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Metabolic bone disease of total parenteral nutrition
1Department of Pediatrics, University of Texas Medical Branch, Galveston, USA.
Insights
Parenteral nutrition-associated metabolic bone disease in children causes osteopenia and fractures. Its causes are multifactorial, including nutrient deficiencies and potential aluminum toxicity, with exact incidence unknown.
Area of Science:
- Pediatric Endocrinology
- Nutritional Science
- Pediatric Gastroenterology
Background:
- Parenteral nutrition-associated metabolic bone disease (PN-MBD) is a significant complication in children.
- Manifestations include osteopenia and fractures, particularly in preterm infants.
- The exact etiology and incidence remain unclear, hindering effective management strategies.
Purpose of the Study:
- To review the current understanding of parenteral nutrition-associated metabolic bone disease in pediatric patients.
- To explore the multifactorial etiology, including nutritional deficiencies and potential toxicities.
- To highlight the challenges in diagnosis and the need for further research.
Main Methods:
- Literature review of existing studies on pediatric PN-MBD.
- Analysis of potential contributing factors such as calcium and phosphate deficiency.
- Discussion of the role of aluminum toxicity and other pathogenetic elements.
Main Results:
- PN-MBD is characterized by osteopenia and fractures in children.
- Calcium and phosphate deficiency are key factors, especially in preterm infants.
- Aluminum toxicity's role is under investigation, and normal reference values are lacking.
Conclusions:
- PN-MBD is a complex condition with multifactorial causes.
- Further research is needed to establish normal reference values and clarify the role of various factors.
- Accurate diagnosis and incidence data are crucial for pediatric patient care.
Abstract:
Parenteral nutrition-associated metabolic bone disease in children is manifested primarily as osteopenia and, on occasion, fractures. The etiology is likely multifactorial, with calcium and phosphate deficiency playing a major role in the preterm infant and with the role of aluminum toxicity yet to be clearly defined in this population. Lack of normal values of bone histomorphometry in the premature infant as well as lack of normal data for biochemical markers of bone turnover in these patients contribute to the uncertainty. Other factors that may play a role in the pathogenesis include lack of periodic enteral feeding; underlying intestinal disease, including malabsorption and inflammation; the presence of neoplasms; and drug-induced alterations in calcium and bone metabolism. The true incidence and prevalence of parenteral nutrition-associated bone abnormalities in pediatric patients remain unknown.