Macrosomic Infants Of Nondiabetic Mothers Research Articles

Troponin T and NT ProBNP Levels in Gestational, Type 1 and Type 2 Diabetic Mothers and Macrosomic Infants.

This study compares NT proBNP and troponin T levels in umbilical cord arterial blood and postnatal echocardiographic findings for infants of gestational and pregestational diabetic mothers and macrosomic infants. Twenty-seven infants of pregestational diabetic mothers, 61 infants of gestational diabetic mothers and 37 macrosomic infants of nondiabetic mothers were prospectively enrolled in this study along with a control group of 58 healthy infants of mothers without any pregestational or gestational disorders as the control group. All enrollees were born after 34 weeks of gestation. For this study, umbilical cord blood was drawn during delivery to determine NT proBNP and troponin T levels. Echocardiography was performed 24-72 h after the delivery. Umbilical cord troponin T and NT proBNP levels were found to be higher in the diabetic and macrosomic groups than in the control group (all of them p < 0.001). NT proBNP levels were positively correlated with interventricular septum thickness in the pregestational and gestational infants of diabetic mothers groups (r = 0.564 and r = 0.560, respectively, p < 0.01). Both pregestational and gestational diabetic mothers were divided into two groups according to HbA1c levels in the third trimester as good (<6.1 %) and suboptimal (>6.1 %) metabolic control. In the good and suboptimal metabolic control diabetic groups, NT proBNP levels were also positively correlated with interventricular septum thickness (r = 0.536 and r = 0.576, respectively, p < 0.01). In the suboptimal metabolic control diabetic group, NT proBNP was only found to be positively correlated with the left ventricular mass index (r = 0.586, p < 0.01). While there was no correlation in the myocardial performance index between infants of diabetic mothers and the control group, the myocardial performance index of macrosomic infants was lower than that of the control group (p = 0.017). Cardiac biomarkers (NT proBNP and troponin T) were elevated in infants of diabetic mothers and macrosomic infants. While there was a positive correlation between NT proBNP levels and cardiac structure in infants of pregestational and gestational diabetic mothers, there was no relationship between NT proBNP levels and cardiac function.

Echocardiographic study of infants of diabetic mothers versus macrosomic infants of non-diabetic mothers - an Egyptian experience

Echocardiographic study of infants of diabetic mothers versus macrosomic infants of non-diabetic mothers - an Egyptian experience

Echocardiographic study of infants of diabetic mothers versus macrosomic infants of non-diabetic mothers - an Egyptian experience

Echocardiographic study of infants of diabetic mothers versus macrosomic infants of non-diabetic mothers - an Egyptian experience

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

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. 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. 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. 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.

Postpartum maternal levels of hemoglobin A1c and cord C-peptide in macrosomic infants of non-diabetic mothers

Postpartum maternal levels of hemoglobin A1c and cord C-peptide in macrosomic infants of non-diabetic mothers

Postpartum maternal levels of hemoglobin A1c and cord C-peptide in macrosomic infants of non-diabetic mothers

Objective: This study was designed to test the hypothesis that macrosomia in infants born to non-diabetic mothers is associated with an increased incidence of hyperinsulinemia and normal maternalglucose regulation in late pregnancy.Methods: Twenty mothers and their macrosomic infants were chosen as the study group, and 20 mothers with their appropriate-for-gestational-age infants werechosen as the control group.Results: No difference in postpartum mean hemoglobin Alc levels was observed between the mothers of macrosomic infants and those of control infants. Cordplasma C-peptide levels were significantly higher in macrosomic than in control infants.Conclusions: This study revealed that macrosomic infants of non-diabetic mothers were significantly more likely to have hyperinsulinemiathan were normal-sized infants, and this hyperinsulinemia was not caused by dysregulation in glucose metabolism.

Beta-cell hyperplasia in macrosomic infants and fetuses of nondiabetic mothers.

