Infants Of Insulin-dependent Mothers Research Articles

Parathyroid function in infants of diabetic mothers.

Serum parathyroid hormone and total and ionized Ca, Mg, and P levels were determined serially from birth to 96 hr of age in 28 infants of diabetic mothers (IDM, 15 Class A, 13 Class B, C, D) and their respective mothers at the time of delivery. In spite of marked decreases in concentrations of serum total and ionized Ca from birth to 24 to 48 hr, there was an insignificant increase in serum PTH values over this period in infants of insulin-dependent mothers. Infants of Class A diabetic mothers had an equivocal PTH response. Nineteen term control infants were similarly examined and had a significant increase in serum PTH postnatally. Relatively higher values of serum ionized Ca at birth in IDM were followed by greater decreases in ionized Ca from birth to 24-48 hr of age, and by decreased neonatal parathyroid function. The data support functional hypoparathyroidism as a basis for the hypocalcemia and hyperphosphatemia of IDM. It is speculated that increased concentrations of serum ionized Ca in utero and suppression of activity in the fetal parathyroid glands may be a cause for the functional hypoparathyroidism.

Observations of plasma osmotic pressure in premature infants

Immediately after delivery, frequent serial determinations of blood glucose in infants of diabetic mothers reveal a consistent and abnormal hypoglucosemia. In order to further characterize this phenomenon, fructose and combined glucosefructose tolerance tests were done on normal infants, infants of gestationally diabetic mothers, and infants of insulin-dependent mothers. All infants efficiently used and converted fructose to glucose as reflected by similar rates of fructose disappearance unaffected by exogenous insulin and by a rise in blood glucose concentration. Two hours after a combined glucose-fructose tolerance test, infants of diabetic mothers had a strikingly different and higher blood glucose concentration. Intravenous administration of fructose to mothers before delivery abolished the usual hypoglucosemia in normal infants and in infants of gestational diabetic mothers; in infants of insulin-dependent mothers, the hypoglucosemia was not abolished but the rate of glucose disappearance after delivery was slowed initially. Although the transplacental gradient of fructose was large (maternal > fetal), the amount transported to the baby was sufficient to alter glucose homeostasis. Fructose administered intravenously immediately after delivery shortened the duration and minimized the symptoms of hypoglycemia. Since fructose may not stimulate insulin release by the pancreas, and since gluconeogenesis from fructose is efficient in infants of diabetic mothers, fructose has important therapeutic advantages over glucose in these infants.