RT Journal Article
SR Electronic
T1 Metabolic bone disease of prematurity: causes, recognition, prevention, treatment and long-term consequences
JF Archives of Disease in Childhood - Fetal and Neonatal Edition
JO Arch Dis Child Fetal Neonatal Ed
FD BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health
SP F560
OP F566
DO 10.1136/archdischild-2018-316330
VO 104
IS 5
A1 Amish Chinoy
A1 Mohamed Zulf Mughal
A1 Raja Padidela
YR 2019
UL http://fn.bmj.com/content/104/5/F560.abstract
AB Metabolic bone disease of prematurity (MBDP) is characterised by skeletal demineralisation, and in severe cases it can result in fragility fractures of long bones and ribs during routine handling. MBDP arises from prenatal and postnatal factors. Infants who are born preterm are deprived of fetal mineral accumulation, 80% of which occurs in the third trimester. Postnatally, it is difficult to maintain a comparable intake of minerals, and medications, such as corticosteroids and diuretic therapy, lead to bone resorption. With improvements in neonatal care and nutrition, the incidence of MBDP in preterm infants appears to have decreased, although the recent practice of administering phosphate supplements alone will result in secondary hyperparathyroidism and associated bone loss, worsening MBDP. Postnatal immobilisation and loss of placental supply of oestrogen also contribute to skeletal demineralisation. There is no single diagnostic or screening test for MBDP, with pitfalls existing for most radiological and biochemical investigations. By reviewing the pathophysiology of calcium and phosphate homeostasis, one can establish that plasma parathyroid hormone is important in determining the aetiology of MBDP – primarily calcipaenia or phosphopaenia. This will then direct treatment with the appropriate supplements while considering optimal physiological calcium to phosphate ratios.