Selenate fortification of infant formulas improves the selenium status of preterm infants.

The purpose of this study was to determine whether selenate fortification of infant formula would improve the selenium status of relatively well, growing, preterm infants during the first 12 wk of enteral feeding. A high-selenium group (n = 7, mean body weight = 1312 g) received selenate-fortified preterm and full-term infant formulas containing 0.36 and 0.22 mumol Se/L, respectively, and a low-selenium group (n = 10, mean body weight = 1262 g) received non-selenium-fortified preterm and full-term infant formulas containing 0.12 and 0.11 mumol Se/L, respectively. There were no significant differences in growth between the two groups throughout the study. The high-selenium group had significantly greater mean selenium intakes than did the low-selenium group from weeks 2 to 12. Plasma selenium concentrations decreased over the study period in the low-selenium group. Plasma selenium-dependent glutathione peroxidase activity was greater in the high-selenium group at week 12 only. Red blood cell selenium concentrations decreased over time in both groups and were significantly greater in the high-selenium group at weeks 4, 8, and 12. Plasma selenium concentrations were significantly correlated with plasma glutathione peroxidase activity for all infants on study day 1 and at weeks 4 and 12. Selenium intake of all infants was significantly correlated with plasma glutathione peroxidase activity at 12 wk. Selenate fortification of infant formulas can improve the selenium status of preterm infants. Current selenium contents of infant formulas and recommendations for dietary intakes of selenium for some preterm infants may be inadequate.

The infant of the diabetic mother.

The history of the medical success in treatment of the pregnant diabetic woman and her infant in the twentieth century illustrates how the combined efforts of dedicated clinicians and researchers have resulted in dramatic improvements in outcome for this patient group. This article discusses fetal growth, metabolic complications of the infant of the diabetic mother, risk of respiratory distress syndrome, hypertrophic cardiomyopathy, and congenital anomalies.

Glucose metabolism in the infant weighing less than 1100 grams.

We studied the rate of endogenous glucose production and disappearance in a group of 10 clinically stable < 1100 gm infants in the first week of life, using stable-isotope (6,6-2H-glucose) dilution analysis for a 2-hour study period. Plasma glucose and insulin concentrations at 2 hours were 5.4 +/- 2.5 mmol/L (97 +/- 15 mg/dl) and 71.4 +/- 2.9 pmol/L, respectively, and did not change during the study period. The rate of glucose disappearance was 37 +/- 10 mumol/kg (6.77 +/- 0.55 mg/kg) per minute. The rate of endogenous glucose production was 12.3 +/- 11 mumol/kg (2.22 +/- 0.61 mg/kg) per minute. The exogenous glucose infusion rate was 25.2 +/- 8.4 mumol/kg (4.54 +/- 0.47 mg/kg) per minute. Endogenous glucose production was correlated with plasma glucose concentration (r = 0.76; p < 0.05) and the rate of glucose disappearance (r = 0.75; p < 0.05); plasma glucose concentration was correlated with the rate of disappearance (r = 0.87; p = < 0.01) and insulin concentrations (p < 0.05). We conclude that infants who weight < 1100 gm utilize three to four times more glucose per kilogram of body weight than adults, reflecting their higher ratio of brain to body weight. Endogenous glucose production provided only approximately one third of the glucose needed--a mandate for the exogenous infusion of glucose to prevent the development of hypoglycemia.

Effect of intrauterine exposure to cocaine on acetylcholinesterase in primary cultures of fetal mouse brain cells.

The effect of in utero exposure to cocaine on the developmental pattern of acetylcholinesterase (AChE), a major regulator of the central nervous system neurotransmitter acetylcholine, was studied in fetal brain cell cultures collected from mice on gestational day 15 after maternal exposure to cocaine from gestational days 6-14. A significant decrease in total and specific activity (expressed per mg of protein) of acetylcholinesterase was seen throughout the culture period in the cells grown from the cocaine-exposed animals as compared to controls (p less than .002). Similarly, the total protein content of the brain cells grown from the cocaine-exposed animals was significantly decreased as compared to controls (p less than .03). Utilizing AChE as a biochemical marker, these studies have shown that in utero exposure to cocaine has an adverse effect on the normal developmental pattern of the production of acetylcholinesterase in cholinergic neurons in the fetal mouse brain.

Zinc and copper balances in preterm infants.

