Aluminium absorption in infancy

The use of aluminium-containing medications and aluminium contamination of infant formulae is common. We aimed to determine whether aluminium absorption occurs after antacid ingestion. Plasma and urinary levels of aluminium were measured before and after antacid therapy in seven infants whose mean gestational age was 36 ± 2 weeks and postnatal age 11 ± 5 days. Antacid therapy (400-800 μmol aluminium) was given with feeds for 2 days.
Plasma aluminium levels increased and reached toxic levels (0.64 ± 0.33 μmol/L vs 3.48 ± 2.86 μmol/L, P = 0.029). Urinary aluminium: creatinine ratio also increased. These results demonstrate that infants absorb aluminium from antacids and raise the concern of aluminium toxicity.     

Elevated plasma aluminum levels in normal infants receiving antacids containing aluminum

Aluminum toxicity is a documented cause of encephalopathy, anemia, and osteomalacia. Excretion is primarily renal; therefore, patients with renal insufficiency are at risk for aluminum accumulation and toxicity. This has been demonstrated in uremic children treated with aluminum-containing antacids. The purpose of this study was to determine whether plasma aluminum levels were elevated in infants with normal renal function during prolonged aluminum-containing antacid use. Ten study infants (mean age = 5.8 months), who had been receiving antacids for at least 1 week, were compared with 16 control infants (mean age = 9.8 months) not receiving antacids. The study patients consumed 123 +/- 16 mg/kg per day (mean +/- SEM) of elemental aluminum for an average of 4.7 weeks. Their plasma aluminum level (37.2 +/- 7.13 micrograms/L) was significantly greater than that of the control group (4.13 +/- 0.66 micrograms/L) (P less than .005). It is concluded that plasma aluminum levels may become elevated in infants with normal renal function who are consuming high doses of aluminum-containing antacids. The safety of antacids containing aluminum should not be assumed and they should be used judiciously in infants, with careful monitoring of the aluminum dose and plasma level.     

Prospective evaluation of aluminum loading from formula in infants with uremia

Assessment of potential aluminum loading from regular ingestion of a commercial infant formula (Similac PM 60/40), as the only milk substitute, was made in 14 infants aged 9.6 +/- 4.4 months who were also undergoing continuous cycling peritoneal dialysis. Tissue aluminum accumulation was assessed by serial measurements of plasma aluminum levels, from the increment in plasma aluminum after a standardized deferoxamine infusion, and from quantitative histomorphometry of bone and measurements of total bone aluminum content. Initial mean plasma aluminum levels were 0.61 +/- 0.32 mumol/L, (normal 0.30 +/- 0.04 mumol/L), and values were less than 0.92 mumol/L during the follow-up of 20 +/- 8 months. Plasma aluminum levels increased from 0.59 +/- 0.18 to 0.88 +/- 0.22 mumol/L after a single dose of deferoxamine. The histochemical stain for bone aluminum was negative for all patients, and the bone aluminum content was 0.27 +/- 0.22 mmol/kg dry weight (normal 0.08 +/- 0.04 mmol/kg dry weight). Thus the infant formula Similac PM 60/40 can be safely used in infants with chronic renal failure.     

Carnitine status and blood ammonium levels in low birth weight infants

Forty-three low birth weight infants appropriate for gestational age (AGA) were monitored to evaluate carnitine status in relation to blood ammonium levels. The infants were grouped into three depending on blood ammonium level on postnatal day 7: 62.9 +/- 3.8 mumol/L in group 1 (N = 13), 38.9 +/- 8.4 mumol/L in group 2 (N = 23), and 24.5 +/- 2.9 mumol/L in group 3 (N = 9). Plasma free carnitine levels decreased in all three groups (p less than 0.001) and plasma short chain acylcarnitine increased only in group 1 (p less than 0.002), compared to findings in normal infants. The blood ammonium level positively and negatively correlated to plasma short chain acylcarnitine (p less than 0.002) and plasma free carnitine levels (p less than 0.002), respectively. The reabsorption rate of free carnitine in renal tubules (RRFC) was decreased at rates of 37.5, 27.5, and 25% of infants in groups 1, 2, and 3, respectively. The acylcarnitine/free carnitine clearance ratio (RAFCC) was decreased in groups 1 (p less than 0.01) and 2 (p less than 0.05) compared with group 3. Thus, an accumulation of short chain acyl moieties and insufficiency in renal absorption of free carnitine are putative causes of lowered plasma free carnitine in infants with higher blood levels of ammonium. The possibility that the carnitine status regulates blood ammonium levels in low birth weight infants warrants continued investigation.     

