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Vitamin D and bronchopulmonary dysplasia in preterm infants

K E Joung¹, H H Burris^2,3,4, L J Van Marter^2,4,5

¹Goryeb Children's Hospital/Morristown Medical Center, Morristown, NJ, USA.

Journal of Perinatology : Official Journal of the California Perinatal Association

|July 29, 2016

Insights

This study found no association between vitamin D levels and bronchopulmonary dysplasia (BPD) in extremely preterm infants. Current supplementation ensures sufficient vitamin D levels by 36 weeks corrected age, regardless of BPD development.

Area of Science:

Neonatology
Pediatric Pulmonology
Nutritional Science

Background:

Vitamin D deficiency is linked to childhood asthma, but its role in bronchopulmonary dysplasia (BPD) among preterm infants remains unclear.
Preterm infants, especially those born before 29 weeks gestation, exhibit lower 25-hydroxyvitamin D (25(OH)D) levels at birth and are susceptible to nutritional deficits.
Understanding vitamin D's impact on BPD is crucial for optimizing infant respiratory health outcomes.

Purpose of the Study:

To investigate the association between 25-hydroxyvitamin D (25(OH)D) concentrations at birth and 36 weeks corrected gestational age with the incidence of BPD in extremely preterm infants.
To determine if cord blood or later-life vitamin D levels correlate with the development of BPD in infants born before 29 weeks gestation.

Main Methods:

Umbilical cord blood and venous blood samples were collected from 44 preterm infants (gestational age <29 weeks) at birth and 36 weeks corrected age.
25(OH)D levels were measured using chemiluminescence, with multivariable logistic models adjusting for gestational age and other confounding factors.
Infant survival and BPD development were tracked up to 36 weeks corrected age.

Main Results:

No significant association was found between 25(OH)D levels at birth or 36 weeks corrected age and the odds of developing BPD or mortality.
Median 25(OH)D levels were similar between infants who developed BPD and those who did not, both at birth and at 36 weeks corrected age.
All infants in the cohort achieved 25(OH)D levels above 30 ng/mL by 36 weeks corrected age, considered sufficient.

Conclusions:

In extremely preterm infants, neither cord blood nor 36-week corrected age 25(OH)D levels are associated with BPD development.
Current vitamin D supplementation protocols appear effective in achieving sufficient levels in this vulnerable population by 36 weeks corrected age.
Further research may explore other factors influencing BPD in extremely preterm infants, as vitamin D status does not seem to be a primary determinant.

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Abstract

Objective:

Vitamin D deficiency is associated with asthma and reactive airway disease in childhood but its potential contribution to bronchopulmonary dysplasia (BPD) in preterm infants is unknown. Preterm infants have lower levels of 25-hydroxyvitamin D (25(OH)D) at birth and are at risk for nutritional deficiencies after birth. The objective of the study was to evaluate the association of 25(OH)D concentrations at birth and at 36 weeks' corrected gestational age with BPD in preterm infants born before 29 completed weeks of gestation.

Study Design:

We collected umbilical cord blood samples from 44 preterm infants (gestational age <29 weeks) delivered at Brigham and Women's Hospital in Boston. In addition, with parental consent we collected venous samples at 36 weeks' corrected age from 20 preterm infants born before 29 weeks' gestation (including 6 infants with previously collected cord blood). Samples were frozen at -80 °C until subsequent measurement of 25(OH)D levels by chemiluminescence. We used multivariable logistic models to adjust for gestational age and considered other confounding variables, including maternal race, age, mode of delivery and infant sex.

Results:

Among 44 infants, 41 (93.2%) survived and 3 (6.8%) died before 36 weeks' corrected age. Median 25(OH)D levels at birth were 30.4 ng ml(-1) in preterm infants who subsequently died or developed BPD and 33.8 ng ml(-1) in infants who survived without BPD (P=0.6). Median 25(OH)D levels at corrected age of 36 weeks were 59.0 ng ml(-1) among survivors without BPD and 64.2 ng ml(-1) among survivors with BPD (P=0.9). Neither cord blood nor 36 weeks' corrected 25(OH)D levels were associated with odds of death or BPD (adjusted odds ratio (OR) 1.00, 95% confidence interval (CI): 0.73 to 1.37; and OR 0.93, 95% CI: 0.61 to 1.43, respectively).

Conclusions:

Among this population of extremely preterm infants neither cord blood nor the 36 weeks' corrected age 25(OH)D levels were associated with development of BPD. Notably, at the current level of supplementation, all extremely preterm infants in our cohort had achieved 25(OH)D levels >30 ng ml(-1) by 36 weeks' corrected age, which is thought to represent sufficiency in adult and pediatric populations.

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