Eur J Endocrinol
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DOI: 10.1530/EJE-08-0429
European Journal of Endocrinology, Vol 159, Issue 6, 693-698
Copyright © 2008 by European Society of Endocrinology
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CLINICAL STUDY

Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids

Marianne K Vihinen, Kaija-Leena Kolho, Merja Ashorn1, Matti Verkasalo and Taneli Raivio

Hospital for Children and Adolescents, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland1 Department of Paediatrics, University of Tampere, Tampere, Finland

(Correspondence should be addressed to M Vihinen, Biomedicum Helsinki 2 C, PO Box 705, 00029 HUCH, Helsinki, Finland; Email: marianne.vihinen{at}helsinki.fi)

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 µg/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 µg/l (P<0.001), serum ICTP from 14.2 to 9.6 µg/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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