Effects of two antibiotics on hepatic function in low birth weight infants: ampicillin vs. cefotaxime

In 21 low birth weight infants with two regimens of antibiotic therapy during the first 3 days of life possible hepatotoxic side effects were studied 8 days after the last administration of the tested drugs. Fourteen of the infants were treated with ampicillin/gentamicin and 7 received cefotaxime/gentamicin. The serum concentrations of total bile acids, the activities of transaminases in serum and the cumulative 15N excretion in urine after administration of 3 mg of 15N-labeled methacetin/kg of body weight were used as markers of hepatotoxic side effects. Neither the concentrations of total bile acids (22.6 +/- 12.1 and 19.4 +/- 10.8 mM, respectively) nor the activities of transaminases (alanine aminotransferase, 0.27 +/- 0.06 vs. 0.30 +/- 0.09 mumol/second/liter; aspartate aminotransferase, 0.46 +/- 0.11 vs. 0.49 +/- 0.10 mumol/second/liter) were different between the two groups. In contrast the cumulative 15N excretion in urine was significantly lower in the group treated with cefotaxime/gentamicin than in the group treated with ampicillin/gentamicin (17.2 +/- 6.4 vs. 33.0 +/- 5.1% of intake; P less than 0.01) and also lower than the reported age-related reference values. On the 28th day of life no differences could be found between the cumulative 15N excretion in the urine of the infants treated with cefotaxime/gentamicin and the reported age-related reference values of this test. The results indicate a limited capacity of the monooxygenase system of the liver of low birth weight infants during the first weeks of life and a specific reversible influence of cefotaxime on this hepatocellular system. Further investigations are required to evaluate the clinical relevance of this drug-specific inhibition of the hepatic monooxygenase pathway.     

Residential deleading: effects on the blood lead levels of lead-poisoned children

Acute elevations of venous blood lead levels (PbB) are periodically reported in children with chronic lead poisoning, during deleading of their houses. To evaluate this phenomenon 114 preschool children who entered the Massachusetts Childhood Lead Poisoning Prevention Program case management system during 1984 and 1985 were retrospectively studied. PbB increased from a mean (+/- SE) of 1.76 +/- 0.03 mumol/L (36.4 +/- 0.6 micrograms/dL) prior to deleading to 2.03 +/- 0.07 mumol/L (42.1 +/- 1.5 micrograms/dL) during deleading (P less than .001). Among 41 subjects for whom deleading was done by dry scraping and sanding, the mean mid-deleading PbB was higher than the pre-deleading PbB by 0.44 +/- 0.12 mumol/L (9.1 +/- 2.4 micrograms/dL). However, when deleading was done by covering or replacement of painted surfaces in the residences of 12 subjects, mid-deleading PbB decreased 0.11 +/- 0.12 mumol/L (2.25 +/- 2.4 micrograms/dL) (P less than .005). In a subset of 59 subjects who had no chelation therapy and were available for follow-up 250 +/- 14 days after completion of deleading, PbB had decreased from 1.72 +/- 0.04 mumol/L (35.7 +/- 0.9 micrograms/dL) to 1.24 +/- 0.04 mumol/L (25.5 +/- 0.9 micrograms/dL) (P less than .001). The long-term effect of deleading is a significant reduction in PbB. However, deleading resulted in a significant, albeit transient, increase in PbB.     

