Tissue carnitine reserves of newborn infants

This study assessed the tissue reserves of carnitine at birth in a group of neonates (n = 22) of varying gestational age dying within 24 h of birth, prior to possible changes in carnitine status induced by postnatal intervention. Tissue carnitine concentration was highest in the muscle in each infant. The mean (+/- SD) muscle carnitine concentration of 8.4 +/- 3.6 nmol/mg noncollagen protein (NCP) in very immature infants (less than or equal to 1000 g birth weight) was significantly lower than the corresponding mean (+/- SD) values of 14.0 +/- 3.2 nmol/mg NCP in larger preterm infants (1001-2500 g; P less than 0.01) and 19.4 +/- 2.6 nmol/mg NCP in term infants (greater than or equal to 2501 g; P less than 0.001). Muscle carnitine concentration correlated positively with gestational age (r = 0.832; P less than 0.001) and with body dimensions. Liver and heart carnitine concentrations did not correlate significantly with gestation or body dimensions. The mean (+/- SD) liver carnitine concentration for all the neonates as a group was 4.1 +/- 1.5 nmol/mg NCP. The mean (+/- SD) heart carnitine concentration was 4.7 +/- 1.3 nmol/mg NCP. In comparison to adult controls, tissue carnitine concentrations were markedly lower in neonates, particularly in immature newborns. These data suggest that newborn infants, especially premature babies, are born with limited tissue reserves of carnitine and are therefore at an increased risk for developing carnitine deficiency and its adverse effects in the postnatal period, particularly if maintained on carnitine-free intravenous nutrition for prolonged periods of time.     

Higher serum retinol-binding protein concentration in Indonesian neonates in Surabaya than Japanese neonates in Kobe.

The concentrations of serum retinol-binding protein (RBP), prealbumin (PA) and vitamin A of Indonesian neonates were compared with those of Japanese neonates. The mean serum concentrations of both PA and vitamin A did not differ significantly in Indonesian and Japanese neonates. Indonesian neonates had significantly higher serum RBP (2.75 +/- 0.87 mg/dl, mean +/- SD) than Japanese neonates (1.65 +/- 0.55 mg/dl, p less than 0.01). The molar ratio of vitamin A:RBP in Indonesian infants was significantly lower than in Japanese infants (p less than 0.02), and this in turn is indicative of increased concentrations of retinol-free RBP in the plasma of Indonesian neonates. The results suggest that RBP metabolism in Indonesian neonates differs from that in Japanese neonates.     

Newborns Vitamin A in Relation to Sex and Birth Weight

Cord serum vitamin A values were determined in 256 male and 294 female neonates born in Tehran. The mean cord serum vitamin A values (micrograms/dl +/- SD) was 24.04 +/- 6.87 and ranged from 3.16 to 49.71 micrograms/dl. Males had significantly lower mean cord serum vitamin A values than females (P less than 0.001), and the prevalence of low serum vitamin A (below 20 micrograms/dl) was higher in male neonates than female ones (35 and 21 per cent, respectively). Serum retinol values increased gradually with birth weight. The mean serum vitamin A for premature neonates was significantly lower than term neonates. A significant r value for the linear correlation between cord serum retinol and parity was obtained for mothers aged more than 35 years.     

Serum vitamin A in premature and term neonates

Serum vitamin A was determined in premature and term neonates by a specific spectrofluorometric method. Premature neonates (N = 42; gestational age = 32 +/- 0.4 weeks) had a serum vitamin A level (14.9 +/- 0.98 microgram/dl) significantly lower (P less than 0.001) than that of term neonates (N = 51; 22.4 +/- 0.99 microgram/dl). The vitamin A mean serum values of infants of 36 weeks' gestational age were not statistically different from those of the term neonates. Linear regression analysis for serum vitamin A values vs gestational age showed no significant correlation. A linear correlation (P less than 0.05), however, was found between serum vitamin A and serum protein protein concentrations, perhaps indicative of a lower concentration of retinol-binding protein. Since vitamin A is involved in the promotion of mucous-secreting cells, the premature neonate may be at greater risk than the term infant for diseases involving the mucosal epithelium, including necrotizing enterocolitis.     

