
AbstractAntenatal corticosteroids (ACS) administration to pregnant women for threatened preterm labor is standard obstetric care to reduce neonatal respiratory distress syndrome and the associated respiratory morbidity. While ACS stimulates surfactant production in the fetal lung, the effects of ACS upon the subsequent growth and development of the lung are unclear. Follow‐up studies outside of the neonatal period have been primarily limited to spirometry, and most subjects evaluated were born prematurely. To our knowledge, no study has assessed both airway and parenchymal function in infants or adults following ACS exposure. We hypothesized that ACS impairs lung growth and performed infant pulmonary function testing, which included spirometry, alveolar volume (VA) and lung diffusion (DL). As a pilot study, we limited our assessment to infants whose mothers received ACS for threatened preterm labor, but then proceeded to full term delivery. This approach evaluated a more homogenous population and eliminated the confounding effects of preterm birth. We evaluated 36 full‐term infants between 4 to 12 months of age; 17 infants had ACS exposure and 19 infants had no ACS exposure. Infants exposed to ACS had a significantly lower forced vital capacity compared with non‐ACS exposed infants (250 vs 313 mL; P = .0075). FEV0.5 tended to be lower for the ACS exposed group (205 vs 237 mL; P = .075). VA and DL did not differ between the two groups. These findings suggest that ACS may impair subsequent growth of the lung parenchyma.
Adult, Male, Respiratory Distress Syndrome, Newborn, Pulmonary function, Infant, Pilot Projects, Lung diffusion, Lung growth, Respiratory Function Tests, Lung volume, Young Adult, Spirometry, Adrenal Cortex Hormones, Pregnancy, Prenatal Exposure Delayed Effects, Humans, Female, Lung
Adult, Male, Respiratory Distress Syndrome, Newborn, Pulmonary function, Infant, Pilot Projects, Lung diffusion, Lung growth, Respiratory Function Tests, Lung volume, Young Adult, Spirometry, Adrenal Cortex Hormones, Pregnancy, Prenatal Exposure Delayed Effects, Humans, Female, Lung
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