Publications by authors named "Rakhee Bowker"

6 Publications

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Evaluation of vitamin D protocol in the neonatal intensive care unit at Rush University Medical Center.

JPEN J Parenter Enteral Nutr 2021 Jun 14. Epub 2021 Jun 14.

Division of Neonatology, Department of Pediatrics, Rush University Medical Center, Chicago, Illinois, USA.

Background: In 2017, the neonatal intensive care unit (NICU) at Rush University Medical Center (RUMC) implemented a protocol to provide individualized vitamin D supplementation dosing for very low-birth-weight (VLBW) and very preterm infants. This study evaluated the association of demographic and socioeconomic factors, vitamin D dose, and health indicators, including bone mineral status, measured by alkaline phosphatase and phosphorus levels; linear growth velocity; and occurrence of fractures.

Method: This retrospective cross-sectional study included 227 VLBW or very preterm infants (34 VLBW, 12 very preterm, and 181 VLBW and very preterm) born in and discharged from the RUMC NICU between February 1, 2017, and October 31, 2019. Vitamin D dose was classified as adjusted (supplemental dose of 800 IU/day, n = 169) or standard (recommended dose of 400 IU/day, n = 58), per the protocol. Binary logistic and linear regression models were constructed to test the associations between infant and maternal characteristics and vitamin D dose group and between vitamin D dose group and health indicators.

Results: The analysis found a statistically significant association between maternal age, gestational age, infant birth weight, and race/ethnicity and receipt of an adjusted vitamin D dose. No significant associations were found between health indicators and vitamin D dose.

Conclusion: Sociodemographic factors may influence vitamin D deficiency in VLBW and very preterm infants in the NICU. At this time, there is insufficient evidence to support a tailored approach, but further research in this area is warranted.
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http://dx.doi.org/10.1002/jpen.2138DOI Listing
June 2021

Maternal production of milk for infants in the neonatal intensive care unit.

Semin Perinatol 2021 Mar 2;45(2):151381. Epub 2021 Jan 2.

Department of Pediatrics, Division of Neonatology, Rush University Medical Center, Chicago, USA.

Mother's own milk (MOM) feeding is a cost-effective strategy to reduce risks of comorbidities associated with prematurity and improve long-term health of infants hospitalized in the Neonatal Intensive Care Unit (NICU). Significant racial and socioeconomic disparities exist in MOM provision in the NICU, highlighting the importance of developing strategies to reduce these disparities. Mothers of infants in the NICU experience many health concerns which may negatively impact lactation physiology. Objective measures of lactation physiology are limited but may assist in identifying mothers at particular risk. Several strategies to assist mothers of hospitalized infants are essential, including maternal education, qualified lactation professionals, early and frequent milk expression with a hospital-grade double electric breast pump, and providing support for transitioning to direct breastfeeding prior to discharge from the NICU.
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http://dx.doi.org/10.1016/j.semperi.2020.151381DOI Listing
March 2021

Mother's own milk dose is associated with decreased time from initiation of feedings to discharge and length of stay in infants with gastroschisis.

J Perinatol 2020 08 28;40(8):1222-1227. Epub 2020 Jan 28.

Section of Neonatology, Department of Pediatrics, Rush University Medical Center, Chicago, IL, 60612, USA.

Objective: To determine if mother's own milk (MOM) dose after gastroschisis repair is associated with time from feeding initiation to discharge. Secondary outcomes included parenteral nutrition (PN) duration and length of stay (LOS).

Study Design: Retrospective study of 44 infants with gastroschisis examined demographics, gastroschisis type, PN days, timing of nutrition milestones, feeding composition, and LOS.

Results: MOM dose was significantly associated with shorter time to discharge from feeding initiation (adjusted hazard ratio [HR] for discharge per 10% increase in MOM dose, 1.111; 95% CI, 1.011-1.220, p = 0.029). MOM dose was also significantly associated with shorter LOS (adjusted HR for discharge per 10% increase in MOM dose, 1.130; 95% CI, 1.028-1.242, p = 0.011).

Conclusions: MOM dose was significantly associated with a decrease in time to discharge from feeding initiation and LOS in a dose-dependent manner. Mothers of gastroschisis patients should receive education and proactive lactation support to optimize MOM volume for feedings.
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http://dx.doi.org/10.1038/s41372-020-0595-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7223788PMC
August 2020

Intestinal microcirculation and necrotizing enterocolitis: The vascular endothelial growth factor system.

Semin Fetal Neonatal Med 2018 12 6;23(6):411-415. Epub 2018 Sep 6.

