Maternal iron needs increase sixfold during pregnancy, but obesity interferes with iron absorption. We hypothesized that maternal obesity impairs fetal iron status. Three hundred and sixteen newborns with risk factors for infantile iron deficiency anemia (IDA) were studied to examine obesity during pregnancy and neonatal iron status. Erythrocyte iron was assessed by cord blood hemoglobin (Hb), zinc protoporphyrin/heme (ZnPP/H) and reticulocyte-ZnPP/H, and storage iron by serum ferritin. Women with body mass index (BMI) 30 kg m⁻², as compared with non-obese women, delivered larger offspring with higher reticulocyte-ZnPP/H and lower serum ferritin concentrations (P<0.05 for both). With increasing BMI, the estimated body iron was relatively lower (mg kg⁻¹) and the ratio of total Hb-bound iron (mg) per total body iron (mg) increased. Maternal diabetes compromised infant iron status, but multivariate analysis demonstrated that obesity was an independent predictor. Obesity during pregnancy and excessive weight gain are independent risk factors for iron deficiency in the newborn.

Meeting antibiotic stewardship goals in the neonatal intensive care unit (NICU) is challenging because of the unique nature of newborns and the lack of specificity of clinical signs of sepsis. Antibiotics are commonly continued for 48 hours pending culture results and clinical status. The goal of this study was to examine if the implementation of a 48-hour automatic stop (autostop) order during NICU admissions would decrease antibiotic use at UnityPoint Health–Meriter. An observational double-cohort study was performed in a level 3 NICU. Antibiotic use was evaluated before and after the autostop initiative. The admission order set included 48 hours of ampicillin and gentamicin coverage. After the autostop initiation, total doses given per patient decreased by 35% and doses per patient-day decreased by 25% (P < .0001). The greatest effect was a 66% decrease in the use of vancomycin, an antibiotic not included in the admission order set. Providers proactively continued antibiotics for infants in whom they had high suspicion for sepsis and in those with positive blood or cerebral spinal fluid culture results. An admission-order autostop was highly effective at decreasing antibiotic usage with no doses intended for a pathogen missed. Fewer doses of certain antibiotics outside of the admission order set were administered, particularly vancomycin, which results in our speculation that provider awareness of the antibiotic stewardship initiative might have altered prescribing practices.

Background: Maternal anemia and several complications of pregnancy can affect fetal iron acquisition. Aim: Because it is unknown whether the effects of demographic and maternal risk factors (RF) are summative, we examined cord iron status in newborns with multiple RF for acquiring iron deficiency. Methods: Cord blood indices from healthy control newborns with and without RF for newborn or infant iron deficiency were studied. Results: Newborns with greater RF had poorer erythrocyte and storage iron status. Poorest status was seen if mothers with comorbid obesity and diabetes delivered large-for-gestation newborns. Findings highlight the importance of identifying RF.

Maternal iron deficiency anemia, obesity, and diabetes are prevalent during pregnancy. All are associated with neonatal brain iron deficiency (ID) and neurodevelopmental impairment. Exosomes are extracellular vesicles involved in cell–cell communication. Contactin-2 (CNTN2), a neural-specific glycoprotein, and brain-derived neurotrophic factor (BDNF) are important in neurodevelopment and found in exosomes. We hypothesized that exosomal CNTN2 and BDNF identify infants at risk for brain ID. Umbilical cord blood samples were measured for iron status. Maternal anemia, diabetes, and body mass index (BMI) were recorded. Cord blood exosomes were isolated and validated for the exosomal marker CD81 and the neural-specific exosomal marker CNTN2. Exosomal CNTN2 and BDNF levels were quantified by ELISA. Analysis of CNTN2 and BDNF levels as predictors of cord blood iron indices showed a direct correlation between CNTN2 and ferritin in all neonates (n = 79, β = 1.75, p = 0.02). In contrast, BDNF levels inversely correlated with ferritin (β = −1.20, p = 0.03), with stronger association in female neonates (n = 37, β = −1.35, p = 0.06), although there is no evidence of a sex-specific effect. Analysis of maternal risk factors for neonatal brain ID as predictors of exosomal CNTN2 and BDNF levels showed sex-specific relationships between infants of diabetic mothers (IDMs) and CNTN2 levels (Interaction p = 0.0005). While male IDMs exhibited a negative correlation (n = 42, β = −0.69, p = 0.02), female IDMs showed a positive correlation (n = 37, β = 0.92, p = 0.01) with CNTN2. A negative correlation between BNDF and maternal BMI was found with stronger association in female neonates (per 10 units BMI, β = −0.60, p = 0.04). These findings suggest CNTN2 and BNDF are respective molecular markers for male and female neonates at risk for brain ID. This study supports the potential of exosomal markers to assess neonatal brain status in at-risk infants.

Iron is essential for fetal organ development, but the effect of isolated iron deficiency on nephrogenesis is unknown. Human premature infants are at risk for disrupted nephrogenesis because glomerular development is incomplete until 36-wk gestation. We modeled the effects of iron on postnatal glomerulogenesis in four groups of immature rats from P4 to P12: dam fed controls (DF), dam fed with sham gastrostomy surgery (DF + SS), iron-deficiency anemia (IDA), fed iron-deficient formula through gastrostomy apart from the dam, and IDA plus simultaneous enteral iron rescue (IDA+Fe). Hematocrit, plasma ferritin, and body and kidney tissue iron contents were measured. Tissue was examined. Rats grew similarly, but IDA rats exhibited lower hematocrit, plasma ferritin, and body and kidney iron contents than DF, DF + SS, or IDA + Fe. IDA exhibited 1.7 fewer radial glomerular counts (RGCs), 26% reduced glomerular density, and 29% less planar glomerular surface area than DF, with partial improvement in IDA + Fe. Compared with DF or DF + SS, we observed elevated plasma CRP levels and tubulointerstitial fibrosis in the IDA and IDA + Fe groups. IDA reduced glomerular density, glomerular surface area, and promoted fibrosis. Iron substantially rescued renal growth and development, supporting the critical role of iron in late nephrogenesis.