Aim: To characterise the change in serum and urinary bone markers in the early postnatal period, and to assess the effect of systemic corticosteroid on bone metabolism in preterm infants.
Methods: Bone formation was quantified by measurement of serum concentrations of bone specific alkaline phosphatase (BALP) and osteocalcin. Bone resorption was measured by monitoring creatinine adjusted urinary deoxypyridinoline (Dpd) concentration. Blood and urinary samples were collected from corticosteroid treated infants (n = 19) immediately before the start (Td-pre), three weeks after the start (Td-end), and two (Td-post2) and four weeks (Td-post4) after the end of the dexamethasone course. Untreated patients (n = 30) had specimens taken at week 3 (Twk-3), 6 (Twk-6), 8 (Twk-8), and 10 (Twk-10) of postnatal age.
Results: Serum concentrations of BALP and osteocalcin at Td-end were significantly lower than pretreatment levels and the levels at the corresponding time point (Twk-6) of the non-treatment group. In contrast, urinary Dpd concentration at Td-end was not significantly decreased compared with the pretreatment level. However, it was significantly lower than the urinary Dpd concentration at Twk-6 of the non-treatment group. The rate of increase in lower leg length was significantly higher in the non-treatment group between weeks 3 and 6 than in the corresponding period during dexamethasone treatment in the corticosteroid group.
Conclusion: Systemic corticosteroid causes appreciable suppression of serum BALP and osteocalcin and, to a lesser extent, urinary Dpd. The results suggest that corticosteroid inhibits bone growth mainly by decreasing bone formation.
- alkaline phosphatase
- BALP, bone specific alkaline phosphatase
- Dpd, deoxypyridinoline
- VLBW, very low birth weight
- BPD, bronchopulmonary dysplasia
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