Metabolic bone disease of prematurity

Abstract

Metabolic bone disease (MBD) is a significant complication that commonly affects extremely preterm (Gestation under 28 weeks) or very low birth weight (Birth weight under 1,500 g) infants. Reduced bone mineralization is the pathognomonic feature of MBD. Many hormonal and nutritional factors contribute to its pathogenesis. Conditions such as bronchopulmonary dysplasia, necrotising enterocolitis, and medications such as glucocorticoids and loop diuretics increase the risk. MBD is often asymptomatic and can present with failure to wean off the ventilator and/or long bone and rib fractures. Serum phosphate and alkaline phosphatase levels can help in early diagnosis but lack sensitivity and specificity. Plain X-rays of bones have low sensitivity because significant demineralization needs to occur before the diagnostic changes become visible. Dual Energy X ray absorptiometry (DEXA) is a more specific and sensitive diagnostic tool but it is not portable and involves increased radiation exposure to the infant. Early enteral feeding, fortification of preterm human milk with calcium, phosphorus and supplementation of vitamin D have an important role in the prevention of MBD. Current evidence suggests that MBD can reduce bone mineral contents and height in childhood but may not affect eventual adult height and bone mineralization. However there are uncertainties about its role in development of osteoporosis in adulthood. Future research is required to evaluate the long term outcomes such as the risk of fractures and skeletal deformities following MBD, and the role of systematic physical activity programs and maternal vitamin D deficiency in the condition.