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Neonatology. 2018;113(4):366-378. doi: 10.1159/000487388. Epub 2018 Mar 7.

Update on Vitamin E and Its Potential Role in Preventing or Treating Bronchopulmonary Dysplasia.

Author information

1
Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
2
Division of Neonatology, Department of Pediatrics, Oregon Health and Science University, Portland, Oregon, USA.
3
Division of Neonatology, Department of Pediatrics, Albert Einstein College of Medicine and the Children's Hospital at Montefiore, Bronx, New York, USA.
4
Division of Allergy, Immunology and Pulmonary Medicine, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
5
Division of Allergy-Immunology, Department of Medicine, Northwestern University School of Medicine, Chicago, Illinois, USA.
6
Division of Neonatology, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Abstract

Vitamin E is obtained only through the diet and has a number of important biological activities, including functioning as an antioxidant. Evidence that free radicals may contribute to pathological processes such as bronchopulmonary dysplasia (BPD), a disease of prematurity associated with increased lung injury, inflammation and oxidative stress, led to trials of the antioxidant vitamin E (α-tocopherol) to prevent BPD with variable results. These trials were all conducted at supraphysiologic doses and 2 of these trials utilized a formulation containing a potentially harmful excipient. Since 1991, when the last of these trials was conducted, both neonatal management strategies for minimizing oxygen and ventilator-related lung injury and our understanding of vitamin E isoforms in respiratory health have advanced substantially. It is now known that there are differences between the effects of vitamin E isoforms α-tocopherol and γ-tocopherol on the development of respiratory morbidity and inflammation. What is not known is whether improvements in physiologic concentrations of individual or combinations of vitamin E isoforms during pregnancy or following preterm birth might prevent or reduce BPD development. The answers to these questions require adequately powered studies targeting pregnant women at risk of preterm birth or their premature infants immediately following birth, especially in certain subgroups that are at increased risk of vitamin E deficiency (e.g., smokers). The objective of this review is to compile, update, and interpret what is known about vitamin E isoforms and BPD since these first studies were conducted, and suggest future research directions.

KEYWORDS:

Bronchopulmonary dysplasia; Chronic lung disease of prematurity; Oxidative stress; Tocopherol; Vitamin E; α-Tocopherol; γ-Tocopherol

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