Abstract
Premature infants, particularly those born before the 28th week of gestation, are at a significant risk for reduced bone mineral content because a major part of fetal bone mineralization occurs during the third trimester of gestation with maximum close to the term labor. After birth, another important reduction of bone mineral density occurs due to early start of bone remodeling, relatively fast bone growth, and low mineral intake (compared with intake during intrauterine development).
These postnatal changes are responsible for a disease known as metabolic bone disease of prematurity (MBD). Incidence of MBD (30-55%) remains unchanged despite improvements of neonatal intensive care during the last 20 years.
Although occurrence of pathological fractures due to MBD appears to have decreased, the risk of this early complication is still over 10%. Changes seen in the bones of ex-preterm newborns in childhood and in young adults (reduction of final height and, eventually, of bone mineral density) suggest that it could be a significant risk factor for the development of early osteoporosis in adulthood.
The risk factors contributing to the development of MBD of prematurity have been well described. Diagnosis of metabolic bone disease is done by biochemical analysis.
Low serum levels of phosphorus and high levels of alkaline phosphatase are suggested as a gold standard, despite the strong evidence of limited use of these parameters. The key of successful treatment is consistent prevention, which is based on early and optimal delivery of calcium, phosphorus and vitamin D through parenteral and enteral nutrition.
This article reviews the pathophysiology, incidence, diagnostics, therapy and consequnces of MBD of prematurity.