Mineral Homeostasis and Effects on Bone Mineralization in the Preterm Neonate.
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.
['Karpen|Heidi E|HE|']
D000138:Acidosis D001238:Asphyxia Neonatorum D001851:Bone Diseases, Metabolic D002113:Calcification, Physiologic D002116:Calcitonin D002118:Calcium D006706:Homeostasis D006801:Humans D007231:Infant, Newborn D007234:Infant, Premature D010281:Parathyroid Hormone D010288:Parenteral Nutrition D010758:Phosphorus D012279:Rickets D014807:Vitamin D
Bone mineralization Parathyroid hormone Nutrition Bone density Calcium Phosphorus Rickets of prematurity