The objective of this study was to test the hypothesis that macrosomic infants of nondiabetic mothers have beta-cell hyperplasia in their pancreases. Pancreatic tissues were examined from 10 macrosomic fetuses and liveborn infants and from 10 comparison cases matched for gestational age and gender. None of the mothers had a history of diabetes and all had normal glucose screening during pregnancy. Tissues were stained with hematoxylin and eosin and a monoclonal antibody against beta cells and were analyzed using an image analysis program to evaluate the size and surface area of beta-cell clusters. Brain/liver weight ratios were calculated and compared. The total surface area and cluster size of beta cells in the pancreases of macrosomic subjects were significantly larger than in the comparison pancreases. The study subjects lacked macroscopic and histopathologic findings expected in infants of diabetic mothers. We conclude that some macrosomic fetuses and infants of nondiabetic mothers manifest beta-cell hyperplasia. This corresponds to the higher insulin levels in macrosomic infants of nondiabetic mothers described in previous clinical studies. In macrosomic fetuses the stimulus for beta-cell hyperplasia may not involve aberrant maternal glucose levels.

Beta-cell hyperplasia in macrosomic infants and fetuses of nondiabetic mothers.

The objective of this study was to test the hypothesis that macrosomic infants of nondiabetic mothers have beta-cell hyperplasia in their pancreases. Pancreatic tissues were examined from 10 macrosomic fetuses and liveborn infants and from 10 comparison cases matched for gestational age and gender. None of the mothers had a history of diabetes and all had normal glucose screening during pregnancy. Tissues were stained with hematoxylin and eosin and a monoclonal antibody against beta cells and were analyzed using an image analysis program to evaluate the size and surface area of beta-cell clusters. Brain/liver weight ratios were calculated and compared. The total surface area and cluster size of beta cells in the pancreases of macrosomic subjects were significantly larger than in the comparison pancreases. The study subjects lacked macroscopic and histopathologic findings expected in infants of diabetic mothers. We conclude that some macrosomic fetuses and infants of nondiabetic mothers manifest beta-cell hyperplasia. This corresponds to the higher insulin levels in macrosomic infants of nondiabetic mothers described in previous clinical studies. In macrosomic fetuses the stimulus for beta-cell hyperplasia may not involve aberrant maternal glucose levels.

Macrosomic infants of nondiabetic mothers and elevated C-peptide levels in cord blood

C-peptide concentrations in the cord blood of 29 macrosomic neonates born of nondiabetic mothers were higher than in 23 control infants whose birth weight was appropriate for gestational age, and there was a significant direct correlation between birth weight and C-peptide concentration. Six of the macrosomic infants studied (20%) had hypoglycemia in the first 24 hours of life, compared with none of the infants born with appropriate weight. We conclude that chronic fetal hyperinsulinemia may be one of the causes of macrosomia and neonatal hypoglycemia in infants of nondiabetic mothers. (J P EDIATR 1995;127:481-4)

Hyperinsulinemia in macrosomic infants of nondiabetic mothers.

We tested the hypothesis that macrosomic infants of nondiabetic mothers are more likely to have hyperinsulinemia and increased subcutaneous fat. Plasma insulin concentrations were measured in cord blood from 50 macrosomic infants and 32 normal-sized (control), term infants. All mothers had had a normal 50-g 1-h GCT. Skin-fold measurements of the triceps and subscapular area were done on 44 macrosomic infants with a Halpern caliper. No difference was observed in GCT between mothers of macrosomic (5.8 +/- 1.0 mM) and normal (5.7 mM) infants. The insulin level in macrosomic infants (18.75 +/- 19.08 microU/ml) was significantly higher than in control infants (8.67 +/- 6.64 microU/ml). Macrosomia was a predictor of hyperinsulinemia and vice versa (R2 = 0.26). Maternal height, prepregnancy weight, and weight gain were predictors for macrosomia (R2 = 0.26). No differences were noted in anthropometric measurements between hyperinsulinemic and normoinsulinemic infants. A subset of macrosomic infants have hyperinsulinemia. Maternal anthropometric factors as well as hyperinsulinemia are correlated with macrosomia. The macrosomia may be causally related to the high insulin levels.

Fingernail nitrogen content in infants of diabetic mothers and in macrosomic neonates.

Fingernail nitrogen content (FNC) was determined on nail trimmings obtained within 24 h of birth from 21 infants of diabetic mothers and 82 infants of nondiabetic mothers. Macrosomic infants of nondiabetic mothers had higher mean FNC than their normally grown peers. Both normally grown and macrosomic infants of diabetic mothers had higher mean FNC than normally grown infants of diabetic mothers. These data suggest that fetal macrosomia and maternal diabetes may independently increase the rate of nitrogen accretion in fingernails.