Background: Serum ferritin measurements are used in clinical populations to estimate total body iron stores and the risk of subsequent iron deficiency or overload. The lack of normative newborn serum ferritin concentration data between 23 and 41 weeks has led to difficulty in establishing the incidence and degree of abnormal iron status in the neonatal period. Objectives: The primary objective of this review was to summarize the maternal and gestational factors that determine ferritin concentrations in full-term and pre-term newborn infants and to generate comprehensive reference values. The secondary objective was to assess serum ferritin concentrations in newborn infants at risk for abnormal fetal iron metabolism, including maternal diabetes mellitus, intrauterine growth restriction and maternal smoking during pregnancy. Methods: Serum ferritin and gestational age data at birth from 457 low-risk pre-term and term infants of 23–41 weeks gestation obtained from 35 published studies reviewed from a period of 25 years and from recently collected data from our centers were assessed by regression analysis. Slopes and intercepts of the high-risk groups were compared with the standard curve. Results: Umbilical cord serum ferritin concentrations increased with advancing gestational age, from a mean of 63 µg/l at 23 weeks to 171 µg/l at 41 weeks gestation (p < 0.001). The infants of diabetic mothers had a lower intercept than the control infants (p < 0.001). Conclusions: Iron deficiency and overload have been implicated in neurodevelopmental impairments. Normative cord serum ferritin data may permit a more precise assessment of infants who are at risk for abnormal iron status at birth.

Sixteen metabolites were quantified from 11–24 μl volumes in three different brain regions (hippocampus, striatum, and cerebral cortex) during postnatal development. Rat pups from the same litter were repeatedly measured on postnatal days 7, 10, 14, 21, and 28 using a completely noninvasive and longitudinal study design. Metabolite quantification was based on ultra‐short echo‐time ¹H NMR spectroscopy at 9.4 T and LCModel processing. Most of the brain metabolites were quantified with Cramer‐Rao lower bounds (CRLB) less than 20%, which corresponded to an estimated concentration error <0.2 μmol/g. Taurine and total creatine were quantified with CRLB ≤ 5% from all 114 processed spectra. The resulting high reliability and reproducibility revealed significant regional and age‐related changes in metabolite concentrations. The most sensitive markers for developmental and regional variations between hippocampus, striatum, and cerebral cortex were N‐acetylaspartate, myo‐inositol, taurine, glutamate, and choline compounds. Absolute values of metabolite concentrations were in very good agreement with previously published in vitro results based on chromatographic measurements of brain extracts. The current data may serve as a reference for studies focused on developmental defects and pathologies using neonatal rat models. Magn Reson Med 50:24–32, 2003.

Cognitive deficits in human infants at risk for gestationally acquired perinatal iron deficiency suggest involvement of the developing hippocampus. To understand the plausible biological explanations for hippocampal injury in perinatal iron deficiency, a neurochemical profile of 16 metabolites in the iron-deficient rat hippocampus was evaluated longitudinally by ¹H NMR spectroscopy at 9.4 T. Metabolites were quantified from an 11–24 μL volume centered in the hippocampus in 18 iron-deficient and 16 iron-sufficient rats on postnatal day (PD) 7, PD10, PD14, PD21 and PD28. Perinatal iron deficiency was induced by feeding the pregnant dam an iron-deficient diet from gestational d 3 to PD7. The brain iron concentration of the iron-deficient group was 60% lower on PD7 and 19% lower on PD28 (P < 0.001 each). The concentration of 12 of the 16 measured metabolites changed over time between PD7 and PD28 in both groups (P < 0.001 each). Compared with the iron-sufficient group, phosphocreatine, glutamate, N-acetylaspartate, aspartate, γ-aminobutyric acid, phosphorylethanolamine and taurine concentrations, and the phosphocreatine/creatine ratio were elevated in the iron-deficient group (P < 0.02 each). These neurochemical alterations suggest persistent changes in resting energy status, neurotransmission and myelination in perinatal iron deficiency. An altered neurochemical profile of the developing hippocampus may underlie some of the cognitive deficits observed in human infants with perinatal iron deficiency.

Iron deficiency (ID) is common in pregnant women and infants, particularly in developing countries. The relation between maternal and neonatal iron s