Enhanced feeding in very-low-birth-weight infants may cause electrolyte disturbances and septicemia – A randomized, controlled trial

Moltu, Sissel J.; Strømmen, Kenneth; Blakstad, Elin Wahl; Almaas, Astrid Nylander; Westerberg, Ane Cecilie; Brække, Kristin; Rønnestad, Arild; Nakstad, Britt; Berg, Jens Petter; Veierød, Marit B.; Haaland, Kirsti; Iversen, Per Ole; Drevon, Christian A.

doi:10.1016/j.clnu.2012.09.004

Cited by 140 publications

(179 citation statements)

References 27 publications

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“…It was reported that IUGR infants had reduced serum P concentration, and showed hypophosphatemia (Moltu et al, 2013) and that bone mineralization was affected (Abrams et al, 1988;. In the present study, IUGR pigs had lower P level in the LDM than NBW pigs.…”

Section: Discussionsupporting

confidence: 53%

“…However, the safety of early nutrient enhancement of IUGR needs to be further evaluated, as it may cause adult obesity (Desai et al, 2005;Desai et al, 2007) and more severe mineral disturbance (Moltu et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

“…Most of these studies focus on bone development and calcium or phosphorus metabolism via determining mineral concentrations in serum or bone (Prestridge et al, 1993;. However, essential minerals are abundant in tissues, in which they are critical for electrolyte balance and nutrient metabolism through being involved in the activities of enzymes (Moltu et al, 2013;Gupta et al, 2014;Gharibzahedi & Jafari, 2017). For example, Mg-deficient foetal livers of IUGR mice are accompanied by low monounsaturated fatty acids (MUFAs), high polyunsaturated fatty acids (PUFAs), and low desaturase and elongase mRNA expression (Gupta et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Altered tissue mineralization, increased hepatic lipid and inhibited autophagy in intrauterine growth retardation piglets

Wang¹,

Zheng²,

Siyal³

et al. 2018

SA J. An. Sci.

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Mineral homeostasis is often disrupted in intrauterine growth retardation (IUGR) infants. Most studies focus on calcium or phosphorus metabolism of IUGR infants via determining serum mineral concentrations instead of tissues. This study was conducted to investigate the effects of IUGR on the mineralization and physiological functions of tissue in a piglet model. Six normal birth weight (NBW) and six IUGR neonatal piglets were slaughtered at 35 days. Mineral concentrations in blood and selected tissues (liver, kidney, lungs, heart, and longissimus dorsi muscle (LDM)), hepatic lipid, mRNA expressions of magnesium (Mg) metabolism, and autophagy were analysed. Results showed that IUGR pigs showed significantly lower phosphorus (P) in LDM, and lower Mg in the liver and LDM, and higher Mg in lungs than NBW pigs. There were no significant differences in concentrations of selenium (Se), calcium (Ca), copper (Cu), aluminium (Al), and lithium (Li) in selected tissues. IUGR pigs had similar mRNA expression of TRPM7 and MagT1 to NBW pigs, but significantly lower expressions of HNF1B and Mrs2 in the liver than NBW pigs. Hepatic triglyceride was significantly increased, and MAP1LC3B expression was significantly decreased in IUGR pigs compared with those of NBW pigs. These result suggested that IUGR pigs had tissue mineralization disturbance, especially for Mg, and liver dysfunction (increased hepatic lipid and inhibited autophagy). Hepatic Mg deficiency might result from increased Mg efflux via reducing HNF1B expression. ______________________________________________________________________________________

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Altered tissue mineralization, increased hepatic lipid and inhibited autophagy in intrauterine growth retardation piglets

Wang¹,

Zheng²,

Siyal³

et al. 2018

SA J. An. Sci.

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“…66 The authors terminated the study early as there was an increased rate of sepsis in the intervention group and an association between low serum phosphate levels in the intervention group (despite increased phosphate delivery) and sepsis. In our study both groups received similar intake of electrolytes and there was no significant difference in the incidence of abnormalities in electrolytes.…”

Section: Resultsmentioning

confidence: 99%

Nutritional Evaluation and Optimisation in Neonates (NEON) trial of amino acid regimen and intravenous lipid composition in preterm parenteral nutrition: a randomised double-blind controlled trial

