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Vitamin A in prevention of bronchopulmonary dysplasia
Hercília Guimarães1, Maria Beatriz Guedes, Gustavo Rocha
1São João Hospital, Porto, Portugal. herciliaguimaraes@gmail.com
Insights
Vitamin A supplementation may reduce death or bronchopulmonary dysplasia (BPD) in preterm infants. Antenatal vitamin A combined with neonatal supplementation shows promise in preventing BPD, especially in deficient areas.
Area of Science:
- Neonatology
- Pediatric Pulmonology
- Nutritional Science
Background:
- Bronchopulmonary dysplasia (BPD) affects a significant portion of very preterm infants.
- Oxygen toxicity and lower vitamin A levels may contribute to BPD pathogenesis.
- Vitamin A is crucial for fetal lung growth, surfactant production, and immune modulation.
Purpose of the Study:
- To evaluate the role of vitamin A supplementation in preventing BPD in very low birth weight (VLBW) infants.
- To assess the impact of antenatal and neonatal vitamin A administration on BPD development.
- To explore the long-term neurodevelopmental outcomes associated with vitamin A supplementation.
Main Methods:
- Review of evidence on vitamin A supplementation in VLBW infants.
- Analysis of parenteral vitamin A administration as a preventive therapy for BPD.
- Examination of antenatal vitamin A administration combined with neonatal supplementation.
Main Results:
- Parenteral vitamin A supplementation is a recommended preventive therapy for BPD (NNT 12).
- No clear benefit or harm on long-term neurodevelopmental status or cerebral palsy was observed.
- Antenatal vitamin A with neonatal supplementation may be more effective in preventing BPD in vitamin A-deficient areas.
Conclusions:
- Vitamin A supplementation shows promise in reducing BPD and mortality in VLBW infants.
- Further trials are needed to evaluate intravenous vitamin A emulsions, prenatal/postnatal combinations, and high-dose vitamin A in extremely low birth weight (ELBW) infants.
Abstract:
Bronchopulmonary dysplasia (BPD) remains one of the most serious challenges in the care of the very preterm infants, affecting approximately one-quarter of infants born < 1500g birth weight and 30% < 1000g. Oxygen toxicity may contribute to its pathogenesis. Vitamin A concentrations are lower in BPD infants which may result in a reduction of the antioxidant protection. It has been found to up regulate genes necessary for fetal lung growth and increase surfactant production in animal models and is also involved in the modulation of immunological and inflammatory responses by regulation of cytokine production. Retinoic acid plays a key role in lung development improving alveolar septation. Evidence exists that vitamin A supplementation for very low birth weight (VLBW) infants, beyond that routinely given in multivitamin preparations, is associated with a reduction in death or BPD. So, parenteral administration of vitamin A to the newborn is one of the current recommended preventive therapies for BPD (number needed to treat 12; 95% CI: 6-94; The information on long-term neurodevelopmental status suggests no evidence of either benefit or harm. Estimates for cerebral palsy range from a number needed to treat of 11 to a number needed to harm of 33. Nowadays, it seems that administration of antenatal vitamin A to the mother in late pregnancy associated with neonatal supplementation can better prevent the development of BPD in areas of endemic vitamin A deficiency. The benefits, in terms of vitamin A status, safety and acceptability of delivering vitamin A in an intravenous emulsion compared with repeat intramuscular injections, the association of vitamin A prenatal and postnatal, as well as the effectiveness and safety of administered high dose vitamin A in ELBW infants await evaluation and should be assessed in further trials.
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