Modification of serum fatty acids in preterm infants by parenteral lipids and enteral docosahexaenoic acid/arachidonic acid: A secondary analysis of the Mega Donna Mega trial.

Arachidonic acid Docosahexaenoic acid Extremely preterm infants Intravenous lipid emulsion LCPUFA Parenteral nutrition

Journal

Clinical nutrition (Edinburgh, Scotland)
ISSN: 1532-1983
Titre abrégé: Clin Nutr
Pays: England
ID NLM: 8309603

Informations de publication

Date de publication:
06 2023
Historique:
received: 24 01 2023
revised: 13 04 2023
accepted: 14 04 2023
medline: 16 6 2023
pubmed: 30 4 2023
entrez: 30 4 2023
Statut: ppublish

Résumé

Preterm infants risk deficits of long-chain polyunsaturated fatty acids (LCPUFAs) that may contribute to morbidities and hamper neurodevelopment. We aimed to determine longitudinal serum fatty acid profiles in preterm infants and how the profiles are affected by enteral and parenteral lipid sources. Cohort study analyzing fatty acid data from the Mega Donna Mega study, a randomized control trial with infants born <28 weeks of gestation (n = 204) receiving standard nutrition or daily enteral lipid supplementation with arachidonic acid (AA):docosahexaenoic acid (DHA) (100:50 mg/kg/day). Infants received an intravenous lipid emulsion containing olive oil:soybean oil (4:1). Infants were followed from birth to postmenstrual age 40 weeks. Levels of 31 different fatty acids from serum phospholipids were determined by GC-MS and reported in relative (mol%) and absolute concentration (μmol l Higher parenteral lipid administration resulted in lower serum proportion of AA and DHA relative to other fatty acids during the first 13 weeks of life (p < 0.001 for the 25th vs the 75th percentile). The enteral AA:DHA supplement increased the target fatty acids with little impact on other fatty acids. The absolute concentration of total phospholipid fatty acids changed rapidly in the first weeks of life, peaking at day 3, median (Q1-Q3) 4452 (3645-5466) μmol l Our data show that parenteral lipids aggravate the postnatal loss of LCPUFAs seen in preterm infants and that serum AA available for accretion is below that in utero. Further research is needed to establish optimal postnatal fatty acid supplementation and profiles in extremely preterm infants to promote development and long-term health. ClinicalTrials.gov, identifier: NCT03201588.

Sections du résumé

BACKGROUND & AIM
Preterm infants risk deficits of long-chain polyunsaturated fatty acids (LCPUFAs) that may contribute to morbidities and hamper neurodevelopment. We aimed to determine longitudinal serum fatty acid profiles in preterm infants and how the profiles are affected by enteral and parenteral lipid sources.
METHODS
Cohort study analyzing fatty acid data from the Mega Donna Mega study, a randomized control trial with infants born <28 weeks of gestation (n = 204) receiving standard nutrition or daily enteral lipid supplementation with arachidonic acid (AA):docosahexaenoic acid (DHA) (100:50 mg/kg/day). Infants received an intravenous lipid emulsion containing olive oil:soybean oil (4:1). Infants were followed from birth to postmenstrual age 40 weeks. Levels of 31 different fatty acids from serum phospholipids were determined by GC-MS and reported in relative (mol%) and absolute concentration (μmol l
RESULTS
Higher parenteral lipid administration resulted in lower serum proportion of AA and DHA relative to other fatty acids during the first 13 weeks of life (p < 0.001 for the 25th vs the 75th percentile). The enteral AA:DHA supplement increased the target fatty acids with little impact on other fatty acids. The absolute concentration of total phospholipid fatty acids changed rapidly in the first weeks of life, peaking at day 3, median (Q1-Q3) 4452 (3645-5466) μmol l
CONCLUSIONS
Our data show that parenteral lipids aggravate the postnatal loss of LCPUFAs seen in preterm infants and that serum AA available for accretion is below that in utero. Further research is needed to establish optimal postnatal fatty acid supplementation and profiles in extremely preterm infants to promote development and long-term health.
CLINICAL TRIAL REGISTRY
ClinicalTrials.gov, identifier: NCT03201588.

Identifiants

pubmed: 37120902
pii: S0261-5614(23)00133-4
doi: 10.1016/j.clnu.2023.04.020
pmc: PMC10512593
mid: NIHMS1932044
pii:
doi:

Substances chimiques

Docosahexaenoic Acids 25167-62-8
Fatty Acids 0
Arachidonic Acid 27YG812J1I
Phospholipids 0

Banques de données

ClinicalTrials.gov
['NCT03201588']

Types de publication

Randomized Controlled Trial Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

962-971

Subventions

Organisme : NEI NIH HHS
ID : R01 EY017017
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY030904
Pays : United States
Organisme : NICHD NIH HHS
ID : U54 HD090255
Pays : United States

Informations de copyright

Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.

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Auteurs

Ulrika Sjöbom (U)

Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Learning and Leadership for Health Care Professionals at the Institute of Health and Care Science at Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden. Electronic address: ulrika.sjobom@gu.se.

Mats X Andersson (MX)

Department of Biological and Environmental Sciences, University of Gothenburg, Gothenburg, Sweden. Electronic address: mats.andersson@bioenv.gu.se.

Aldina Pivodic (A)

Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: aldina.pivodic@gu.se.

Anna-My Lund (AM)

Lund University, Skåne University Hospital, Department of Clinical Sciences Lund, Pediatrics, Lund, Sweden. Electronic address: anna-my.lund@med.lu.se.

Mireille Vanpee (M)

Department of Women's and Children's Health, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden. Electronic address: mireille.vanpee@regionstockholm.se.

Ingrid Hansen-Pupp (I)

Lund University, Skåne University Hospital, Department of Clinical Sciences Lund, Pediatrics, Lund, Sweden. Electronic address: ingrid.pupp@med.lu.se.

David Ley (D)

Lund University, Skåne University Hospital, Department of Clinical Sciences Lund, Pediatrics, Lund, Sweden. Electronic address: david.ley@med.lu.se.

Dirk Wackernagel (D)

Department of Neonatology, Karolinska University Hospital and Institute, Astrid Lindgrens Children's Hospital, Stockholm, Sweden. Electronic address: dirk.wackernagel@regionstockholm.se.

Karin Sävman (K)

Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Region Västra Götaland, Department of Neonatology, The Queen Silvia Children's Hospital, Sahlgrenska University Hospital, Gothenburg, Sweden. Electronic address: karin.savman@pediat.gu.se.

Lois E H Smith (LEH)

The Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: lois.smith@childrens.harvard.edu.

Chatarina Löfqvist (C)

Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Learning and Leadership for Health Care Professionals at the Institute of Health and Care Science at Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden. Electronic address: chatarina.lofqvist@gu.se.

Ann Hellström (A)

Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: ann.hellstrom@medfak.gu.se.

Anders K Nilsson (AK)

Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: anders.k.nilsson@gu.se.

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