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Two-year outcomes after dextrose gel prophylaxis for neonatal hypoglycaemia
  1. Rebecca Griffith1,
  2. Joanne Elizabeth Hegarty2,
  3. Jane M Alsweiler1,2,
  4. Greg D Gamble3,
  5. Robyn May3,
  6. Christopher Joel Dorman McKinlay3,4,
  7. Benjamin Thompson5,6,
  8. Trecia Ann Wouldes7,
  9. Jane E Harding3
  1. 1 Department of Paediatrics: Child and Youth Health, The University of Auckland, Auckland, New Zealand
  2. 2 Newborn Services, Auckland City Hospital, Auckland, New Zealand
  3. 3 Liggins Institute, University of Auckland, Auckland, New Zealand
  4. 4 Kids First Neonatal Care, Counties District Health Board, Auckland, New Zealand
  5. 5 Optometry and Vision Science, University of Waterloo, Waterloo, Ontario, Canada
  6. 6 Optometry and Vision Science, University of Auckland, Auckland, New Zealand
  7. 7 Psychological Medicine, University of Auckland, Auckland, New Zealand
  1. Correspondence to Professor Jane E Harding, Liggins Institute, University of Auckland, Auckland 1142, New Zealand; j.harding{at}


Objective To determine the effect of prophylactic dextrose gel for prevention of neonatal hypoglycaemia on neurodevelopment and executive function at 2 years’ corrected age.

Design Prospective follow-up of a randomised trial.

Setting New Zealand.

Patients Participants from the pre-hypoglycaemia Prevention with Oral Dextrose (pre-hPOD) trial randomised to one of four dose regimes of buccal 40% dextrose gel or equivolume placebo.

Main outcome measures Coprimary outcomes were neurosensory impairment and executive function. Secondary outcomes were components of the primary outcomes, neurology, anthropometry and health measures.

Results We assessed 360 of 401 eligible children (90%) at 2 years’ corrected age. There were no differences between dextrose gel dose groups, single or multiple dose groups, or any dextrose and any placebo groups in the risk of neurosensory impairment or low executive function (any dextrose vs any placebo neurosensory impairment: relative risk (RR) 0.77, 95% CI 0.50 to 1.19, p=0.23; low executive function: RR 0.50, 95% CI 0.24 to 1.06, p=0.07). There were also no differences between groups in any secondary outcomes. There was no difference between children who did or did not develop neonatal hypoglycaemia in the risk of neurosensory impairment (RR 1.05, 95% CI 0.68 to 1.64, p=0.81) or low executive function (RR 0.73, 95% CI 0.34 to 1.59, p=0.43).

Conclusion Prophylactic dextrose gel did not alter neurodevelopment or executive function and had no adverse effects to 2 years’ corrected age, but this study was underpowered to detect potentially clinically important effects on neurosensory outcomes.

  • neonatology
  • neurology
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  • Contributors Contributed equally to this paper: RG and JoH. Conceptualisation/ design: JoH, JMA, BT and JaneH. Assessments: RG, JoH, CJDMcK and TAW. Data analysis: RG, RM, GDG and JaneH. Contributed analysis tools: GDG and RM. Drafted the initial manuscript: RG.

  • Funding This study was funded by Lottery Health Research (241266), Cure Kids (3561), philanthropic donations to the University of Auckland Foundation (F-ILG-LRSR), Health Research Council of New Zealand (15-216), Gravida, National Centre for Growth and Development (SCH-14-14 Hegarty), Eunice Kennedy Shriver National Institute of Child Health & Human Development, National Institutes of Health (R01HD091075). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. RG received a fellowship in 2016 from the New Zealand Diabetes Foundation.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Ethics approval Ethics approval was obtained from the Health and Disability Ethics Committees of New Zealand (13/NTA/8) and caregivers gave written informed consent.

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

  • Data availability statement Data are available upon reasonable request. Published data are available to approved researchers under the data sharing arrangements provided by the Maternal and Perinatal Central Coordinating Research Hub (CCRH), based at the Liggins Institute, University of Auckland ( Metadata, along with instructions for data access, are available at the University of Auckland’s research data repository, Figshare ( Data access requests are to be submitted to Data Access Committee via De-identified published data will be shared with researchers who provide a methodologically sound proposal and have appropriate ethical and institutional approval. Researchers must sign and adhere to the Data Access Agreement that includes a commitment to using the data only for the specified proposal, to refrain from any attempt to identify individual participants, to store data securely and to destroy or return the data after completion of the project. The CCRH reserves the right to charge a fee to cover the costs of making data available, if required.

  • 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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