Weight gain: a response to transfusion in selected preterm infants

A group of low-birth-weight infants with daily weight gains that were below the expected mean for postnatal age were examined to determine the effects of RBC transfusion on their weight gain. The mean hemoglobin concentration (+/- SD) in 13 infants (birth weight less than 1,500 g) prior to transfusion was 8.5 +/- 1.6 g/dL and 11.4 +/- 2.1 g/dL after transfusion. When a comparison was made between the daily weight gain for the week prior to transfusion with the week following transfusion, the mean daily weight gain (+/- SD) increased from 20.8 +/- 4.6 g to 28.0 +/- 6.3 g. Among the six infants with pretransfusion hemogloblin concentrations of less than 7.5 g/dL, the increase in daily weight gain was greatest (a rise from 22.6 +/- 4.0 g to 34.1 +/- 4.9 g). Improvements in weight gain were associated with a decrease in metabolic rates as determined by declines in oxygen consumption.     

Increased parenteral amino acid administration to extremely low-birth-weight infants during early postnatal life

BACKGROUND: Early administration of parenteral amino acids to infants with extremely low birth weight (birth weight < or = 1,000 g) has been encouraged to foster growth. However, excessive intravenous intake of amino acids may cause metabolic acidosis and uremia in extremely low birth weight infants. The hypothesis for this study was that extremely low birth weight infants would tolerate slightly increased early postnatal parenteral amino acid administration and benefit. METHODS: The peak daily parenteral amino acid dosage was increased from 3 g/kg (standard group) to 4 g/kg (modified group). The corrected parenteral amino acid dosage was computed to account for enteral protein intake and keep the combined daily intravenous amino acid and enteral protein intake at or below 3 g . kg -1 . d -1 in the standard group and 4 g . kg -1 . d -1 in the modified group. The primary outcome measure was plasma bicarbonate concentration as an indicator of acid-base status. Data were collected for patient demographics, nutritional intake, serum bicarbonate and serum urea nitrogen concentrations, and outcome. RESULTS: The corrected parenteral amino acid intake of the modified group was 16% greater at postnatal week 1 (3.30 +/- 0.83 g . kg -1 . d -1; mean, +/-1 SD) and 18% greater (3.86 +/- 0.94 g . kg -1 . d -1 ) at postnatal week 2 than the parenteral amino acid intake of the standard group. In the modified group, the mean serum bicarbonate concentration was 19.1 +/- 1.8 mEq/dL at week 1 and 23.9 +/- 2.9 mEq/dL at week 2, with no difference between the groups. At week 1, serum urea nitrogen concentrations were the same in both groups. The mean serum urea nitrogen concentration of the modified group at postnatal week 2 (18.2 +/- 8.8 mg/dL) was unchanged from postnatal week 1, but was greater than that of the standard group at postnatal week 2. Weight gain was the same in both groups. Corrected parenteral amino acid intake at postnatal week 1 correlated directly with weight gain from birth to postnatal week 2 ( P < 0.03) in both groups. CONCLUSIONS: Infants with extremely low birth weight tolerated parenteral amino acid intake of approximately 4 g . kg -1 . d -1. Mild increases of mean serum urea nitrogen concentration and mean weight gain were associated with increased parenteral amino acid administration without significant acidosis.     

