Arch Dis Child Fetal Neonatal Ed doi:10.1136/archdischild-2011-301025
Catherine M Harrison1, Alan T Gibson2
1Neonatal Medicine, Leeds Teaching Hospitals Trust, Leeds, UK
2Neonatal Intensive Care, Sheffield Teaching Hospitals NHS Trust, Sheffield, UK
Correspondence to Alan T Gibson, Sheffield Teaching Hospitals NHS Trust, Neonatal Intensive Care, Consultant Neonatologist, Jessop Wing, Sheffield, S10 2SF, UK; alan.gibson at sth.nhs.uk
Received 12 September 2011; Accepted 15 February 2012; Published Online First 3 May 2012
(First portion of text of the article)
In the newborn preterm infant a combination of inadequate reserves and increased loss of essential minerals is common and frequently compounded by difficulties in obtaining an intake sufficient to replace losses and restore reserves. Deficiencies in calcium and phosphate and disturbed balance between them are frequently encountered, and may lead to significant impairment of bone deposition. Osteopenia of prematurity – also known as neonatal rickets, rickets of prematurity or neonatal metabolic bone disease – is a common and important concern in neonatology, and effective management is hindered by difficulties in accurately assessing calcium and phosphate status and the ‘quality’ of bone deposition.
It is well known that preterm infants are at risk of reduced bone mineral content (BMC) and subsequent bone disease and that many factors may contribute to this.
The majority of calcium and phosphate accretion and bone mineralisation occur in the third trimester of pregnancy and from 24 weeks of gestation onwards, it has been estimated that the fetus in utero gains about 30 g in weight each day, and this daily requirement includes 310 mg of calcium and 170 mg phosphorus.1
It has been shown that BMC and bone mineral density (BMD) correlate positively with gestational age, birth weight, body area and length.2
Mineral deposition may be affected before an infant is born as a number of prenatal factors, particularly placental function, have been shown to play a part in the development of osteopenia.
The placenta converts vitamin D to 1,25-dihydrocholecalciferol which enables phosphate to be transported across the placenta.3
A reduced ability to do so explains the higher incidence of postnatal rickets that may be seen in infants with intrauterine growth restriction suggesting that chronic injury to the placenta may limit the ability to transfer phosphate.4 Poor mineralisation may also occur in …
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