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.