Optimization of gentamicin therapy in very low birth weight infants

In order to optimize gentamicin (G) therapy we studied G pharmacokinetics in 48 preterm infants (gest. age 31.6 +/- 3.4, range 25-37 wk; birth weight 1.5 +/- 0.5 kg, range 0.7-2.5 kg). They received IV G twice daily (5.2 +/- 0.6 mg/kg/day). After at least 2 days of treatment trough and peak levels were measured for 2 successive doses. Trough levels were significantly higher in infants less than 1 kg receiving 5 mg/kg/day than in other infants (1-2.5 kg) who received the same dose (3.1 +/- 1.0 vs. 2.3 +/- 0.5 micrograms/ml; p less than 0.01). Mean G t 1/2 was significantly longer in infants under 1 kg than in those weighing 1-2.5 kg (7.9 +/- 1.9 and 6.5 +/- 1.6 hr, respectively; p less than 0.01). These differences could be attributed to lower G clearance in infants less than 1 kg (31 +/- 6 vs. 39 +/- 8 ml/kg/hr; p less than 0.005). There was no difference in G distribution volume between less than 1 kg and 1-2.5 kg infants (0.35 +/- 0.07 and 0.38 +/- 0.13 L/kg, respectively). A correlation was found between clearance and t 1/2 for the total group (r = 0.57, p less than 0.01). No correlation was detected between BUN and clearance or between gestational age and clearance. Our data suggest that G dose in infants less than 1 kg should be reduced to 3.5-4 mg/kg/day in order to avoid excessive levels associated with nephrotoxicity.     

Low blood and plasma carnitine levels in children receiving long-term parenteral nutrition

Total and free carnitine and acylcarnitine concentrations were analyzed in whole blood and plasma in 12 children with a mean age of 68.4 +/- 42.9 months who had received carnitine-free total parenteral nutrition (TPN) for an average of 4 years. The purpose of the study was to see if the children had become carnitine deficient and, if so, whether this correlated with poor lipid clearance. Compared to controls, the TPN-dependent children had significantly decreased concentrations of total and free carnitine in blood (26.6 +/- 9.4 (SD) mumols/L vs. 43.3 +/- 9.1 mumols/L, p less than 0.001, and 17.1 +/- 7.7 mumols/L vs. 35.2 +/- 8.1 mumols/L, p less than 0.001, respectively). Similar results were found in plasma (total carnitine of 19.0 +/- 8.0 mumols/L vs. 41.9 +/- 5.2 mumols/L, p less than 0.001, and free carnitine of 15.7 +/- 7.3 mumols/L vs. 36.1 +/- 5.2 mumols/L, p less than 0.001, respectively). The acylcarnitine concentration in plasma was decreased in the TPN children (3.3 +/- 1.5 mumols/L vs. 5.8 +/- 3.0 mumols/L, p less than 0.01) compared to controls. Despite the low carnitine concentrations, serum triglyceride levels and serum free fatty acid levels were within the normal range. There was no correlation between carnitine concentrations in plasma and serum triglyceride and free fatty acid levels. Our data show that children receiving carnitine-free TPN for many years developed markedly decreased concentrations of carnitine in blood and plasma. However, no adverse effects of the low carnitine levels were found on triglyceride and free fatty acid metabolism under stable conditions.     