Preterm infants are at risk for copper and zinc depletion if sufficient quantities of these nutrients are not provided in a bioavailable form in postnatal life. The purpose of this study was to determine whether the use of a whey-predominant, 50% medium chain triglyceride formula with relatively high concentrations of zinc and copper would promote the achievement of the in utero accretion rate for zinc and copper in the preterm infant. Two groups of five preterm infants were fed a diet containing 12.5 mg/L of zinc and either 0.9 mg/L or 2.1 mg/L of copper. Seventy-two-hour metabolic balance studies were performed at an average postconceptual age of 34 weeks and an average weight of 1,549 g. All infants were in positive zinc balance and nine of ten achieved the in utero accretion rate for zinc for a 34-week gestation fetus (greater than or equal to 0.432 mg/d). Three infants receiving the high copper formula and two receiving the lower copper formula were in positive copper balance. Two infants from each group achieved the in utero accretion rate for copper for a 34-week gestation fetus (0.088 mg/d). A formula that provides 12.5 mg/L of zinc permits positive zinc balance and zinc retention similar to in utero rates. A formula that provides as much as 2.1 mg/L of copper, however, may not always permit positive copper balance.

Serum zinc concentrations in growing premature infants.

Serial serum zinc concentrations were measured in 31 relatively well, growing premature infants during the first 26 weeks of life. Zinc concentrations declined progressively from 17.9 mumol (1.17 mg/l) at birth (normal adult value) to 8.9 mumol (0.58 mg/l) at 6 weeks of age despite a zinc intake of greater than 13.7 mumol (900 micrograms)/kg/day after the second week of life. The serum zinc increased after 16 weeks of age to 10.7 mumol/dl (0.7 mg/l). No infant demonstrated clinical signs of zinc deficiency. This data may serve as a reference against which serum zinc concentrations in other premature infants may be compared in order to help define the deficiency state.

Urinary copper losses in infants receiving free amino acid solutions.

Plasma amino acids and the 24-h urinary excretion of copper and amino acids were measured in 18 infants receiving 0.4 g N/kg/day as free amino acids as part of a total parenteral nutrition regimen. Urinary copper excretion correlated positively with total excretion of alpha-amino nitrogen, in general, and the excretion of glycine, methionine, histidine, and lysine, in particular. Infants who received FreAmine II as compared to FreAmine III generally had increased plasma concentrations of glycine and methionine and increased urinary excretion of total alpha-amino nitrogen, glycine, methionine, and of copper. Chronic losses of copper in the urine of infants receiving free amino acid solutions may contribute to copper depletion and the development of a copper deficiency syndrome.

Serum copper concentrations in sick and well preterm infants.

In order to define the range of serum copper concentrations in preterm infants and to determine the effect of growth upon these values, serial serum copper concentrations were measured in 26 preterm infants over their first six weeks of life. Fourteen healthy, growing preterm infants (Group I) had mean serum copper concentrations below 32 microgram/dl throughout the study. Clinical and hematologic signs of copper deficiency which responded promptly to the oral administration of copper sulfate were noted in five of these 14 infants. Twelve ill preterm infants (Group II-A), who received parenteral nutrition without supplemental copper and had slow rates of growth, had mean serum copper concentrations above 50 micrograms/dl after the first week of life. Seven surviving from Group II-A (Group II-B) had a decrease in mean serum copper concentrations to values similar to those in Group I after two weeks of oral feedings and resumption of normal growth. Our findings suggest that preterm infants who have normal growth while receiving oral feedings are at significant risk for developing copper deficiency.

Caffeine secretion into breast milk.

Serum and milk concentrations of caffeine were measured in 5 breast-feeding mothers after a standardised oral dose of caffeine. Peak concentrations of caffeine in serum and milk were attained 60 minutes later. Binding of caffeine by constituents of serum and breast milk was low (25 and 3.2% respectively). In breast milk, caffeine binding is associated with the cream layer, and correlates with the butter fat content. Caffeine does not diffuse freely into breast milk and concentrations in milk are lower than in maternal serum.

Clinical pharmacology of hexachlorophene in newborn infants.

Bathing with soap containing hexachlorophene was instituted during two major staphylococcal epidemics in a Neonatal Intensive Care Unit. Infants who weighed less than 1,200 gm, those with a postconceptional age of less than 35 weeks, and those with large areas of abraded skin were at highest risk to achieve elevated blood HCP concentrations. T 1/2 of HCP ranged from 6.1 to 44.2 hours and appeared to follow first order kinetics. Time of peak blood concentrations of HCP following a bath ranged from 6 to 10 hours. One infant with liver disease achieved a concentration of HCP of 4,350 ng/ml after seven baths and developed clinical symptoms consistent with HCP toxicity.

Micromethod for measuring hexachlorophene in whole blood by gas-liquid chromatography.

We describe a micromethod for measuring hexachlorophene by use of gas-liquid chromatography with a 63Ni electron capture detector. The procedure requires 100 micronl of blood for extractions of hexachlorophene, and dichlorophene is added as an internal standard. CV is 3.4% over the concentration range of 500 to 1300 microng of hexachlorophene per liter of whole blood. This procedure permits repeated measurements of hexachlorophene in newborns who are being washed with soap containing hexachlorophene.