Diminished IgG, but not complement C3 or C4 or factor B, precedes nosocomial bacterial sepsis in very low birth weight neonates

The significance of low serum IgG and complement proteins in very low birth weight (VLBW; less than 1500 g) neonates is not known. Therefore serum IgG, C3, C4 and Factor B were quantitated weekly by rate nephelometry in 15 VLBW neonates who developed proven nosocomial bacterial or candidal sepsis (Group A) and 27 VLBW neonates who did not develop sepsis (Group B). In the first week of life the serum IgG of neonates in Group A was 295 +/- 33 mg/dl (mean +/- SEM) and in Group B it was 440 +/- 21 mg/dl (P less than 0.01). In the second week, the IgG of Group A was 270 +/- 32 mg/dl and that of Group B was 473 +/- 38 mg/dl (P less than 0.01). If the IgG was less than 350 mg/dl in the first week or less than 230 mg/dl in the second week, the relative risk of acquiring sepsis was greater than or equal to 5 (95% confidence interval in the first week, 1.7 to 11.2). The serum IgG was measured before the onset of sepsis in 14 of the 15 neonates in Group A. In the week before sepsis the IgG of the 14 neonates was less than 440 mg/dl (range, 45 to 433 mg/dl) in all cases, was below the mean IgG of Group B in 12 of 14 cases (P = 0.006 vs. Group B) and was greater than 2 SD below the mean IgG of Group B in 4 of 14 cases (P = 0.0003 vs. Group B).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cord blood and postnatal serum leptin and its relationship to steroid use and growth in sick preterm infants

OBJECTIVE: To study the effect of prenatal and postnatal glucocorticoids use on serum leptin and weight gain in sick preterm infants and its correlation with caloric intake. METHODS: Serum leptin was measured in 24 neonates at day 1 (cord), 14 and 28 by radioimmunoassay. Total caloric intake (enteral and parenteral) and weight were measured on days 14 and 28 of life. RESULTS: Mean birth weight and gestational age of study infants were 864 +/- 273 g (mean +/- SD) (range 520-1755 g), and 26.6 +/- 2.4 weeks (23-32 weeks) respectively. Cord blood leptin was greater in infants whose mothers received antenatal steroids (1.98 +/- 1.05 ng/ml vs 0.94 +/- 0.39 ng/ml, p=0.004). Serum leptin increased postnatally from 1.52 +/- 1.0 ng/ml at birth to 2.2 +/- 1.3 ng/ml on day 28 of life (p=0.03). Mean serum leptin had an inverse exponential relationship with postnatal weight gain by day 28 of life (R2=0.56). Total caloric intake on days 14 and 28 of life did not correlate with postnatal weight gain. CONCLUSIONS: Increased serum concentration of leptin following glucocorticoids may be associated with poor weight gain in sick preterm infants.     

Pharmacokinetics of intravenous clindamycin in newborn infants

We studied 12 newborn infants (gestational ages 26-39 wk [mean +/- SD, 30.6 +/- 4.7]; birth weight 640-2700 g, [mean, 1,322 +/- 688]; postnatal age 1-24 days [mean, 9.6 +/- 8.5]) who received clindamycin phosphate for suspected or proven necrotizing enterocolitis (ten patients) or suspected anaerobic septicemia (two patients) in doses of 3.2-11 mg/kg every six hours. Range of mean serum concentration of clindamycin at steady state was between 12.7 and 40 micrograms/ml (therapeutic range = 2-10 micrograms/ml). High concentrations could be attributed to elimination T1/2 (6.3 +/- 2.1 hr) 100% longer than in older children or adults. Clindamycin clearance (61.6 +/- 31.6 hr ml/kg/hr) was lower than in older children or adults. Because of the observed prolongation in T1/2 and correspondingly lower clearance, the IV dose of clindamycin in newborn infants should be reduced to 15-20 mg/kg/day given in four daily doses.     

The effect of glucocorticosteroids on serum, liver, and lung vitamin A and retinyl ester concentrations.