Renal calcification incidence in very low birth weight infants

Serial ultrasound examinations were performed on 31 neonates with birth weights of less than 1,500 g for the detection of renal calcifications. Renal calcifications occurred in 20 (64%) of the infants at a mean age of 39.3 +/- 26.7 days of life. Infants with renal calcifications had shorter gestations (28.2 +/- 1.8 v 31 +/- 1.4 weeks, P less than .004) and lighter birth weights (924 +/- 195 v 1,338 +/- 100 g, P less than .004) than those infants without renal calcifications (n = 11). Furosemide administration was more common in the infants with renal calcifications (65% v 9.1%, P less than .001). The mean total dose of furosemide administered before renal calcifications were noted was 9.59 +/- 7.25 mg/kg. The 20 neonates with renal calcifications had a mean urine calcium level of 12.0 +/- 6.8 mg/kg/24 hours, mean urine calcium to creatinine ratio of 1.32 +/- 1.03 (range 0.3 to 4.45), and a mean alkaline phosphatase concentration of 961 +/- 327 IU. Initial parathyroid hormone levels were not different between the two groups, and subsequent determinations in infants with renal calcifications did not differ significantly from initial values. Renal calcifications are fairly common among very low birth weight infants, particularly in those receiving supplemental calcium and furosemide therapy. Although long-term implications of such findings are not known, close monitoring of renal function by serial determinations of urine calcium and urine calcium to creatinine ratios may identify those infants at risk for renal calcifications.     

Inorganic sulfate metabolism in the very low birthweight infant

The effect of vitamin D supplementation on inorganic sulfate metabolism was examined in very low birth weight (less than 1,500 g) infants at biweekly intervals after birth until 6 weeks of postnatal age. Baseline serum sulfate concentrations were significantly higher in all infants (471 +/- 24 mumol/l, n = 80) than in adults (299 +/- 25 mumol/l, n = 17). In controls, the levels did not change significantly over the ensuing 6 weeks, although serum creatinine declined. Urinary sulfate excretion rose significantly to near adult levels by 2 weeks. Both urine and serum sulfate were correlated with weight gain but not with estimated glomerular filtration rate, suggesting that factors other than renal clearance have a preponderant influence on serum sulfate in these infants. At 6 weeks, the mean serum sulfate in the high-dose group (receiving 2,170 +/- 23 U/day of vitamin D, n = 41) was significantly higher than in controls (receiving 360 +/- 22 U/day, n = 40). In all infants, there was a significant correlation (r = 0.36, p less than 0.001) between serum sulfate and 25(OH)-vitamin D concentrations, but not other analytes or clinical variables, suggesting that vitamin D may be one of the factors modulating sulfate metabolism in the newborn period.     

Plasma creatinine in the first month of life.

The creatinine-kinetics method of analysis was used to study the changes, during the first month of life, in plasma creatinine levels in 34 newborn infants receiving no treatment with drugs. Plasma creatinine values during the first 5 days of life ranged from 188 to 17 mumol/l. After day 5 plasma levels were fairly stable throughout the first month, with a mean value of 35 +/- 2 (range 12-62) mumol/l. Twenty-two infants receiving treatment with gentamicin-ampicillin-cloxacillin were also studied. Seven of them had raised plasma creatinine concentrations after day 5, well beyond the range of concentrations found for infants receiving no drugs. Plasma creatinine, measured by the kinetic method, appears to provide a useful index of renal function in the neonatal period.     

Circulating levels of biologically active and immunoreactive intact parathyroid hormone in human newborns

We evaluated circulating levels of biologically active and immunoreactive intact parathyroid hormone [iPTH-(1-84)] in 47 newborns at birth and eight hypocalcemic preterm infants during the first 10 d of life. Use of two sensitive detection systems, the cytochemical bioassay and an immunoradiometric assay specific for intact parathyroid hormone, enabled us to compare plasma concentrations of PTH-like bioactivity (bioPTH) and iPTH-(1-84). Mean umbilical venous plasma bioPTH was elevated in nondiabetic term and preterm newborns [22.5 +/- 3.1 (+/- SEM) and 15.8 +/- 2.5 ng-equiv/L, respectively] compared with normal adult subjects (9.8 +/- 2.6 ng-equiv/L; p less than 0.01). Umbilical bioPTH was suppressed in five term infants of diabetic mothers (2.6 +/- 0.4 ng-equiv/L). In contrast, iPTH-(1-84) was low in term and preterm nondiabetic infants' and term infants of diabetic mothers' umbilical samples (5.4 +/- 1.5, 4.3 +/- 1.5, and 2.4 +/- 1.0 ng/L, respectively). Umbilical venous bioPTH was highly correlated with the magnitude of the transplacental calcium gradient (r = 0.90; p less than 0.05). In eight preterm infants studied longitudinally, by 24-36 h of life, declining plasma total and ionized calcium (1.71 +/- 0.04 and 0.78 +/- 0.03 mmol/L, respectively) were accompanied by a significant rise in both bioPTH (41.2 +/- 6.3 ng-equiv/L) and iPTH-(1-84) (56.3 +/- 11.6 ng/L). These data indicate that the 3rd trimester fetoplacental circulation contains levels of bioPTH several-fold higher than those of immunoreactive intact hormone. We also conclude that even hypocalcemic preterm newborn infants can significantly elevate circulating levels of PTH.     

