Accuracy of transcranial ultrasound in the detection of mild white matter lesions in newborns.

Cranial Ultrasound (cUS) may not be sensitive enough to detect subtle white matter (WM) injuries. Our study compared serial cUS with MRI at term equivalent age (TEA) to determine if it is possible to identify an ultrasound representation of subtle diffuse WM injuries such as punctate lesions (PWMLs) and diffuse excessive high signal intensity (DEHSI). Fifty-six very preterm infants were scanned sequentially from birth to TEA, an MRI was performed at TEA. Each echodensity found on cUS was classified as absent, transient (≤7 days), or prolonged (>7 days). A transient periventricular echodensity was detected in seven infants (12.5%), and a prolonged echodensity in 15 (26.8%). MRI examinations were performed in all 56 infants. No altered signal intensity was found in 18 infants (32.1%). DEHSI was detected in 14 infants (25%), and PWMLs were detected in eight babies (14.3%). Both abnormalities were found in 16 infants (28.6%). The positive predictive values of the prolonged echodensity for DEHSI and PWMLs were 86.7% and 46.7% respectively. However, a significant statistical correspondence (p=0.002, Odds Ratio 11.9) was found comparing DEHSI with cUS abnormal echodensities. Serial cUS during the neonatal period in preterm infants is essential and cannot be replaced with MRI at TEA. MRI seems to be more reliable in detecting mild or moderate WM abnormalities. However, serial cUS performed by an experienced neonatologist can provide valuable information on early WM changes such as prolonged echodensities that could potentially lead to a diffuse injury.

Developmental aspects of the offspring of diabetic mothers.

This study examined the effect of some maternal factors on the pre- and postnatal development of a group of infants of diabetic mothers (IDMs). Body weight, length and head circumference were measured at birth and at 3, 6, 12, 24, 36, and 48 months of age. No differences were observed in pre- and postterm growth when IDMs were subdivided according to the maternal White class or pregnancy complications. Poor metabolic control during pregnancy resulted in excessive and abnormal prenatal growth; the fetal weight increased progressively during the last 3 weeks of gestation, while little or no increase was observed in fetal length or the head circumference which at 37 weeks both were already higher than (length) or similar to (head circumference) those of normal babies at term. Children of mothers with poor metabolic control during pregnancy showed significantly higher values for weight and weight/height ratio in infancy than children of well controlled mothers. Female offspring contributed most to the differences.

Endocrine pancreatic function in insulin-dependent diabetic pregnant women.

In order to better understand the role of A- and B-cell function in diabetic pregnancy, we studied four groups of pregnant women at week 34-36 of gestation. Seventeen were healthy controls (C), 24 had gestational diabetes (GD), 16 had type 2 diabetes (NIDD) and 37 had type 1 diabetes (IDD). At times -20, 0, 20, 30, 45, 60, 90 and 120 min from the beginning of a 30 min infusion of 30 g of arginine intravenously, plasma glucose, glucagon (IRG) and C-peptide (CPR) were measured. Plasma glucose was higher in diabetic than in control subjects. IRG values were also higher in the GD and the NIDD women. CPR values were similar to, or slightly higher than control values in the GD and the NIDD and were much lower in the IDD women. All three variables increased during the arginine infusion in all groups, with the exception that CPR remained unchanged in the IDD. The CPR/IRG molar ratio was similar in control, GD and NIDD women; in the IDD, it was much smaller than in the other groups and was not affected by arginine. In all the diabetic patients, IRG was negatively correlated with the maternal weight gain and in the IDD IRG was positively correlated with the increase in the insulin need and with the CPR levels. In conclusion diabetes appeared to enhance the A-cell function also in pregnancy, possibly impairing the 'facilitated anabolism' and stressing the 'accelerated starvation' which are typical of normal pregnancy. Glucagon was confirmed as one possible determinant of the insulin resistance seen in diabetic pregnancy.