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Vitamin A deficiency and severe bronchopulmonary dysplasia in very low birthweight infants
R P Verma1, K M McCulloch, L Worrell
1Department of Pediatrics, University of Illinois, Chicago 60612, USA.
Insights
Persistent vitamin A deficiency in preterm infants is linked to a higher risk of severe bronchopulmonary dysplasia. This deficiency also correlates with delayed enteral feeding and lower vitamin A intake in these vulnerable infants.
Area of Science:
- Neonatalogy
- Nutritional Science
- Pediatric Pulmonology
Background:
- Preterm infants frequently exhibit low serum vitamin A levels.
- Prolonged vitamin A deficiency may contribute to bronchopulmonary dysplasia development.
Purpose of the Study:
- To investigate the association between persistent vitamin A deficiency and severe bronchopulmonary dysplasia in very low birthweight infants.
Main Methods:
- Retrospective analysis of 22 infants with birthweight <= 1250g requiring mechanical ventilation.
- Serum vitamin A concentrations measured serially from enteral feeding onset.
- Comparison of infants with low (< or = 11 mcg/dL) versus higher (> 11 mcg/dL) serum vitamin A levels after 10 days of age.
Main Results:
- Severe bronchopulmonary dysplasia incidence was significantly higher in the low vitamin A group (11/13) compared to the higher vitamin A group (1/9).
- The low vitamin A group experienced more pulmonary air leaks, ventilator days, and antibiotic treatments.
- Infants with low vitamin A were older at enteral feeding onset and had lower daily vitamin A intake.
Conclusions:
- Persistent vitamin A deficiency in very low birthweight infants is associated with increased severe bronchopulmonary dysplasia.
- Vitamin A deficiency correlates with delayed enteral feeding and reduced vitamin A intake.
- Findings support earlier reports linking vitamin A deficiency to adverse respiratory outcomes in preterm infants.
Abstract:
Preterm infants often have abnormally low serum vitamin A concentrations. Persistence of vitamin A deficiency for a prolonged postnatal period may contribute to the development of bronchopulmonary dysplasia. We retrospectively analyzed data from 22 infants with birthweight < or = 1250 g who had hyaline membrane disease requiring mechanical ventilation with oxygen and in whom serum vitamin A concentrations had been measured at the onset of enteral feeding and every 2 weeks thereafter. Thirteen infants (low serum vitamin A group) had one or more serum vitamin A concentrations < or = 11 mcg/dL at > 10 days of age. In 9 infants (higher serum vitamin A group) all serum vitamin A concentrations were > 11 mcg/dL at > 10 days of age. Mean birthweight, mean gestational age, sex, race, incidence of antenatal maternal glucocorticoid treatment and ventilatory support on the first day of life were similar for the two groups. Severe bronchopulmonary dysplasia was as defined as characteristic radiographic changes and either discharge from the hospital with supplemental oxygen or death from respiratory failure at > 28 days of age following mechanical ventilation with oxygen since birth. The incidence of severe bronchopulmonary dysplasia was significantly higher in the low serum vitamin A group (11/13, 3 deaths vs. 1/9, no deaths; p=0.001). The incidence of pulmonary air leak, the number of ventilator days, the number of days of postnatal glucocorticoid treatment for chronic lung disease, the number of episodes of suspected sepsis and the number of days of antibiotic treatment also were higher in the low serum vitamin A group. Low serum vitamin A group infants were older at the onset of enteral feeding (21 days vs. 8 days; p = 0.001) and during feeding their average daily enteral intake of vitamin A was lower (713 IU vs. 1255 IU; p = 0.001) when compared with infants in the higher serum vitamin A group. Our retrospective analysis of data from these infants confirms earlier reports from other workers that persistent marked vitamin A deficiency in very low birthweight infants is associated with a high incidence of severe bronchopulmonary dysplasia, delayed onset of enteral feeding and low enteral intake of vitamin A.
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