Adrenal function in thalassemia major following long-term treatment with multiple transfusions and chelation therapy. Evidence for dissociation of cortisol and adrenal androgen secretion

Eight patients with beta-thalassemia who were given long-term treatment with combined multiple transfusions and chelation therapy underwent adrenal testing. The six male and two female patients ranged in age from 7 to 19 years. Six of eight patients had delayed bone ages and height greater than 2.5 SDs below the mean. Of the six patients more than 13 years of age, two had clinical evidence of isolated adrenarche and only one had evidence of true puberty. Cortisol levels were similar in patients and controls at zero time (10.6 +/- 1.8 micrograms/dL [292 +/- 50 nmol/L] vs 10.8 +/- 1.4 micrograms/dL [298 +/- 39 nmol/L]) and at 60 minutes (26.6 +/- 2.5 micrograms/dL [734 +/- 69 nmol/L] vs 24.9 +/- 1.9 micrograms/dL [687 +/- 52 nmol/L]) after insulin hypoglycemia (all values are the mean +/- SE). During an eight-hour infusion of ACTH, cortisol responses in the patients with thalassemia were not significantly different from those of controls. Baseline levels of the adrenal androgens dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) were significantly lower in the subjects with thalassemia compared with controls of similar bone age and pubertal status. The prolonged ACTH infusion caused a significant increase in the DHEA level (79.2 +/- 14.7 ng/dL [2.74 +/- 0.51 nmol/L] vs 538.6 +/- 38.1 ng/dL [18.67 +/- 4.79 nmol/L]) and the DHEA-S level (37.5 +/- 10.8 micrograms/dL [1.02 +/- 0.29 mumol/L] vs 70.5 +/- 18.3 micrograms/dL [1.19 +/- 0.50 mumol/L]) in the patients. The patients' peak stimulated levels of DHEA-S were significantly lower than those of the controls, whereas peak levels of DHEA were similar in the patients and the controls. These results indicate that combined multiple transfusions and chelation therapy preserve the integrity of the ACTH-cortisol axis in patients with thalassemia. The reduced levels of adrenal androgens, short stature, and delayed puberty noted in our patients suggest, however, that alternative approaches to the therapy of thalassemia are needed.     

Early neonatal hyperkalaemia in the extremely premature newborn infant

The incidence of hyperkalaemia in 43 consecutive infants born at less than 28 weeks gestation and cared for in our neonatal intensive care unit was documented. Plasma K levels were related to indices of renal function as well as to the degree of illness in the infants. The mean gestational age was 26.0 weeks (range 24-27 weeks) and the mean birthweight was 815 g (range 395-1170 g). Twenty-six of the infants (60%) had at least one plasma K greater than 5.5 mmol/L and 13 (30%) had a maximum plasma K greater than 7 mmol/L. The mean postnatal age at which the plasma K exceeded 7 mmol/L was 25 h (range 10-39 h). Five infants with plasma K greater than 7 mmol/L developed cardiac arrhythmias and four died of this complication. Only one infant had a large intraventricular haemorrhage. Only two of 16 infants with an initial plasma K less than 5 mmol/L had a maximum plasma K greater than 7 mmol/L, compared with eight of 10 with an initial plasma K greater than 6 mmol/L (P less than 0.005). Plasma K also correlated directly with plasma urea (P less than 0.001) and plasma creatinine (P less than 0.025), and inversely with urine volume (P less than 0.05). Plasma K did not correlate with K intake, arterial pH, presence of asphyxia, severity of respiratory illness, gestation or birthweight. The rapidity with which the plasma K concentration reached potentially hazardous levels in some infants makes it imperative to measure plasma K within 6 h of birth and to continue to monitor levels at least every 6 h for the first 48 h in all infants born at less than 28 weeks gestation.     

