Abstract
Few studies have explored the importance of riboflavin deficiency in premature infants. Infants receiving human milk during the first 2 weeks become biochemically riboflavin-deficient, partly through photodegradation of riboflavin during the banking and delivery of human milk. Animal studies have shown that the metabolic lesions of riboflavin deficiency in sucking neonates differ in important ways from those seen later after weaning. Techniques are described for non-invasive study of functional riboflavin requirements by premature infants. It appears prudent to supplement human milk-fed babies with at least 300 micrograms riboflavin/day; but the potential danger of over supplementation in infants exposed to phototherapy is discussed.
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