Background Determine the tube-related complications and feeding outcomes of infants discharged home from the NICU with nasogastric (NG) tube feeding or gastrostomy (G-tube) feeding. Material & Methods We performed a chart review of 335 infants discharged from our NICU with home NG tube or G-tube feeding between January 2009 – December 2013. The primary outcome was the incidence of feeding tube-related complications requiring emergency department (ED) visits, hospitalizations, or deaths. Secondary outcome was feeding status at 6 months post-discharge. Univariate and multivariate analyses were conducted. Results There were 322 infants discharged with home enteral tube feeding, 84 NG tube and 238 G-tube, with available out-patient data for the 6 month post-discharge period. A total of 115 ED visits, 28 hospitalizations, and 2 deaths were due to a tube-related complication. The incidence of tube-related complications requiring an ED visit was significantly higher in the G-tube group compared to the NG tube group (33.6% vs 9.5%, p < 0.001). Two patients died due to a G-tube related complication. By 6 months post-discharge, full oral feeding was achieved in 71.4% of infants in the NG tube group compared to 19.3% in the G-tube group (p < 0.001). Type of feeding tube and percentage of oral feeding at discharge were significantly associated with continued tube feeding at 6 months post-discharge. Conclusion Home NG tube feeding is associated with fewer ED visits for tube-related complications compared to home G-tube feeding. There may be some infants who could benefit from a trial home NG tube feeding.

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.

BackgroundPhytosterols in soybean oil (SO) lipids likely contribute to parenteral nutrition-associated liver disease (PNALD) in infants. No characterization of phytosterol metabolism has been done in infants receiving SO lipids.MethodsIn a prospective cohort study, 45 neonates (36 SO lipid vs 9 control) underwent serial blood sample measurements of sitosterol, campesterol, and stigmasterol. Mathematical modeling was used to determine pharmacokinetic parameters of phytosterol metabolism and phytosterol exposure.ResultsCompared to controls, SO lipid-exposed infants had significantly higher levels of sitosterol and campesterol (p<0.01). During SO lipid infusion, sitosterol and campesterol reached half of steady-state plasma levels within 1.5 days and 0.8 days, respectively. Steady-state level was highest for sitosterol (1.68 mg/dL), followed by campesterol (0.98 mg/dL), and lowest for stigmasterol (0.01 mg/dL). Infants born < 28 weeks gestational age had higher sitosterol steady-state levels (p=0.03) and higher area under the curve for sitosterol (p=0.03) during the first 5 days of SO lipid (AUC5) than infants born ≥ 28 weeks gestational age.ConclusionPhytosterols in SO lipid accumulate rapidly in neonates. Very preterm infants receiving SO lipid have higher sitosterol exposure, and may have poorly developed mechanisms of eliminating phytosterols that may contribute to their vulnerability to PNALD.

Objective to describe neonatal intensive care unit (NICU) medical interventions and NICU mortality by birth weight and major anomaly types for infants with trisomy 13 (T13) or 18 (T18). Study Design retrospective cohort analysis of infants with T13 or T18 from 2005–12 in the Pediatrix Medical Group. We classified infants into 3 groups by associated anomaly type: neonatal surgical, non-neonatal surgical, and minor. Outcomes were NICU medical interventions and mortality. Results 841 infants were included from 186 NICUs. NICU mortality varied widely by anomaly type and birth weight, from 70% of infants <1500g with neonatal surgical anomalies to 31% of infants ≥2500g with minor anomalies. Infants ≥1500g without a neonatal surgical anomaly comprised 66% of infants admitted to the NICU; they had the lowest rates of NICU medical interventions and NICU mortality. Conclusions Risk stratification by anomaly type and birth weight may help provide more accurate family counseling for infants with T13 and T18.

Summary The cholesterol molecule is at the center of the pathophysiology of many vascular diseases. Whole-body cholesterol pools are maintained by a balance of endogenous synthesis, dietary absorption and elimination from our bodies. While the cellular aspects of cholesterol metabolism received significant impetus from the seminal work of Goldstein and Brown investigating LDL receptor trafficking, how dietary cholesterol was absorbed and eliminated was relatively neglected. The identification of the molecular defect a rare human disorder, Sitosterolemia, led to elucidation of a key mechanism of how we regulate the excretory pathway in the liver and in the intestine. Two proteins, ABCG5 and ABCG8, constitute a heterodimeric transporter that facilitates the extrusion of sterols from the cell into the biliary lumen, with a preference for xenosterols. This mechanism explained how dietary xenosterols are prevented from accumulating in our bodies. In addition, this disease has also highlighted the potential harm of xenosterols; macrothrombocytopenia, liver disease and endocrine disruption are seen when xenosterols accumulate. Mouse models of this disease suggest that there are more dramatic alterations of physiology, suggesting that these highly conserved mechanisms have evolved to prevent these xenosterols from accumulating in our bodies.