Vitamin A and its active metabolites are important factors in promoting normal respiratory epithelial differentiation and growth. Glucocorticoids, often used to treat chronic lung diseases in infancy and childhood, are known to increase serum retinol concentrations. To determine the effects of exogenous steroids on serum retinol and retinol-binding protein concentrations (as well as on liver and lung total vitamin A, retinol, and retinyl ester concentrations), 32 weanling Sprague-Dawley rats were divided into four equal experimental groups. Eight animals were vitamin A sufficient and received 7 days of intraperitoneal dexamethasone at 0.5 mg/kg/day (group SD), 8 were vitamin A sufficient and received placebo (group SP), 8 were made vitamin A deficient and subsequently received dexamethasone (group DD), and 8 were vitamin A deficient and received placebo (group DP). Dexamethasone increased serum retinol concentrations in the SD group (2.27 +/- 0.20 mumol/L) when compared with control (SP, 1.64 +/- 0.46 mumol/L, p less than 0.001) as well as with pretreatment baseline values (1.21 +/- 0.23 mumol/L, p less than 0.001). Lung total vitamin A, retinol, and individual retinyl esters were depleted by 56 +/- 19% in the SD group, whereas liver values were depleted by 36 +/- 23%. In the vitamin A-sufficient groups the relative percentages of four major retinyl esters (palmitate, stearate, oleate, and linoleate) did not change in either tissue after steroid exposure. The vitamin A-deficient groups had no detectable tissue vitamin A, and dexamethasone did not increase serum retinol concentrations in the DD group. Serum retinol-binding protein concentrations were significantly higher in both steroid-treated groups when compared with control.(ABSTRACT TRUNCATED AT 250 WORDS)     

Vitamin A status of neonates with bronchopulmonary dysplasia

We prospectively assessed and compared the vitamin A status of two groups of preterm neonates (less than 1500 g birth weight, less than 32 wk gestation), one who developed clinical and radiographic evidence of bronchopulmonary dysplasia (BPD) (n = 10), and the other (control) who developed no significant lung disease (n = 8). The infants with BPD in this study required prolonged mechanical ventilation and supplemental O2 therapy, and had a higher incidence of cardiorespiratory complications when compared to controls. Their mean plasma vitamin A concentrations were significantly lower than those of controls at four sampling times in the 1st postnatal month. In contrast to the controls, infants with BPD showed a substantial decline in their plasma vitamin A concentrations from the initial values, and a high percentage of individual values of plasma vitamin A concentration in these infants were less than 10 micrograms/dl during the 8-wk postnatal period of observation. Delayed establishment of gastrointestinal feeding and a lower vitamin A intake in these infants relative to controls may have accounted for this decline. Our data show that preterm neonates who develop BPD have suboptimal plasma vitamin A concentrations for extended periods of time postnatally. We speculate that the necrotizing bronchiolitis and squamous metaplasia of conducting airways associated with vitamin A deficiency could influence the orderly repair of lung injury in susceptible neonates who are mechanically ventilated and could contribute to the pathophysiology of BPD in these infants.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypouricemia in neonates with syndrome of inappropriate secretion of antidiuretic hormone

A prospective study of serum levels of uric acid in 23 hyponatremic neonates was performed. Infants on diuretic medications or with renal failure were excluded. The infants were separated into two groups: group I consisted of 11 neonates with clinical evidence of syndrome of inappropriate secretion of antidiuretic hormone (SIADH), (mean +/- SD serum sodium 127 +/- 1.36 mEq/liter). Group II included 12 infants with hyponatremia (mean serum sodium 128 +/- 1.10 mEq/liter) associated with decreased effective vascular volume manifest by a fractional sodium excretion less than 1%. The groups were similar for gestational and postnatal ages, birth weight, clinical conditions, and concurrent use of drugs. The serum urate concentration in neonates with SIADH was 2.46 +/- 0.54 mg/dl; serum urate concentration in group II infants was 8.49 +/- 2.45 mg/dL (p less than 0.001). Water restriction in the group I infants with SIADH resulted in a rise in mean serum urate concentration (p less than 0.001). Fractional excretion of urate was elevated during hyponatremia in the group I infants (to 78 +/- 0.13%) and fell to 51 +/- 0.08% after correction (p less than 0.001). In group I infants, a direct correlation was found between fractional excretion of urate and sodium (r = 0.7667, p less than 0.001). These results indicate that hypouricemia is common in infants with suspected SIADH and seems to be due to increased urate clearance secondary to volume expansion.     

