Abstract
BackgroundDiminished bone mineral density (BMD) is of significant concern in pediatric inflammatory bowel disease (IBD). Exact etiology is debatable. The recognition of fibroblast growth factor 23 (FGF23), a phosphaturic hormone related to tumor necrosis factor alpha (TNF-α) makes it plausible to hypothesize its possible relation to this pathology.MethodsIn this follow up case control study, BMD as well as serum levels of FGF23, calcium, phosphorus, alkaline phosphatase, creatinine, parathyroid hormone, 25 hydroxy vitamin D3 and 1, 25 dihydroxy vitamin D3 were measured in 47 children with IBD during flare and reassessed in the next remission.ResultsLow BMD was frequent during IBD flare (87.2%) with significant improvement after remission (44.7%). During disease flare, only 21.3% of patients had vitamin D deficiency, which was severe in 12.8%. During remission, all patients had normal vitamin D except for two patients with Crohn’s disease (CD) who remained vitamin D deficient. Mean value of serum FGF23 was significantly higher among patients with IBD during flare compared to controls. It showed significant improvement during remission but not to the control values. 1, 25 dihydroxy vitamin D3, FGF23, serum calcium and urinary phosphorus were significant determinants of BMD in IBD patients.ConclusionsWe can conclude that diminished BMD in childhood IBD is a common multifactorial problem. Elevated FGF23 would be a novel addition to the list of factors affecting bone mineral density in this context. Further molecular studies are warranted to display the exact interplay of these factors.
Highlights
Diminished bone mineral density (BMD) is of significant concern in pediatric inflammatory bowel disease (IBD)
While some studies recommend the use of oral vitamin D and calcium for prevention of bone loss in patients with IBD [5], no sufficient evidence exists of vitamin D deficiency in these patients [6,7,8] or of their benefit from vitamin D supplementation [9]
The aim was to assess relation of serum FGF-23 to BMD among children with IBD. Subjects and methods This follow up case control clinical study included 47 children with IBD (27 with ulcerative colitis "Ulcerative colitis (UC)" and 20 with Crohn’s disease "CD") recruited from amongst IBD patients followed up at the Pediatric Gastroenterology Unit, Ain Shams University Faculty of Medicine over the period from December 2008 to December 2010
Summary
Diminished bone mineral density (BMD) is of significant concern in pediatric inflammatory bowel disease (IBD). Children with inflammatory bowel disease demonstrate decreased bone mineral density [1]. Fibroblast growth factor 23 (FGF23) belongs to the group of phosphatonins, which enhance renal phosphate excretion and inhibit renal 25-hydroxy-vitamin D3 1α hydroxylase [10]. The PHEX (phosphate-regulating with homologies to endopeptidases on the X chromosome) gene encodes a Zinc-metalloendopeptidase expressed primarily in osteoblasts and odontoblasts. Studies seemed to confirm the hypothesis of proteolytic degradation of FGF-23 by PHEX [15]. The down-regulation of the PHEX gene results in decreased degradation of FGF-23 and a subsequent increase in its circulating levels [16]
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