et al. 2016

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Health. This issue may be freely reproduced for the purposes of private research and study and extracts (or indeed, the full report) may be included in professional journals provided that suitable acknowledgement is made and the reproduction is not associated with any form of advertising.The WestminsterResearch online digital archive at the University of Westminster aims to make the research output of the University available to a wider audience. Copyright and Moral Rights remain with the authors and/or copyright owners.Whilst further distribution of specific materials from within this archive is forbidden, you may freely distribute the URL of WestminsterResearch: ((http://westminsterresearch.wmin.ac.uk/).In case of abuse or copyright appearing without permission e-mail repository@westminster.ac.uk This journal is a member of and subscribes to the principles of the Committee on Publication Ethics (COPE) (www.publicationethics.org/). EFFICACY AND MECHANISM EVALUATION Efficacy and Mechanism EvaluationEditorial contact: nihredit@southampton.ac.ukThe full EME archive is freely available to view online at www.journalslibrary.nihr.ac.uk/eme. Print-on-demand copies can be purchased from the report pages of the NIHR Journals Library website: www.journalslibrary.nihr.ac.uk Criteria for inclusion in the Efficacy and Mechanism Evaluation journalReports are published in Efficacy and Mechanism Evaluation (EME) if (1) they have resulted from work for the EME programme, and (2) they are of a sufficiently high scientific quality as assessed by the reviewers and editors. EME programmeThe Efficacy and Mechanism Evaluation (EME) programme was set up in 2008 as part of the National Institute for Health Research (NIHR) and the Medical Research Council (MRC) coordinated strategy for clinical trials. The EME programme is broadly aimed at supporting 'science driven' studies with an expectation of substantial health gain and aims to support excellent clinical science with an ultimate view to improving health or patient care.Its remit includes evaluations of new treatments, including therapeutics (small molecule and biologic), psychological interventions, public health, diagnostics and medical devices. Treatments or interventions intended to prevent disease are also included.The EME programme supports laboratory based or similar studies that are embedded within the main study if relevant to the remit of the EME programme. Studies that use validated surrogate markers as indicators of health outcome are also considered.For more information about the EME programme please visit the website: http://www.nets.nihr.ac.uk/programmes/eme This reportThe research reported in this issue of the journal was funded by the EME programme as project number 08/99/04. The contractual start date was in February 2010. The final report began editorial review in January 2015 and was accepted for publication in October 2015. The authors have been wholly responsible for all data collection, analysis and interpretation, and for writing up their work. The EME edit...

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“…It is highly probable that in extremely preterm infants, longterm parenteral supplementation with commercial AA solutions, which deviate from physiological fetal plasma AA concentrations, causes unbalanced plasma AAs in the preterm newborn and is partially responsible for worse short and long-term outcomes. Norwegian pediatricians observed a higher occurrence of septicemia in the verylow-birth-weight infants (63% vs. 29%) that received an enhanced feeding protocol (AA = 3.5 g/kg/day) within 24 h after birth [25]. In connection with these critically important functions of AAs, we assume that long-term supplementation with poorly balanced AAs from commercial AA-infusions (in utero and/or postpartum) could have led to worse outcomes of extremely preterm infants in our pilot study.…”

Section: Discussionmentioning

confidence: 99%

The effect of intraumbilical fetal nutrition via subcutaneously implanted port system on amino acid concentration by severe IUGR human fetuses

Winarno

Bapayeva

Bergner

et al. 2015

Geburtshilfe Frauenheilkd

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Objective: To determine if intrauterine intraumbilical supplementation with amino acids (AA) and glucose can improve neonatal outcome of severe growth restricted human fetuses (IUGR). Methods: Prospective pilot study of intrauterine treatment of severe IUGR fetuses [n = 14, 27 weeks of gestation (range 23-31)] with cerebroplacental ratio < 1, with longterm intraumbilical AA and glucose supplementation (10% of feto-placental blood volume/day) using a perinatal port system alone (n = 5) or combined with hyperbaric oxygenation (n = 1, HBO) vs. control group (n = 8). Results:The duration of continuous intraumbilical AA/ glucose supplementation was 11 (6-13) days. Daily intravascular fetal nutrition significantly prolonged the brain sparing to delivery interval by 24 (14-33) days vs. 5.6 (2-12) days in controls. Fetal nutrition reduced blood flow resistance in the placental circulation but did not affect the Doppler profile of cerebral arteries. Higher weight gain of 113.5 (36-539) g was observed following supplementation compared to 33.3 (8-98) g in the control group (P< 0.05). In spite of this, fetuses below 28 weeks of gestation did not sufficiently benefit from infused commercial AA. We found a reduced fetal plasma concentration of the essential AA histidine, threonine, lysine and arginine, and non-essential AA taurine, in severe IUGR fetuses in both groups. Longterm supplementation with a commercial AA formula led to a slight, but not significant, reduction of histidine, threonine, lysine, arginine, asparagine and glutamine. However, the concentration of tryptophan and glutamic acid slightly increased. HBO can be combined with AA supplementation via a port system. In one case, the port system was also successfully used for fetal blood transfusion. Conclusions: Intravascular treatment of IUGR with fetal nutrition can prolong pregnancy with severe placental insufficiency and brain sparing for many weeks. However, rather than normalizing AA concentrations, an enhanced AA imbalance was observed in IUGR fetuses following supplementation. These deviations in AA concentrations prevent the recommendation for use of commercial AA solutions for prenatal treatment of extreme preterm IUGR fetuses.

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Enhanced feeding in very-low-birth-weight infants may cause electrolyte disturbances and septicemia – A randomized, controlled trial

Cited by 140 publications

References 27 publications

Altered tissue mineralization, increased hepatic lipid and inhibited autophagy in intrauterine growth retardation piglets

Altered tissue mineralization, increased hepatic lipid and inhibited autophagy in intrauterine growth retardation piglets

Nutritional Evaluation and Optimisation in Neonates (NEON) trial of amino acid regimen and intravenous lipid composition in preterm parenteral nutrition: a randomised double-blind controlled trial

The effect of intraumbilical fetal nutrition via subcutaneously implanted port system on amino acid concentration by severe IUGR human fetuses

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