Endocrine Abstracts

(ENDOCRINE)Metabolic bone disease of prematurity (MBDP) occurs due to under-mineralisation of the preterm skeleton postnatally, as the baby misses the large amounts of mineral accretion that occurs during the third trimester, coupled with postnatal feeding regimes being unable to replicate this in utero mineral supply. Furthermore, postnatal risk factors such as reduced movements, parenteral nutrition and certain medications can worsen MBDP. If left unmanaged or mismanaged, it can lead to osteopenia, rickets, and eventually fractures. As there are rarely clinical signs of early MBDP, it is identified biochemically on laboratory screening, typically with elevated alkaline phosphatase and reduced serum phosphate. However, it is the plasma parathyroid hormone (PTH) that can help to differentiate between primarily calcipenia (elevated PTH) or phosphopenia (normal PTH), and thus guide treatment. Management should focus on preventative measures, including reducing risk factors and ensuring feeding regimens provide optimal calcium and phosphorus. Prophylactic phosphate supplementation is not recommended, as this can worsen MBDP in a primarily calcipenic state, by worsening the secondary hyperparathyroidism. Where the issue is primarily calcipenia, calcium supplementation will be needed. In primarily phosphopenic state, phosphate supplementation is required, but calcium supplementation may also be needed, to maintain an optimal calcium:phosphorus ratio, which facilitates optimal absorption of these minerals. Controversies remain about the long-term implications of MBDP, and the role of vitamin D. Current research is focused on the use of physical therapies to assist bone development in MBDP.