Mineral homeostasis and bone mass in children treated for acute lymphoblastic leukemia

Clinical observations of bone pain, abnormal gait, and unusual fractures during remission of leukemia led us to assess mineral status in a cohort of 16 children with acute lymphoblastic leukemia treated with intensive chemotherapy. During maintenance and 6 months after the completion of therapy, blood and urine were analyzed for calcium and magnesium and blood for osteocalcin, vitamin D, and parathyroid hormone. Bone mineral content and bone width of the distal one third of the radius of the nondominant arm was measured by single-photon absorptiometry. During therapy, mild ionic hypocalcemia (less than 1.19 mmol/L) and hypomagnesemia (less than 0.77 mmol/L) were demonstrated in 9 and 8 of 16 children, respectively; hypercalciuria (8/16) and hypomagnesiuria (12/16) were also observed. Plasma osteocalcin values correlated with plasma magnesium levels (r = 0.54; p less than 0.05). Oral magnesium supplements normalized plasma magnesium, calcium, and osteocalcin levels, all of which were normal at the postchemotherapy study. Plasma 1,25-dihydroxyvitamin D levels were nondetectable (less than 8 ng/ml) in 12 of 13 patients receiving therapy and in 7 of 14 patients not receiving therapy; alkaline phosphatase activity increased significantly after therapy (179 +/- 86 to 340 +/- 101 units/L), and parathyroid hormone levels were normal in both studies. Bone mineral content/bone width ratio was less than 1 SD below the mean for age- and sex-related population standards in 70% of patients. These data indicate that alterations in magnesium, calcium, and vitamin D metabolism in children treated for acute lymphoblastic leukemia may be instrumental in inducing or sustaining altered bone turnover during chemotherapy.     

Plasma creatinine in the first month of life

The creatinine-kinetics method of analysis was used to study the changes, during the first month of life, in plasma creatinine levels in 34 newborn infants receiving no treatment with drugs. Plasma creatinine values during the first 5 days of life ranged from 188 to 17 mumol/l. After day 5 plasma levels were fairly stable throughout the first month, with a mean value of 35 +/- 2 (range 12-62) mumol/l. Twenty-two infants receiving treatment with gentamicin-ampicillin-cloxacillin were also studied. Seven of them had raised plasma creatinine concentrations after day 5, well beyond the range of concentrations found for infants receiving no drugs. Plasma creatinine, measured by the kinetic method, appears to provide a useful index of renal function in the neonatal period.     

The natural history of direct hyperbilirubinemia associated with extracorporeal membrane oxygenation.

