A randomized trial of two levels of iron supplementation and developmental outcome in low birth weight infants.

OBJECTIVES: To investigate the effect of increased iron intakes on hematologic status and cognition in low birth weight infants. STUDY DESIGN: We randomly assigned 58 infants to receive formula with 13.4 mg iron/L (normal iron) or 20.7 mg iron/L (high iron). At baseline, discharge, and at 3, 6, 9, and 12 months' corrected age, we assessed anthropometry; infections; red blood cell hemoglobin, catalase, glutathione peroxidase, red blood cell fragility (hydrogen peroxide test), and superoxide dismutase values; plasma malondialdehyde, ferritin, iron, transferrin, zinc and copper levels; and diet intake. Griffiths' Development Assessment was done at 3, 6, 9, and 12 months only. RESULTS: No statistical differences (P <.05) were noted for weight, catalase or malondialdehyde levels, red blood cell fragility, or Griffith's Development Assessment. Iron intakes were greater in the high iron group except at 12 months. Hemoglobin (high iron, 123 +/- 9; normal iron, 118 +/- 8) was not different at 3 months (P =.07). Plasma zinc levels (high iron, 70 +/- 14; normal iron, 89 +/- 27) and copper levels (high iron, 115 +/- 26; normal iron, 132 +/- 27; P =.06) at 12 months suggested inhibition of absorption by high iron formula. Glutathione peroxidase levels were higher in the high iron group. The total number of respiratory tract infections was greater in the high iron group (3.3 +/- 0.9) than in the normal iron group (2.5 +/- 0.9). CONCLUSION: In terms of cognitive outcome, there is no advantage associated with elevated iron intake for low birth weight infants.

Thiamine, riboflavin, pyridoxine, and vitamin C status in premature infants receiving parenteral and enteral nutrition.

BACKGROUND: There is a paucity of data about water soluble vitamin status in low birthweight infants. Therefore, the authors' objective was to assess current feeding protocols. METHODS: The authors measured serum concentrations for riboflavin, pyridoxine, and vitamin C and functional assays for thiamine and riboflavin longitudinally in 16 premature infants (birthweight, 1,336 +/- 351 g; gestational age, 30 +/- 2.5 weeks) before receiving nutrition (time 1, 2 +/- 1 days), during supplemental or parenteral nutrition (time 2, 16 +/- 10 days) and while receiving full oral feedings (time 3, 32 +/- 15 days). In plasma, vitamin C was measured colorimetrically, and riboflavin and pyridoxine were measured using high-performance liquid chromatography. The erythrocyte transketolase test as a functional evaluation of thiamine and the erythrocyte glutathione reductase test for riboflavin were measured colorimetrically. RESULTS: At time 1, nutrient intake of vitamins were negligible because infants were receiving intravenous glucose and electrolytes only. Intakes differed between time 2 and time 3 for thiamine (510 +/- 280 and 254 +/- 115 microg. kg-1. d-1, respectively), riboflavin (624 +/- 305 and 371 +/- 193 microg. kg-1. d-1, respectively), and pyridoxine (394 +/- 243 and 173 +/- 85 microg/100 kcal, respectively), but not for vitamin C (32 +/- 17 and 28 +/- 12 mg. kg-1. d-1, respectively). Blood levels at times 1, 2, and 3 were for thiamine (4.9 +/- 2.7%, 3.3 +/- 6.6%, and 4.1 +/- 9% erythrocyte transketolase test, respectively), riboflavin (0.91 +/- 0.31, 0.7 +/- 0.3, 0.91 +/- 0.18 erythrocyte glutathione reductase test, respectively), riboflavin (19.5 +/- 17, 23.3 +/- 8.6, 17.6 +/- 10 ng/mL, respectively), pyridoxine (32 +/- 25, 40 +/- 16, 37 +/- 26 ng/mL, respectively), and vitamin C (5.2 +/- 3, 5 +/- 2.2, 10 +/- 5 microg/mL, respectively) and did not differ at those times. CONCLUSIONS: Current intakes of these vitamins, except for possibly vitamin C, during parenteral and enteral nutrition seem to result in adequate plasma concentrations and normal functional indices.

Molybdenum requirements in low-birth-weight infants receiving parenteral and enteral nutrition.

