Abstract
Retinol stores accumulate in fetal tissue during gestation. Hence, the premature infant faces extrauterine adaptation with less total reserves of retinol than does the term infant. Retinol-binding protein in serum is also lower in the premature infant population. The parenteral retinol supplementation frequently required for these infants has only recently become adequate by the finding of methods to avoid large losses of retinol onto intravenous tubing. Retinol is an essential vitamin for epithelial cell function; nearly 40% of lung cells are of epithelial origin. The premature infant’s lung often is the initial site of difficulties during extrauterine adaptation, and respiratory system epithelial-cell damage and chronic lung disease frequently develop. Because these infants have associated low retinol reserves, retinol supplementation to help repair pulmonary injury is being considered. Some of these relationships are beginning to be clarified by basic research on the metabolism and function of retinol in lung.