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Commentary on amino acid homeostasis in the preterm infant.

Delivering adequate amounts of nutrients to premature infants at all times is challenging because the infant’s immature gastrointestinal tract is initially unable to accept feedings, necessitating the use of parenteral nutrition. Although the rate of survival of these infants has improved, growth failure is nearly universal, and multiple recent studies have documented the poor growth and nutritional deficits in this population of infants. At the time of birth, about 18% of extremely low-birthweight infants are less than the 10th percentile for weight and length, but at 36 weeks’ corrected gestational age or before discharge, most of these same babies are below their birth centiles for weight and length. In addition, many remain very small throughout infancy [1]. Protein deficits, especially those occurring in the first week of life contribute substantially to poor growth [2]. Delaying amino acid (AA) supplementation for even few days in the postnatal period can result in negative nitrogen balance, and approximately 1.1– 2.5 g/kg per day of AA intake with caloric intake of 30–60 kcal/kg per day can change protein balance from significantly negative to neutral or positive [3, 4]. The consistencies of these findings are despite differences in the composition of the AA solutions used in the studies. Therefore, early administration of AA at a rate equal to or slightly exceeding the rate of protein losses (1.5–2 g/kg per day) is an important clinical strategy in preterm infants to preserve body protein stores, even if caloric intakes remain low. Safety is often cited as a reason to delay initiation of AA, particularly in the sickest, most immature infants. Specific concerns include changes in acid-base status and elevations in blood urea nitrogen (BUN) and ammonia levels. It is, therefore, reassuring that multiple studies have demonstrated no differences in Commentary on Amino Acid Homeostasis in the Preterm Infant