ESPE Abstracts

Introduction: Knowledge of changes in bone-mineral metabolism in patients with inflammatory bowel disease (IBD) is of particular interest, since in many patients bone metabolic disease is an epiphenomenon of the underlying pathology. Impaired bone mineralisation and diminished spinal bone mineral density (BMD) are reported in children with IBD, together with increased incidence of vertebral fracture. The short- and long-term implications of reduced BMD are especially important in pediatric patients.

Material and methods: A descriptive, transversal, case–control study of 39 children with IBD and 46 healthy children, aged 3–17. The following were recorded: clinical histories, bioimpedance, BMD, whole blood count, glucose, urea, creatinine, calcium and phosphor ions, magnesium, alkaline phosphatase, uric acid, PTH, osteocalcin, T₄, TSH, cortisol, insulin, albumin, prealbumin, proteins, iron and lipid metabolism, CRP, orosomucoid, β-CrossLaps, vitamin D, leptin and its soluble receptor, IL6, FGF23, osteoprotegerin, sclerostin, and RANK ligand. Data were analysed using the SPSS 15.0 Statistical Software Package.

Results: The bone-mineral biochemical profile of children with IBD differed from that of the control group, with lower blood calcium and total alkaline phosphatase levels and higher RANKL values. A positive correlation was observed in the IBD group, but not in the control group, between 25(OH)-vitamin D and serum iron and albumin levels and total proteins. A negative correlation was observed with activity markers, suggesting that vitamin D has an anti-inflammatory and immunomodulatory role. Findings confirmed the adverse effect of a greater activity index and higher corticoid dose-rates on bone tissue (according to the BMD z-score). The latter appears to be the most harmful factor for bone.

Conclusion: In pediatric patients, IBD prompts changes in bone metabolism with implications in other areas.