Related Experiment Videos
Elevated serum 1,25 dihydroxyvitamin D concentrations in rickets of very low-birth-weight infants
Insights
Very low birth weight (VLBW) infants developing rickets may have calcium and phosphorus deficiency, not vitamin D metabolism issues. Supplementation rapidly improved bone mineralization in these infants.
Area of Science:
- Pediatrics
- Neonatology
- Nutritional Science
Background:
- Rickets is a significant concern in very low birth weight (VLBW) infants.
- Vitamin D deficiency is often implicated in rickets development.
- Altered vitamin D metabolism has been hypothesized in VLBW infants with rickets.
Purpose of the Study:
- To investigate the potential causes of rickets in VLBW infants.
- To examine the roles of vitamin D metabolites, calcium (Ca), and phosphorus (P) in VLBW infant rickets.
- To assess the efficacy of Ca and P supplementation in treating rickets in VLBW infants.
Main Methods:
- Measurement of serum 1,25 dihydroxyvitamin D (1,25(OH)2D) and 25 hydroxyvitamin D (25OHD) levels.
- Assessment of bone mineralization using infant-adapted direct photon absorptiometry.
- Treatment with a specialized formula supplemented with additional Ca and P.
Main Results:
- Five VLBW infants presented with rickets, extremely low bone mineralization, low 25OHD, and elevated 1,25(OH)2D levels.
- Treatment with Ca and P supplementation led to rapid bone mineralization improvement.
- Concomitant normalization of 1,25(OH)2D, increased 25OHD, and decreased parathyroid hormone levels were observed.
Conclusions:
- Rickets in VLBW infants may stem from Ca and P deficiency rather than vitamin D metabolism abnormalities.
- Adequate Ca and P supplementation is crucial for bone health in VLBW infants.
- Further research is warranted to elucidate the precise mechanisms of rickets in this vulnerable population.
Abstract:
Elevated 1,25 dihydroxyvitamin D concentrations were found in five VLBW infants who developed rickets at two to three months postnatal age or term postconceptual age; 25 hydroxyvitamin D concentrations were low. Bone mineralization was found to be extremely low as measured by infant-adapted direct photon absorptiometry. After treatment with a formula supplemented with additional Ca and P, there was a rapid improvement in bone mineralization with a concomitant decrease of 1,25(OH)2D to normal adult values, whereas 250HD values increased and parathyroid hormone values decreased. In the VLBW infants studied, we suggest that rickets may be caused by Ca and P deficiency rather than by a deficiency of vitamin D metabolism.