Vitamin concentrations in very low birth weight infants given vitamins intravenously in a lipid emulsion: measurement of vitamins A, D, and E and riboflavin

Because total parenteral nutrition with vitamins added to the glucose-amino acid mixture is often associated with a reduction in blood levels of vitamin A (retinol) during the routine treatment of many very low birth weight (VLBW) infants (less than 1500 gm), and because retinol losses in the plastic delivery system can be prevented by adding the vitamins to an intravenous lipid emulsion, seven VLBW infants with a mean birth weight of 900 gm (range 450 to 1360 gm) were given 40% of a unit dose vial, per kilogram of body weight, of a multivitamin preparation (M.V.I. Pediatric) (280 micrograms retinol; 160 IU vitamin D; 2.8 mg tocopherol; 0.68 mg riboflavin) in a lipid emulsion, Intralipid. After treatment with the intralipid-vitamin mixture for 19 to 28 days, plasma vitamin A (retinol) concentrations increased significantly from 11.0 +/- 0.76 (mean +/- SEM) before intralipid to 19.2 +/- 0.97 micrograms/dl after the intralipid-vitamin mixture (p less than 0.01); 25-hydroxyvitamin D concentrations increased from an initial value of 12.6 +/- 2.6 to 20.2 +/- 1.9 mg/dl (p less than 0.01); alpha-tocopherol concentrations increased from an initial value of 0.31 +/- 0.06 to 2.44 +/- 0.13 mg/dl (p less than 0.01); and riboflavin levels increased from 64.1 +/- 7.8 ng/ml to concentrations between 20 and 100 times the initial level. Erythrocyte riboflavin levels increased from 71.8 +/- 14 initially to 166 +/- 41 ng/gm hemoglobin, and erythrocyte flavin-adenine dinucleotide levels increased similarly from 972 +/- 112 initially to 2005 +/- 294 ng/gm hemoglobin. These results show that the addition of M.V.I. Pediatric to Intralipid decreases the extensive in vivo loss of retinol and is associated with an increase in plasma retinol concentrations in VLBW infants. The daily doses of vitamins D (160 IU/kg) and E (2.8 mg/kg) appear sufficient, but the dose of vitamin A (280 micrograms/kg) is insufficient to raise blood levels of all infants into the normal range. The current dose of riboflavin is excessive and may be harmful.     

Vitamin A nutrition in the human foetus. A comparison of Sweden and Ethiopia

The accumulation of vitamin A during foetal development was investigated post mortem in foetuses and newborn infants of well-defined socio-economic groups of Swedish and Ethiopian women. The median vitamin A concentration in the liver was 37.0 micrograms/g in the Swedish foetuses (n = 39) and 9.1 micrograms/g in the Ethiopian ones (n = 49) (p less than 0.001). The liver vitamin A concentration in the Swedish foetuses increased exponentially during the second and third trimesters of pregnancy. This trend was not evident in the Ethiopian material. The mean serum concentration of retinol-binding protein was only slightly lower in the healthy Ethiopian newborns (18.6 mg/l; n = 70.) than in the Swedish newborns. This finding suggests that vitamin A is retained i the foetal circulation in preference to storage, much like the situation in a vitamin A deficiency state in the adult.     

Perinatal rat lung retinol (vitamin A) and retinyl palmitate

The potential role for retinol (vitamin A alcohol) in the differentiation of the developing lung prompted this study in the perinatal rat. High performance liquid chromatography was used to separate, detect, and quantitate retinol and retinyl palmitate in lipid extracts of tissue and serum. Fetal and maternal blood showed the presence of retinol, whereas no retinyl palmitate was detected. On the other hand, fetal and postnatal lungs contained retinyl palmitate as well as retinol. Considerable changes in the content of lung retinyl palmitate were found during lung development. Fetal lungs (17-21 days of gestation) contained 2.3 +/- 0.36 micrograms/g wet weight (mean +/- SD) of retinyl palmitate and 0.14 +/- 0.05 micrograms/g of retinol. Lungs of pups (1-10 days old) contained much less retinyl palmitate, 0.63 +/- 0.20 micrograms/g, whereas the amount of retinol was the same as in fetal lungs. The surprisingly high content of retinyl palmitate in fetal lung and its depletion after birth may be functionally related to retinol action in the developing lung.     

