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Can bisphosphonate treatment be stopped in a growing child with skeletal fragility?
K A Ward1, J E Adams, T J Freemont
1Imaging Science and Biomedical Engineering, University of Manchester, Manchester, M13 9PT, UK. kate.ward@manchester.ac.uk
Insights
Cyclical pamidronate therapy improved bone density and healed fractures in a child with skeletal fragility. However, bone mineral density declined rapidly after treatment cessation, questioning long-term bisphosphonate discontinuation in growing children.
Area of Science:
- Pediatric Endocrinology
- Skeletal Biology
- Pharmacology
Background:
- A 23-month-old male diagnosed with type IV osteogenesis imperfecta experienced a low-trauma femur fracture, osteopenia, and vertebral fractures.
- Genetic testing for COL1A1 and COL1A2 mutations was negative.
Observation:
- Cyclical pamidronate treatment in a 2-year-old with skeletal fragility led to vertebral fracture remodeling and improved bone mineral density (BMD) at radial and spinal sites.
- Discontinuation of bisphosphonate therapy resulted in a rapid decline in BMD within 24 months.
Findings:
- Quantitative CT (QCT) revealed low spinal trabecular volumetric BMD (Z-score -2.4) initially.
- After 4 years of pamidronate, BMD normalized across QCT, DXA, and pQCT, leading to treatment cessation.
- Post-discontinuation, the patient experienced stress fractures and significant reductions in spinal and radial vBMD.
Implications:
- This case highlights the potential for relapse of skeletal fragility and bone density loss upon bisphosphonate cessation in children.
- It raises critical questions about the optimal duration and criteria for discontinuing bisphosphonate therapy in pediatric patients with fragility fractures during their growth phase.
- Reinitiation of IV pamidronate therapy was necessary, underscoring the challenges in managing long-term skeletal health in this population.
Unlabelled:
Cyclical pamidronate therapy in a 2-year-old child with skeletal fragility resulted in remodelling of vertebral fractures and improvement in bone mineral density (BMD) at distal radial and spinal sites. The BMD at both sites decreased precipitously within 24 months of stopping treatment, raising the question as to whether bisphosphonates can be stopped in a growing child with skeletal fragility.
Introduction:
At age 23 months, a male toddler sustained a low trauma fracture of his right femur. Skeletal radiographs revealed generalised osteopenia with multiple vertebral body fractures. He was diagnosed with type IV osteogenesis imperfecta; however, no mutations were found in COL1A1 or COL1A2 genes.
Methods:
This case report presents bone densitometry data before, during and after bisphosphonate treatment. Axial QCT was main outcome from 2 years of age; DXA and pQCT were taken after age 5.
Results:
QCT confirmed that he had low spinal trabecular volumetric BMD (Z-score -2.4). After 4 years of treatment his vertebral fractures had been remodelled and all bone densitometry values (QCT, DXA and pQCT) were within normal range and therefore treatment was discontinued. Shortly after this he suffered stress fractures of his left mid tibia and at the sclerotic metaphyseal line corresponding to his first APD treatment. He had marked reduction in spinal trabecular and distal radial vBMD; change in BMAD was less marked.
Conclusion:
The patient has been restarted on IV APD therapy. This case has led us to consider whether bisphosphonate therapy can be discontinued in a child with fragility fractures before his/her linear growth has ceased?
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