Division of Neonatology, Department of Pediatrics, Ann & Robert H. Lurie Children's Hospital of Chicago, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA; Center for Intestinal and Liver Inflammation Research, Stanley Manne Children's Research Institute, Ann & Robert H. Lurie Children's Hospital of Chicago, Northwestern University, Chicago, IL, USA. Electronic address:

Necrotizing enterocolitis (NEC), a leading cause of morbidity and mortality in preterm neonates, is a devastating disease characterized by intestinal tissue inflammation and necrosis. NEC pathogenesis is multifactorial but remains unclear. Translocation of bacteria and/or bacterial products across a weak intestinal barrier in the setting of impaired mucosal immunity leads to an exaggerated inflammatory response and secondary mucosal epithelial injury. In addition to prematurity, other risk factors for NEC include congenital heart disease, maternal pre-eclampsia with placental vascular insufficiency, severe anemia and blood transfusion - all conditions that predispose the intestine to ischemia. We recently found that maldevelopment of the intestinal microvasculature plays an important role in NEC pathogenesis. Here we review the evidence supporting a role for defective development of the intestinal mucosal microvasculature and perturbations of intestinal blood flow in NEC, emphasizing the importance of vascular endothelial growth factor (VEGF) and the VEGF receptor-2 signaling pathway.
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http://dx.doi.org/10.1016/j.siny.2018.08.008DOI Listing
December 2018

Dimethyloxalylglycine preserves the intestinal microvasculature and protects against intestinal injury in a neonatal mouse NEC model: role of VEGF signaling.

Pediatr Res 2018 02 25;83(2):545-553. Epub 2017 Oct 25.

Division of Neonatology, Department of Pediatrics, Ann and Robert H. Lurie Children's Hospital of Chicago, Northwestern University, Feinberg School of Medicine, Chicago, Illinois.

BackgroundNecrotizing enterocolitis (NEC) is a devastating neonatal disease characterized by intestinal necrosis. Hypoxia-inducible factor-1α (HIF-1α) has a critical role in cellular oxygen homeostasis. Here, we hypothesized that prolyl hydroxylase (PHD) inhibition, which stabilizes HIF-1α, protects against NEC by promoting intestinal endothelial cell proliferation and improving intestinal microvascular integrity via vascular endothelial growth factor (VEGF) signaling.MethodsTo assess the role of PHD inhibition in a neonatal mouse NEC model, we administered dimethyloxalylglycine (DMOG) or vehicle to pups before or during the NEC protocol, and determined mortality and incidence of severe intestinal injury. We assessed intestinal VEGF by western blot analysis and quantified endothelial cell and epithelial cell proliferation following immunofluorescence.ResultsDMOG decreased mortality and incidence of severe NEC, increased intestinal VEGF expression, and increased intestinal villus endothelial and epithelial cell proliferation in experimental NEC. Inhibiting VEGFR2 signaling eliminated DMOG's protective effect on intestinal injury severity, survival, and endothelial cell proliferation while sparing DMOG's protective effect on intestinal epithelial cell proliferation.ConclusionDMOG upregulates intestinal VEGF, promotes endothelial cell proliferation, and protects against intestinal injury and mortality in experimental NEC in a VEGFR2 dependent manner. DMOG's protective effect on the neonatal intestinal mucosa may be mediated via VEGFR2 dependent improvement of the intestinal microvasculature.
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http://dx.doi.org/10.1038/pr.2017.219DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5866158PMC
February 2018

Effect of red blood cell storage time on markers of hemolysis and inflammation in transfused very low birth weight infants.

Pediatr Res 2017 Dec 16;82(6):964-969. Epub 2017 Aug 16.

Division of Neonatology, Department of Pediatrics, College of Physicians and Surgeons, Columbia University, New York, New York.

BackgroundProlonged storage of transfused red blood cells (RBCs) is associated with hemolysis in healthy adults and inflammation in animal models. We aimed to determine whether storage duration affects markers of hemolysis (e.g., serum bilirubin, iron, and non-transferrin-bound iron (NTBI)) and inflammation (e.g., interleukin (IL)-8 and monocyte chemoattractant protein (MCP)-1) in transfused very low birth weight (VLBW) infants.MethodsBlood samples from 23 independent transfusion events were collected by heel stick before and 2-6 h after transfusion.ResultsSerum iron, total bilirubin, NTBI, and MCP-1 levels were significantly increased after transfusion of RBCs (P<0.05 for each comparison). The storage age of transfused RBCs positively correlated with increases in NTBI following transfusion (P<0.001; R=0.44). No associations between storage duration and changes in the other analytes were observed.ConclusionTransfusion of RBCs into VLBW infants is associated with increased markers of hemolysis and the inflammatory chemokine MCP-1. RBC-storage duration only correlated with increases in NTBI levels following transfusion. NTBI was only observed in healthy adults following 35 days of storage; however, this study suggests that VLBW infants are potentially more susceptible to produce this pathological form of iron, with increased levels observed after transfusion of only 20-day-old RBCs.
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http://dx.doi.org/10.1038/pr.2017.177DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5685900PMC
December 2017
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