11 - Hypocalcemia and other abnormalities of mineral homeostasis during the neonatal period

Abstract

This chapter reviews hypocalcaemia and other abnormalities of mineral homeostasis during the neonatal period. It describes three types of neonatal hypocalcaemia based on their time of occurrence in life: early neonatal hypocalcaemia, late neonatal hypocalcaemia, and demineralization and late-late hypocalcaemia. Early neonatal hypocalcaemia is prevalent in premature infants, infants of diabetic mothers, and asphyxiated infants. An exaggeration of the calcitonin surge probably plays a major role in premature and asphyxiated infants, while the infants of diabetic mothers and premature infants may have a prolonged functional hypoparathyroidism. Late neonatal hypocalcaemia occurs in full-term, otherwise healthy infants and is most common in vitamin D-deficient populations. It is much less frequent than early neonatal hypocalcaemia; however, the infants are usually symptomatic often with seizures and the entity always requires treatment with additional calcium and often magnesium supplementation and/or phosphate restriction. Late-late neonatal hypocalcaemia is seen in very premature infants and is associated with severe osteopenia or rickets. Its etiology appears to be a combination of calcium and phosphorus deficiency and an effective vitamin D metabolite deficiency. Both high calcium-high phosphorus formulae and 25-hydroxycholecalciferol to normalize serum 25-hydroxyvitamin D (25-OHD) have improved mineralization and decreased hypocalcaemia. Severe demineralization occurs most frequently when a phosphorus deficiency is superimposed on 25-OHD deficiency. Human milk per se , when fed to the very small premature infant, often produces classical phosphate deficiency rickets.