Source and Quality of Enteral Nutrition Influences Oxidative Stress in Preterm Infants: A Prospective Cohort Study.

BACKGROUND: Preterm infants are at risk of oxidative stress from neonatal intensive care interventions. 8-Oxo-2'-deoxyguanosine (8-oxodG), generated by oxygen radical attack on DNA, is a potential marker of oxidative stress. The aim of the present study was to investigate the impact of quality and source of enteral nutrition (EN) on renal excretion of 8-oxodG in preterm infants. METHODS: Spontaneous urine samples were collected on postnatal days 26-31 in 33 preterm infants. Infants were fed either breast milk (BM), formula (FM), or BM/FM mixtures. Daily iron (Fe) supplementation was started day 28 ± 1 postnatally. 8-oxodG was determined by highperformance liquid chromatography-electrochemical detection (HPLC-EC). RESULTS: The 8-oxodG/creatinine ratio was significantly higher in infants fed FM vs FM/BM (38.7 ± 28.7 vs 16.7 ± 12.2 nmol 8-oxodG/mmol creatinine, P < 0.0001) or BM (11.6 ± 10.4 nmol 8-oxodG/mmol creatinine, P < 0.0001). There was no significant effect of Fe supplementation (P = 0.547). 8-OxodG excretion showed significant interindividual variation but was similar within pairs of twins. CONCLUSION: Quality and source of EN seem to influence oxidative stress in preterm infants. The underlying pathophysiological mechanism is unclear and needs further investigation. It may be speculated that other mechanisms than Fe supplementation contribute to oxidative stress, such as cow's milk protein-mediated up-regulation of the intestinal inflammatory cascade.

Fortification of breast milk in VLBW infants: metabolic acidosis is linked to the composition of fortifiers and alters weight gain and bone mineralization.

BACKGROUND & AIMS: Study objectives were to test (a) whether increased incidence of metabolic acidosis (MA) was caused by introduction of a new commercially available fortifier for breast milk, (b) if so, whether its modification would decrease the incidence of MA and (c) to analyze the impact of MA on growth. METHODS: Double-blind randomized design. Healthy breast-fed infants (≤34 gestational weeks). Primary outcome measure was incidence of MA (BE < -6.0 mmol/L). Secondary outcome measures were growth, bone mineral content (BMC), vital signs, treatment with sodium hydrogen carbonate and Ca and laboratory parameters (pH, pCO2, HCO3⁻, electrolytes). RESULTS: Part 1 (comparison of standard (SF) and new fortifier (NF)): Interim analysis showed MA in 1 out of 7 (SF) and 7 out of 8 (NF) infants, p = 0.01; therefore the study was interrupted; subsequently the fortifier was adapted by modifying mineral components. Part 2 (comparison of SF and reformulated fortifier (RF)): MA occurred in 3 out of 15 (SF) and 6 out of 19 (RF), p = 0.7. When data of all infants studied, those with MA had lower mean weight gain (median: 9 vs. 21 g/kg/d, p < 0.01) and lower BMC (1.6% vs. 1.9% BMC/lean, p = 0.04) at discharge. CONCLUSIONS: When fed fortified breast milk, mild MA spontaneously may develop in 20-30% of VLBW infants. A fortifier with an inappropriate composition may increase the severity and frequency of MA. Our data show that weight gain and BMC seem to be related to acid-base homeostasis. It may be speculated that inadequate growth of fully fed preterm infants is triggered more often by imbalances of acid-base status than previously expected.