Calcium and Phosphorus Metabolism in the Premature Infant

Abstract

During the last trimester of pregnancy, there is a sixfold increase in fetal calcium and phosphorus accumulation. Unsupplemented human breast milk may not provide sufficient calcium and phosphorus for the rapidly growing preterm infant to match the accumulation that should have taken place in utero and to permit normal bone mineralization. Rickets of prematurity may present clinically between the 6th and 12th postnatal week. The clinical diagnosis may be confirmed using simple biochemical tests. Inadequate mineral substrate intake, particularly of phosphorus, is the most common cause, although a delay in the maturation of the renal enzyme, 1-alpha hydroxylase, with low plasma concentrations of 1,25-dihydroxyvitamin D, may also occur. The biochemical response to treatment can be determined by documenting a fall in plasma alkaline phosphatase activity and a rise in plasma phosphate concentration and urinary phosphate excretion.