Ontogeny of thyrotropin releasing hormone and precursor peptide in the rat

Thyrotropin releasing hormone (TRH) and its precursor peptide pGlu-His-Pro-Gly (TRH-Gly) were measured in serum and in a variety of tissues of developing rats using specific RIA. TRH and TRH-Gly immunoreactivities were detected in most tissues. TRH concentrations were highest in pancreas, in which mean (+/- SEM) TRH concentrations were 138 +/- 20 pmol/g wet tissue 2 d before birth and 644 +/- 80 and 586 +/- 86 pmol/g, respectively, 2 and 5 d after birth. Hypothalamic TRH levels gradually increased from 4 d before birth (12 +/- 2.5 pmol/g) to 77 d of postnatal age (348 +/- 33 pmol/g). Hypothalamic concentrations were lower than levels in pancreas until 13 d of age. The mean serum TRH level at 2 d was 80 +/- 20 pmol/L and fell to the adult range by 21 d. TRH-Gly concentrations were highest in small gut (371 +/- 64 pmol/g) during the neonatal period, falling gradually to adult levels (33 +/- 4.8 pmol/g) by 35 d. Mean hypothalamic TRH-Gly concentrations increased to a peak of 62 +/- 4.5 pmol/g at 13 d, falling thereafter. High TRH-Gly concentrations (greater than 100 pmol/g) also were observed in pancreas (at d 2), kidney, and pituitary gland (at d 21). Serum TRH-Gly concentrations were highest (mean 417 +/- 26 pmol/L) on the 2nd postnatal day and gradually decreased to the adult level by 35 d. Changes in the TRH-Gly/TRH ratio were inversely correlated with tissue TRH concentrations in hypothalamus, pancreas, and liver.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical trial of vitamin A supplementation in infants susceptible to bronchopulmonary dysplasia

We conducted a randomized, double-blind, controlled trial to determine whether vitamin A supplementation from early postnatal life could reduce the morbidity associated with bronchopulmonary dysplasia in very low birth weight (VLBW) neonates. Forty VLBW neonates (700 to 1300 g birth weight, 26 to 30 weeks gestational age), who were oxygen dependent and required mechanical ventilation for at least 72 hours after birth, were given by the intramuscular route either supplemental vitamin A (retinyl palmitate 2000 IU) or 0.9% saline solution on postnatal day 4 and every other day thereafter for a total of 14 injections over 28 days. The study groups were comparable in gestational maturity, clinical characteristics, initial lung disease, and vitamin A status at entry into the trial. Vitamin A administration resulted in significantly higher mean plasma concentrations of vitamin A and retinol-binding protein in treated infants compared with controls. Bronchopulmonary dysplasia was diagnosed in nine of 20 infants given vitamin A supplement and in 17 of 20 control infants (P less than 0.008). Four of 19 infants in the vitamin A group and 11 of 20 in the control group required mechanical ventilation on study day 28 (P less than 0.029). The need for supplemental oxygen, mechanical ventilation, and intensive care was reduced in infants given vitamin A supplement compared with controls. Airway infection and retinopathy of prematurity were less frequent in the vitamin A group. We conclude that vitamin A supplementation at the dosage used in this trial in VLBW neonates not only improves their vitamin A status but also appears to promote regenerative healing from lung injury, as evidenced by a decrease in the morbidity associated with bronchopulmonary dysplasia.     

