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Pathological fractures in paediatric patients with inflammatory bowel disease
Sze Choong Wong1, A G Anthony Catto-Smith, Margaret Zacharin
1Department of Endocrinology, The Royal Children's Hospital, Flemington Road, Parkville, 3052, Melbourne, Australia, jarod.wong@rch.org.au.
Insights
Children with inflammatory bowel disease (IBD) face skeletal health risks, including vertebral fractures, due to chronic inflammation, even before steroid treatment. Management focuses on disease control and bone health factors.
Area of Science:
- Pediatric Gastroenterology
- Pediatric Endocrinology
- Rheumatology
Background:
- Paediatric inflammatory bowel disease (IBD), particularly Crohn's disease (CD), is linked to compromised skeletal health.
- Factors contributing to poor bone health include chronic inflammation, glucocorticoid (GC) use, malnutrition, and delayed development.
Observation:
- While low bone mineral density is common, the risk of long bone fractures may not be elevated.
- Emerging evidence indicates a potential increase in vertebral fractures (VFs) among these patients.
- VFs have been observed at diagnosis in paediatric CD, preceding GC exposure, underscoring inflammation's impact.
Findings:
- Chronic inflammation, driven by cytokines, adversely affects skeletal health in paediatric IBD.
- Vertebral fracture risk may be elevated, independent of glucocorticoid exposure.
- A case report highlights multiple VFs in a young girl with CD shortly after diagnosis.
Implications:
- Optimizing IBD control, vitamin D levels, physical activity, and growth is crucial for bone health.
- Bisphosphonates may be considered for symptomatic pathological fractures, requiring expert monitoring.
- Close clinical attention to factors influencing bone health is essential for paediatric IBD patients.
Unlabelled:
Paediatric inflammatory bowel disease (IBD), especially Crohn's disease (CD), is commonly associated with poor skeletal health, related to the direct effects of chronic inflammation, prolonged use of glucocorticoid (GC), poor nutrition, delayed puberty and low muscle mass. Low bone mineral density is commonly reported, although the prevalence of long bone fractures may not be increased in these patients. Emerging evidence however suggests that there may be an increased risk of vertebral fractures (VFs) in this group. VFs presenting at diagnosis of paediatric CD, prior to any GC exposure, have been reported, highlighting the deleterious effect of inflammation on skeletal health. This paper reviews the published literature on pathophysiology of skeletal morbidity and fractures in paediatric IBD, illustrated with a new case report of multiple VFs in a prepubertal girl with CD, soon after diagnosis, who received minimal amounts of oral GC. Optimising control of disease, addressing vitamin D deficiency, encouraging physical activity and ensuring normal growth and pubertal progression are paramount to management of bone health in these patients. Despite the lack of evidence, there may be a place for bisphosphonate treatment, especially in the presence of symptomatic pathological fractures, but this requires close monitoring by clinicians with expertise in paediatric bone health.
Conclusion:
Chronic inflammation mediated by pro-inflammatory cytokines may have adverse effects on skeletal health in paediatric patients with IBD. The risk of vertebral fractures may be increased, even without exposure to glucocorticoid. Clinical monitoring of these patients requires careful attention to the various factors that impact on bone health.
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