants of diabetic mothers. We hypothesized that these factors plus low cord blood calcium (Ca) concentration allow prediction of IDMs who develop neonatal hypocalcemia. We studied 186 IDMs (White class B-RT); gestational age (GA, weeks) was by last menstrual period, confirmed +/- 2 weeks by Ballard score. The goals of glycemic control were: preprandial blood glucose less than 100 mg/dl and 90-minute postprandial blood glucose less than 140 mg/dl. Apgar scores, and cord, 24-, 48- and 72-hour serum calcium (Ca) (mg/dl) and magnesium (Mg; mg/dl) were determined. In univariate analysis, lowest serum Ca correlated with cord blood Ca (r = 0.48, p less than 0.001), GA (r = 0.37, p less than 0.001), and 1-minute Apgar score (r = 0.18, p = 0.09), but did not correlate with cord Mg or with advanced White class. In multiple regression, cord Ca and GA were dominant effects and other variables became insignificant. Lowest Ca (mg/dl) was predicted as follows: lowest Ca = 34.05 - 3.22 (Ca cord) - 0.84 (GA) + 0.10 (GA) (Ca cord). This equation predicts neonatal hypocalcemia (lowest Ca less than 8 mg/dl) with a sensitivity of 72% and a specificity of 75%. Thus, GA and cord Ca allow determination of IDMs at risk for neonatal hypocalcemia.     

Nutritional perturbations in infants of diabetic mothers and intrauterine growth retardation.

The fetal nutritional milieu may have important regulatory influences on fetal growth and maturation. Fetuses of diabetics exposed to excessive glucose in late gestation show delayed maturation, whereas, fetuses subjected to nutrient deprivation resulting from decreased uterine blood flow exhibit restricted growth and accelerated maturation. Under conditions of nutrient deficiency, restricted growth and accelerated maturation may be important adaptations mediated through hormonal and growth factor signalling.