Selenium and human lactation in Australia: milk and blood selenium levels in lactating women, and selenium intakes of their breast-fed infants

A series of 20 mother-infant pairs were studied in Brisbane, Australia, at 6-12 weeks postpartum. The mean selenium concentration in maternal blood was 101 (SD +/- 19) ng/g and in maternal serum 81(+/- 15) ng/g; serum values appeared low in comparison with those reported for lactating women from Japan and the USA, but similar to those from Finland and from a previous Australian study. Breast milk selenium concentrations (11.9 +/- 3.5 ng/g) were also low by international standards, but not as low as in New Zealand or Scandinavia. There was no correlation between selenium concentrations in milk and blood (or serum). The infants' 24-h breast-milk intakes were 856 +/- 172 g, and their 24-h selenium intakes 10.7 +/- 4.1 micrograms (compared to the Australian RDI of 10 micrograms).     

Serum vitamin D metabolites in very low birth weight infants with and without rickets and fractures

Seventy-one very low birth weight (less than or equal to 1500 gm) infants were studied to determine the sequential changes in serum vitamin D metabolite concentrations between infants with and without radiographically documented rickets, fractures, or both (R/F). Usual intake of vitamin D included 20 IU/kg/day from parenteral nutrition or 400 IU/day supplementation with enteral feeding. Radiographs of both forearms and serum samples were obtained at 3, 6, 9, and 12 months. Twenty-two infants had R/F. At 3 months, significantly lower mean (+/- SEM) serum phosphorus levels (4.5 +/- 0.4 vs 6.1 +/- 0.2 mg/dl), higher 1,25-dihydroxyvitamin D (1,25-[OH]2D) concentrations (96 +/- 5 vs 77 +/- 4 pg/ml), and higher free 1,25-(OH)2D index (1,25-[OH]2D:vitamin D binding protein ratio; 5.2 +/- 0.3 x 10(5) vs 4.0 +/- 0.2 x 10(5] were found in the R/F group. These values returned to normal and were similar between groups on subsequent measurements. Serum calcium, magnesium, and 25-hydroxyvitamin D (25-OHD) concentrations were normal and similar between groups. In both groups, serum vitamin D binding concentrations increased initially but remained stable and normal beyond 6 months. We conclude that in very low birth weight infants with R/F, the vitamin D status (as indicated by serum 25-OHD concentrations) is normal, and that lowered serum phosphorus levels, higher serum 1,25-(OH)2D levels, and a higher free 1,25-(OH)2D index support the thesis that mineral deficiency (especially of phosphorus) may be important in the pathogenesis of R/F in small preterm infants.     

Plasma vitamin E concentrations of older infants fed cow's milk or infant formula.

Nutrition of older infants, though important for optimal brain development, is inadequately studied. The beverage choice markedly influences nutrient intake, but little is known regarding nutrition status of older infants, particularly for vitamin E. This study assessed vitamin E intakes and plasma tocopherol concentrations in two groups of healthy infants, 8 to 13 months of age, who had consumed either cow's milk (n = 45) or milk-based formula (n = 55) for a minimum of the 3 preceding months. Mean (+/- SEM) vitamin E intake was significantly lower (p < or = 0.001) by the infants who had consumed cow's milk (CMF) than by infants who had consumed formula (FF); 4.1 +/- 0.25 mg/day and 10.9 +/- 0.57 mg/day, respectively. Mean (+/- SEM) intake of linoleic plus linolenic acids was significantly lower (p < or = 0.005) by CMF infants (3.4 +/- 0.2 g) than by FF infants (9.9 +/- 1.0 g), although mean (+/- SEM) dietary vitamin E to polyunsaturated fat ratio (E/PUFA ratio) was the same in both FF and CMF infants (1.3 +/- 0.1). Plasma alpha-tocopherol concentration (mean +/- SD) was significantly lower (p < or = 0.005) in CMF than in FF infants (0.86 +/- 0.28 mg/dl vs. 1.14 +/- 0.42 mg/dl, respectively). Dietary vitamin E intakes were positively correlated (p < or = 0.05) with plasma alpha-tocopherol concentrations. No correlations were found between plasma alpha-tocopherol concentrations and total fat intake, dietary E/PUFA ratios, erythrocyte polyunsaturated fatty acids > or = C18:2, or number of hours postprandial that blood was drawn.(ABSTRACT TRUNCATED AT 250 WORDS)