Mineral Homeostasis and Effects on Bone Mineralization in the Preterm Neonate

Abstract

Most bone formation and mineralization occurs late in gestation. Accretion of adequate minerals is a key element of this process and is often interrupted through preterm birth. In utero, mineral transport is accomplished via active transport across the placenta and does not require fetal hormone input. Postnatal mineral homeostasis requires a balance of actions of parathyroid hormone, calcitonin, and vitamin D on target organs. Preterm birth, asphyxia, acidosis, and prolonged parenteral nutrition increase the risk of mineral imbalance and metabolic bone disease (MBD). Aggressive postnatal nutrition is key to preventing and treating MBD in preterm infants.

Keywords: Bone density; Bone mineralization; Calcium; Nutrition; Parathyroid hormone; Phosphorus; Rickets of prematurity.