OBJECTIVE--To determine the incidence and natural history of direct hyperbilirubinemia in neonates treated with extracorporeal membrane oxygenation. DESIGN--A prospective series of patients. SETTING--A level 3 neonatal intensive care unit and center for extracorporeal membrane oxygenation in Ohio. PARTICIPANTS--Sixty-seven consecutive patients treated with extracorporeal membrane oxygenation in 33 months. INTERVENTION--None. MEASUREMENTS/RESULTS--Twenty-six (39%) developed direct hyperbilirubinemia. In 14 (54%), bilirubin levels were mildly elevated and occurred only during extracorporeal membrane oxygenation therapy. Levels were more severely elevated in the remaining 12 patients (46 +/- 10 mumol/L [2.7 +/- 0.6 mg/dL] vs 159 +/- 101 mumol/L [9.3 +/- 5.9 mg/dL], P less than .0001). Duration and severity of hyperbilirubinemia were correlated. Hyperbilirubinemia resolved in all patients by 9 weeks after extracorporeal membrane oxygenation therapy. No structural abnormalities or infectious agents were identified as causes. Aluminum levels were evaluated for 40 patients, were not in the toxic range, and did not correlate with hyperbilirubinemia. Multiple linear regression analysis suggested that hyperbilirubinemia in these cases resulted from interaction of injuries, with the primary contributor being hemolysis during extracorporeal membrane oxygenation. CONCLUSIONS--Direct hyperbilirubinemia occurs frequently in patients treated with extracorporeal membrane oxygenation and may be severe. However, direct hyperbilirubinemia typically resolves without short-term sequelae. Hemolysis may be an important contributing factor.     

Molybdenum in the premature infant

The molybdenum (Mo) levels in the plasma and urine of 30 premature and 15 full-term infants have been compared with the Mo intakes and urine uric acid excretion (uric acid/creatinine ratio) produced by the Mo enzyme xanthine oxidase. The Mo intakes of full-term infants were 41 +/- 14 nmol/kg/day (mean +/- SEM). In the premature group breast milk supplied significantly less Mo (4.3 +/- 0.4 nmol/kg/day) than infant formulas (101 +/- 31 nmol/kg/day) or premature formula (255 +/- 13 nmol/kg/day). When fed breast milk, the preterm infants displayed similar or higher plasma and urine Mo and urine uric acid levels than formula-fed infants. For the whole preterm group a significant correlation was determined for urine Mo levels and Mo intakes as well as for plasma Mo and uric acid excretion. The bioavailability of breast milk Mo seems to be higher than formula Mo according to the Mo levels and to their statistical link with uric acid excretion which could be proposed as a functional index of Mo status. These parameters displayed similar values in breast milk-fed prematures and control full-term infants. The Mo needs of formula-fed premature newborns remain to be defined using complete balance trials.     

Effect of amino acid composition of parenteral solutions on nitrogen retention and metabolic response in very-low-birth weight infants

To evaluate the influence of amino acid preparations on the metabolic response of parenterally fed immature newborn infants, nitrogen retention and plasma amino acid concentrations were compared in very-low-birth-weight infants given two parenteral regimens differing only by the composition of the infused amino acids (Travasol 10% blend B and Vamin 7%). The intakes of fluid, nitrogen, and calories were comparable. The nitrogen retention was 72% +/- 7% with Vamin and 65% +/- 6% with Travasol. The differences in plasma amino acid concentrations were consistent with the composition of the amino acid solutions. During the infusion of Vamin the increased intake of aromatic amino acids resulted in high plasma levels of tyrosine (256 +/- 233 mumol/L, range 67 to 894 mumol/L). The infusion of Travasol resulted in high plasma levels of methionine (114 +/- 39 mumol/L, range 53 to 260 mumol/L) and an elevated load of glycine, which was accompanied by an abnormally high urinary loss of this amino acid. Despite these metabolic imbalances, the growth rate over the whole study was adequate. These results emphasize the importance of the composition of amino acid solutions on the metabolic response of the very immature preterm infant.     

Plasma zinc levels in premature infants receiving parenteral nutrition.

Plasma zinc levels in premature infants receiving parenteral nutrition without supplementation of trace elements were evaluated. The mean +/- SE for plasma zinc concentration prior to the start of parenteral nutrition was 53 +/- 6 microgram/dl. During the first two weeks of parenteral nutrition the levels remained low, but did not change significantly. However, from day 14 through day 32 there was a statistically significant (P less than 0.05), progressive decline in plasma zinc values. Perhaps the shortened gestational periods were etiologic in producing the initial low plasma zinc concentration in these patients. Since low-birth-weight infants apparently have a high requirement for zinc, the reduced growth rates of these patients may be related to their apparent zinc deficiencies.