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[Disorders of bone metabolism in premature infants]
Insights
Extremely low birth weight infants often develop rickets due to rapid growth and low mineral intake. Certain drugs and phosphate depletion can worsen this bone disease in premature infants.
Area of Science:
- Neonatal Medicine
- Pediatric Endocrinology
- Nutritional Science
Context:
- Extremely low birth weight (ELBW) infants exhibit rapid growth, increasing their risk of nutritional deficiencies.
- Neonatal rickets, a form of osteopenia, is a significant concern in premature infants.
- Phosphate depletion can lead to hypercalcemia syndrome preceding bone demineralization in some infants.
Purpose:
- To discuss the multifactorial etiology of rickets in extremely low birth weight infants.
- To highlight the role of calciprivic drugs in the development of neonatal rickets.
- To present findings from experimental animal models and clinical cases, offering a parenteral mineral infusion schedule.
Summary:
- ELBW infants are susceptible to rickets (osteopenia) due to rapid growth and insufficient calcium and phosphate intake.
- Adverse effects of drugs like phenytoin, phenobarbital, glucocorticoids, furosemide, and heparin contribute to neonatal rickets.
- Experimental evidence in animals and clinical reports support the link between mineral imbalances and impaired bone mineralization, with a proposed treatment protocol.
Impact:
- Informs clinicians about the risk factors and contributing agents for neonatal rickets.
- Provides a basis for understanding drug-induced bone disease in vulnerable infants.
- Offers practical guidance for mineral supplementation in affected neonates.
Abstract:
Extremely low birth weight infants are particularly prone to rickets (osteopenia) due to their rapid growth and to deficient intake of calcium and phosphate. In some premature infants suffering from phosphate depletion hypercalcemia syndrome may precede bone demineralisation. Additionally, the adverse effects of calciprivic drugs (phenytoin, phenobarbital, glucocorticoids, furosemide, heparin) contributing to the development of neonatal rickets are discussed. Phosphorus depleted or heparin treated experimental animals develop impairment of mineralisation as manifested by rickets or osteomalacia. Some clinical cases of neonatal rickets are reported and a dosage schedule for parenteral infusion of minerals is given.