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Effect of prophylactic dextrose gel on the neonatal gut microbiome
  1. Sophie L St Clair1,
  2. Jane E Harding1,
  3. Justin M O’Sullivan1,
  4. Gregory D Gamble1,
  5. Jane M Alsweiler2,3,
  6. Tommi Vatanen1,4
  7. for the hPOD Study Group
  1. 1 Liggins Institute, The University of Auckland, Auckland, New Zealand
  2. 2 Department of Paediatrics: Child and Youth Health, The University of Auckland, Auckland, New Zealand
  3. 3 Newborn Services, Auckland City Hospital, Auckland, New Zealand
  4. 4 The Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA
  1. Correspondence to Professor Jane E Harding, Liggins Institute, The University of Auckland, Auckland, New Zealand; j.harding{at}auckland.ac.nz

Abstract

Objective To determine the effect of prophylactic dextrose gel on the infant gut microbiome.

Design Observational cohort study nested in a randomised trial.

Setting Three maternity hospitals in New Zealand.

Patients Infants at risk of neonatal hypoglycaemia whose parents consented to participation in the hypoglycaemia Prevention in newborns with Oral Dextrose trial (hPOD). Infants were randomised to receive prophylactic dextrose gel or placebo gel, or were not randomised and received no gel (controls). Stool samples were collected on days 1, 7 and 28.

Main outcome measures The primary outcome was microbiome beta-diversity at 4 weeks. Secondary outcomes were beta-diversity, alpha-diversity, bacterial DNA concentration, microbial community stability and relative abundance of individual bacterial taxa at each time point.

Results We analysed 434 stool samples from 165 infants using 16S rRNA gene amplicon sequencing. There were no differences between groups in beta-diversity at 4 weeks (p=0.49). There were also no differences between groups in any other microbiome measures including beta-diversity (p=0.53 at day 7), alpha-diversity (p=0.46 for day 7 and week 4), bacterial DNA concentration (p=0.91), microbial community stability (p=0.52) and microbial relative abundance at genus level. There was no evidence that exposure to any dextrose gel (prophylaxis or treatment) had any effect on the microbiome. Mode of birth, type of milk fed, hospital of birth and ethnicity were all associated with differences in the neonatal microbiome.

Conclusions Clinicians and consumers can be reassured that dextrose gel used for prophylaxis or treatment of neonatal hypoglycaemia does not alter the neonatal gut microbiome.

Trial registration number 12614001263684.

  • neonatology
  • infant development
  • intensive care units
  • neonatal
  • microbiology

Data availability statement

Data are available in a public, open access repository. Data are available on reasonable request. The sequencing data and subject information to reproduce the microbiome analyses are available in the NCBI Sequence Read Archive under BioProject PRJNA738266.

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Data availability statement

Data are available in a public, open access repository. Data are available on reasonable request. The sequencing data and subject information to reproduce the microbiome analyses are available in the NCBI Sequence Read Archive under BioProject PRJNA738266.

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Footnotes

  • Twitter @DrJOSull

  • Contributors Conceptualisation: JEH, JMO’S, GDG, JMA and TV. Data curation: JEH, JMO’S, GDG and TV. Formal analysis: SLSC, GDG and TV. Funding acquisition: JEH, TV and JMO’S. Investigation: JEH, SLSC, TV and JMO’S. Methodology: JEH, JMO’S, GDG, JMA and TV. Project administration: JEH and TV. Resources: JEH, JMO’S and TV. Supervision: JEH and TV. Writing – original draft: SLSC. Writing – review and editing: SLSC, JEH, JMO’S, GDG and TV. JEH takes overall responsibility for the work as guarantor.

  • Funding The hPOD trial was funded by a grant from the Health Research Council of New Zealand (13/131). The microbiome analyses were funded by the Liggins Institute New Staff Research Fund (3717847). SLSC was funded by a clinical research internship from the Aotearoa Foundation (9909494). JEH was funded in part by a grant from the Eunice Kennedy Shriver National Institute of Child Health & Human Development of the National Institutes of Health (R01HD091075). The content is solely the responsibility of the authors and does not necessarily represent the official views of the Eunice Kennedy Shriver National Institute of Child Health and Human Development or the National Institutes of Health.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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