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Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic
Marianne K Vihinen1, Kaija-Leena Kolho, Merja Ashorn
1Hospital for Children and Adolescents, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland. marianne.vihinen@helsinki.fi
Insights
Children with active inflammatory bowel disease (IBD) have compromised bone formation. Glucocorticoid treatment further suppresses bone turnover, but markers improve rapidly after steroid withdrawal.
Area of Science:
- Pediatric Endocrinology
- Gastroenterology
- Bone Metabolism
Background:
- Children with inflammatory bowel disease (IBD) often experience impaired bone health.
- Systemic glucocorticoids are commonly used to manage IBD flares but can negatively impact bone turnover.
Purpose of the Study:
- To investigate circulating markers of bone turnover in pediatric IBD patients before, during, and after systemic glucocorticoid therapy.
- To assess the effects of glucocorticoids on bone formation and resorption in children with IBD.
Main Methods:
- Studied 22 children with IBD requiring oral steroid therapy, measuring bone formation (PINP) and resorption (ICTP) markers, IGF-I, and SHBG.
- Analyzed bone markers at baseline, 2 and 5 weeks during glucocorticoid treatment, and 1 month post-withdrawal.
- Compared with 22 IBD patients in remission as controls.
Main Results:
- Children with active IBD had lower baseline PINP and IGF-I compared to controls.
- Glucocorticoid treatment significantly decreased PINP, ICTP, and SHBG levels within 2 weeks.
- Serum IGF-I levels increased during glucocorticoid treatment.
- All measured bone markers returned to control levels one month after steroid cessation.
Conclusions:
- Bone formation is compromised in active pediatric IBD.
- Systemic glucocorticoid therapy further suppresses bone turnover in these patients.
- Bone markers demonstrate rapid improvement following glucocorticoid withdrawal.
Objective:
We investigated circulating markers of bone turnover before and during systemic glucocorticoid treatment in paediatric patients with inflammatory bowel disease (IBD).
Methods:
Twenty-two children (mean age, 12.3 years) with IBD necessitating peroral steroid therapy were studied, with special reference to bone formation and resorption markers amino-terminal type I collagen propeptide (PINP) and carboxyterminal telopeptide of type I collagen (ICTP) respectively. In addition, GH-related IGF-I and sex hormone-binding protein (SHBG) were measured. Bone markers were analyzed at the initiation of the glucocorticoid treatment, at 2 and 5 weeks thereafter and at 1 month following the withdrawal of the steroid. Control group comprised 22 IBD patients in remission.
Results:
PINP and IGF-I were already lower before glucocorticoid treatment serum in children with active IBD as compared with control children with IBD in remission (median PINP 271 vs 535 microg/l, P<0.05; IGF-I 23 vs 29 nmol/l, P<0.05). After 2 weeks of glucocorticoid treatment serum PINP levels had declined further, from 271 to 163 microg/l (P<0.001), serum ICTP from 14.2 to 9.6 microg/l (P<0.001), and SHBG from 54 to 35 nmol/l (P<0.001) respectively. By contrast, serum IGF-I increased from 23 to 37 nmol/l (P<0.001). One month after the withdrawal of the glucocorticoid, all bone markers restored to levels similar to the controls.
Conclusions:
Bone formation in children with active IBD appears compromised and systemic glucocorticoid treatment further suppresses bone turnover. After the cessation of the glucocorticoid the bone markers show immediate improvement.
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