BACKGROUND: Molybdenum (Mo) is an essential trace element required by three enzymatic systems, yet there are no reports of Mo deficiency in infants. Low-birth-weight infants (LBW) might be at risk for Mo deficiency because they are born before adequate stores for Mo can be acquired, they have rapid growth requiring increased intakes, and they frequently receive supplemental parenteral nutrition (SPN) and total parenteral nutrition (TPN) unsupplemented with molybdenum. METHODS: To investigate Mo requirements of LBW infants (n = 16; birth weight, 1336+/-351 g; gestational age, 29.8+/-2.5 weeks; M+/-SD), the authors collected all feeds, urine, and feces prior to TPN (baseline, n = 16, collections = 16), during TPN (n = 9, collections = 19), during SPN (n = 13, collections = 17), and after one week of full oral feeds (FOFs) of formula or human milk (FOF, n = 16, collections = 16). RESULTS: Infant weights at collection times were: 1.3+/-0.3 g, 1.27+/-0.4 g, 1.4+/-0.3 g, and 1.7+/-0.5 g, respectively. Mo intake was 0.03+/-0.1 microg/d, 0.34+/-0.1 microg/d, 1.25+/-1.7 microg/d, and 6.1+/-2.5 microg/d. Mo output was 0.64+/-0.6, 0.34+/-0.5, 0.68+/-0.8, and 4.1+/-2.5 microg/d. Mo balance at these times was -0.60+/-0.5, -0.001+/-0.5, 0.57+/-1.9, and 2.0+/-2.9 microg/d. Mo balance increased with time, yet some infants were always in negative balance, even though Mo intakes exceeded recommendations. CONCLUSIONS: The authors speculate that an intravenous intake of 1 microg/kg/d (10 nmol/kg/d) and an oral intake of 4-6 microg/kg/d (40-60 nmol/kg/d) would be adequate for the LBW infant.

Elevated intakes of zinc in infant formulas don not interfere with iron absorption in premature infants.

BACKGROUND: Zinc and iron may share common pathways for absorption and compete for uptake into mucosal cells. We determined whether elevated ratios of zinc to iron would interfere with erythrocyte incorporation of iron in premature infants both during and between feeds. METHODS: In the first experiment, five premature infants (<2500 g birth weight) were enrolled, once receiving full oral feeds by nasogastric tube. They received either high (1200 microg/kg, ratio 4:1) or low (300 microg/kg, ratio 1:1) doses of oral zinc sulfate, together with 300 microg/kg oral 58Fe as chloride in saline with 10 mg/kg vitamin C, between designated feeding periods. Each infant served as its own control and randomly received either high or low doses of zinc or iron and then the alternate dose after 2 weeks. In the second experiment, nine additional premature infants were assigned to the same zinc:iron intake protocol except zinc and iron were given with usual oral feeds (premature formula or human milk) equilibrated before feeding. Iron absorption was measured by the erythrocyte incorporation of 58Fe. RESULTS: High doses of zinc given between feeds significantly inhibited erythrocyte incorporation of iron. 58Fe incorporation (%) with the 1:1 ratio of zinc:iron intake was 7.5 (5.7, 10; geometric mean, -I SD, +1 SD). The percentage of 58Fe incorporation on the 4:1 ratio of zinc:iron intake was 3.6 (2.6, 5.1). Given with feeds, the percentage of 58Fe incorporation on low zinc:iron intake was 7.0 (2.6, 19). Finally, the percentage of 58Fe incorporation on high zinc:iron intake was 6.7 (2.5, 19). CONCLUSION: Elevated intakes of zinc do not interfere with erythrocyte incorporation of iron in premature formulas.

Visual acuity in infants and children with Down syndrome.

The authors used the Teller acuity cards to assess the visual acuity of 51 infants and children with Down syndrome aged between two months and 18 years. The success rate and test times were comparable to those reported for normally developing children. Even those subjects in the study who were free of ocular disorders and/or who were wearing optical correction during testing showed significantly poorer visual acuity than individuals without Down syndrome. The development of visual acuity in infants and children with Down syndrome lags behind that of age-matched peers without Down syndrome, especially after the age of six months. These findings are discussed in terms of the neurological and optical factors that might account for the deficits in visual acuity that were observed.