Abstract
Serial concentration values of 25-hydroxyvitamin D (25-OHD) were determined in the sera of term, premature, and twin infants. In infants born at term with normal concentrations of 25-OHD in cord blood, serial concentrations of 25-OHD remained normal; in infants born at term with low concentrations of 25-OHD in cord blood, serial concentrations of 25-OHD increased. In premature infants with normal concentrations of 25-OHD in cord blood, serial concentrations of 25-OHD decreased; in premature infants with low values of 25-OHD in cord blood, serial concentrations of 25-OHD did not increase until a postconceptual age of 36 to 38 weeks. The concentrations of 25-OHD in the sera of twin infant pairs followed parallel courses. Oral and intravenous supplementation of vitamin D did not significantly increase the concentrations of 25-OHD in serum of premature infants. These findings suggest that a decreased rate of 25-hydroxylation of vitamin D may be a factor impairing homeostasis of 25-OHD in premature infants.
Published Version
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