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Approach to the Pediatric Patient With Glucocorticoid-Induced Osteoporosis
Leanne M Ward1, Sarah A Bakhamis1, Khaldoun Koujok2
1Department of Pediatrics, Faculty of Medicine, University of Ottawa and Division of Endocrinology, Children's Hospital of Eastern Ontario, Ottawa, Ontario, Canada, K1H 8L1.
Insights
Glucocorticoid (GC) therapy can cause pediatric osteoporosis (pGIO). Early fracture identification and intervention, particularly for vertebral fractures, are crucial for managing pGIO and preventing further skeletal harm.
Area of Science:
- Pediatric Endocrinology
- Pediatric Rheumatology
- Pediatric Orthopedics
Background:
- Glucocorticoid (GC) therapy is vital for childhood conditions but causes significant skeletal morbidity.
- Pediatric GC-induced osteoporosis (pGIO) requires careful management to mitigate long-term bone health issues.
Purpose of the Study:
- To outline fundamental clinical-biological principles for managing pediatric GC-induced osteoporosis (pGIO).
- To emphasize key concepts including fracture phenotyping, monitoring, bone density assessment, and therapeutic impact of vertebral reshaping.
Main Methods:
- Review of clinical cases illustrating core management principles for pGIO.
- Focus on longitudinal vertebral fracture assessment and risk-based monitoring strategies.
Main Results:
- Early identification of fractures, including vertebral fractures, is critical for timely intervention in at-risk children.
- Bone mineral density plays a role in pGIO assessment, and vertebral body reshaping impacts therapeutic decisions.
Conclusions:
- Effective pGIO management relies on early fracture detection and intervention, especially when spontaneous recovery is limited.
- While bisphosphonates are first-line, future research needs to explore anabolic agents for preventing fractures in high-risk pediatric populations.
Abstract:
Glucocorticoid (GC) therapy remains the cornerstone of treatment for many conditions of childhood and an important cause of skeletal and endocrine morbidity. Here, we discuss cases that bring to life the most important concepts in the management of pediatric GC-induced osteoporosis (pGIO). Given the wide variety of underlying conditions linked to pGIO, we focus on the fundamental clinical-biological principles that provide a blueprint for management in any clinical context. In so doing, we underscore the importance of longitudinal vertebral fracture phenotyping, how knowledge about the timing and risk of fractures influences monitoring, the role of bone mineral density in pGIO assessments, and the impact of growth-mediated "vertebral body reshaping" after spine fractures on the therapeutic approach. Overall, pGIO management is predicated upon early identification of fractures (including vertebral) in those at risk, and timely intervention when there is limited potential for spontaneous recovery. Even a single, low-trauma long bone or vertebral fracture can signal an osteoporotic event in an at-risk child. The most widely used treatments for pediatric osteoporosis, intravenous bisphosphonates, are currently recommended first-line for the treatment of pGIO. It is recognized, however, that even early identification of bone fragility, combined with timely introduction of the most potent bisphosphonate therapies, may not completely prevent osteoporosis progression in all contexts. Therefore, prevention of first-ever fractures in the highest-risk settings is on the horizon, where there is also a need to move beyond antiresorptives to the study of anabolic agents.
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