Background: Animal studies suggest that total parenteral nutrition (TPN) may alter bacterial colonization of the intestinal tract and contribute to complications. Progressive changes in gut microbiome of infants receiving TPN are not well understood. Methods: Infants with and without TPN/soy lipid were enrolled in a prospective, longitudinal study. Weekly fecal samples were obtained for the first 4 weeks of life. High throughput pyrosequencing of 16S rDNA was used for compositional analysis of the gut microbiome. Results: 47 infants were eligible for analyses, 25 infants received TPN and 22 infants did not (control). Although similar between TPN and control groups in the first week, fecal bacterial alpha diversity was significantly lower in the TPN group compared to controls at week 4 (Shannon index 1.0 vs 1.5, P-value = 0.03). The TPN group had significantly lower Bacteroidetes and higher Verrucomicrobia abundance compared to controls (P-values <0.05), and these differences became more pronounced over time. At the genus level, TPN was associated with lower abundance of Bacteroides and Bifidobacterium in all weeks. Conclusions: TPN is associated with significant loss of biodiversity and alterations in the pattern of gut microbial colonization of infants over time. TPN-associated dysbiosis may predispose infants to adverse NICU outcomes.

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Objective: To determine whether a room air challenge (RAC) correlates with duration of respiratory support for infants with bronchopulmonary dysplasia (BPD). Study design: Prospective study of preterm infants with BPD from 2015–2018. Infants receiving ≤2 liters flow at 36 weeks post-menstrual age (PMA) underwent RAC. Cox regression was used to adjust the duration of respiratory support after 36 weeks PMA for significant covariates. Results: Of 161 infants with BPD, 91 were eligible for RAC; 51 passed and 40 failed. Infants who failed RAC had longer respiratory support after 36 weeks PMA than infants who passed (median 19 weeks (IQR 15–33) versus 2 weeks (IQR 1–8, p<0.001)), which persisted after multivariable adjustment (hazard ratio −1.42, 95% CI −1.94 to −0.91, p<0.001). Infants failing RAC also had more frequent and longer duration of home oxygen use. Conclusion: RAC may help provide anticipatory guidance regarding duration of respiratory support for infants with BPD.

We present the case of a breast-fed preterm infant with postnatally acquired cytomegalovirus (CMV) and severe necrotizing enterocolitis (NEC) associated with CMV. The infant had persistent severe thrombocytopenia with clinical deterioration despite multiple platelet transfusions and maximal medical treatment. Surgical intervention was not feasible owing to the instability of the infant's condition. Upon identification of CMV in urine, intravenous ganciclovir was initiated with significant clinical improvement. We also present a literature review of cases of CMV-related NEC or other gastrointestinal complications in preterm and term infants.

Consumption of a high salt (HS) diet results in vascular oxidant stress and impairs endothelium‐dependent relaxation in a variety of human and experimental models. Nuclear factor erythroid‐2‐related factor 2 (Nrf2) is a transcription factor that induces the expression of many critical antioxidant genes. We measured protein expression of Nrf2 and its cytosolic inhibitor, kelch‐like ECH‐associated protein 1 (Keap1), in mesenteric and cerebral arterial homogenates from Sprague‐Dawley (SD) rats fed HS (4% NaCl), low salt (LS), or HS with low dose angiotensin II (ANG II) infusion to restore normal plasma ANG II levels. While Nrf2 expression was similar between groups, Keap1 expression was significantly lower in ANG II‐infused rats (p < 0.05). The Nrf2:Keap1 ratio normalized to LS was significantly increased in both mesenteric (LS = 100.00% ± 19.76; HS = 176.34% ± 29.98; HS + ANG II = 561.44% ± 210.39) and cerebral (LS = 100.00% ± 16.21; HS = 181.67% ± 69.31; HS + ANG II = 677.55% ± 172.38) arterial beds. The dietary supplement Protandim, shown to induce Nrf2 expression, improved endothelium‐dependent relaxation to acetylcholine in salt‐fed SD rats (HS = 0.50 μm ± 0.96; HS + Protandim = 6.67 μm ± 1.28; p = 0.008) and hamsters (HS = 1.33 μm ± 0.52; HS + Protandim = 5.60 μm ± 0.68; p < 0.001 ). Together, these data suggest a functional role for the Nrf2 antioxidant defense system in preventing salt‐induced vascular dysfunction.