Bone Mineral Density in Children and Young Adults with Crohnʼs Disease

Semeao, Edisio; Jawad, Abbas F.; Zemel, Babette S.; Neiswender, Kristin M.; Piccoli, David A.; Stallings, Virginia A.

doi:10.1097/00054725-199908000-00003

Cited by 62 publications

(25 citation statements)

References 25 publications

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“…The diminished BMD during flare with significant improvement in remission agrees with previous similar results in IBD patients using either total body or lumbar spine bone mineral density [38-40]. Herzog et al [41] and Ahmed et al [42] reported significant values of 26% and 22% respectively.…”

Section: Discussionsupporting

confidence: 88%

Fibroblast growth factor 23 contributes to diminished bone mineral density in childhood inflammatory bowel disease

et al. 2012

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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.

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Section: Discussionsupporting

confidence: 88%

Fibroblast growth factor 23 contributes to diminished bone mineral density in childhood inflammatory bowel disease

et al. 2012

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“…A close relationship between height Z-score and BMD is well documented based on cross-sectional studies in young patients with IBD 39-41 . Although BMD Z-scores measured via dual-energy X-Ray absorptiometry (DXA) are underestimated in kids with low height Z-scores, bone mineralization deficits may persist after adjustments for size.…”

Section: Part a Screening And Monitoring Bone Health In Children Andmentioning

confidence: 88%

“…Of note is that most of the studies were retrospective. Some investigators found a negative relationship between cumulative glucocorticoid dose and BMD, 395657404158 where others did not 10, 12, 22, 48 . However, glucocorticoids are known to cause osteoblast cell dysfunction and premature apoptosis 596061 , impaired intestinal absorption of calcium 62 and increased urinary calcium excretion 63 .…”

Section: Part a Screening And Monitoring Bone Health In Children Andmentioning

confidence: 99%

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Skeletal Health of Children and Adolescents With Inflammatory Bowel Disease

Pappa¹,

Thayu²,

Sylvester³

et al. 2011

J. pediatr. gastroenterol. nutr.

113

102

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Objectives Current evidence, albeit sparse, points to suboptimal bone health in children and adolescents with inflammatory bowel disease (IBD) when compared to healthy peers. In this clinical report we aimed to: a) review the current literature regarding the pathogenesis of suboptimal bone health and its clinical consequences and long term outcome in children with IBD, b) provide recommendations regarding screening and monitoring bone health, c) review the evidence on available measures and agents to prevent compromise and improve bone health d) summarize the gaps in knowledge and point to research directions. Methods Six experts in pediatric bone health and IBD reviewed the available literature specific to their area of expertise. Evidence was rated using an adjusted evidence rating system. Results The mechanism of suboptimal bone health in children with IBD lays in reduced bone formation and resorption. This could lead to reduced bone mineral density (BMD), which may predispose to fractures and suboptimal peak bone mass. Factors contributing to this derangement are: inflammation, delayed growth and puberty, lean mass deficits, and use of glucocorticoids. Improvement in linear growth and repletion of lean mass may help improve bone health in children with IBD. The role of vitamin D, calcium, exercise, biologics and bisphosphonates is under investigation. Conclusions We recommend: screening and monitoring BMD in children with IBD and certain identified risk factors, control of inflammation with steroid-sparing techniques, nutritional support in children with growth delays and/or lean mass deficits, optimization of vitamin D status, and weight bearing physical activity. Gaps in knowledge are numerous and require investigation.

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“…IBD is a key risk factor for bone loss and fractures in children 1–7 as well as adults 8–13 . Multiple factors are thought to contribute to IBD effects on bone including nutritional status 3,14–19 , reduced physical activity/muscle 1,20 , glucocorticoid use 1 and inflammatory cytokines 21,22 .…”

Section: Introductionmentioning

confidence: 99%

Colitis-induced Bone Loss is Gender Dependent and Associated with Increased Inflammation

Irwin

Lee

Young

et al. 2013

Inflammatory Bowel Diseases

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Background Patients with inflammatory bowel disease (IBD) are at increase risk for bone loss and fractures. Therefore, in the present study, we examined the effect of experimental IBD on bone health. Methods We used a murine model of colitis, H. hepaticus-infected IL-10 deficient animals. Molecular and histological properties of bone and intestine were examined to identify the immunopathological consequences of colitis in male and female mice. Results At 6 weeks post-infection we observed significant trabecular bone loss in male but surprisingly not in female mice. This was true for both distal femur and vertebral locations. In addition, H. hepaticus infection suppressed osteoblast markers only in males. Consistent with effects on bone health, male mice with H. hepaticus infection had more severe colitis as determined by histology and elevated levels of inflammatory cytokines in the colon. While H. hepaticus levels in the stool appeared similar in male and female mice 1-week after infection, by 6-weeks H. hepaticus levels were greater in male mice, indicating that H. hepaticus survival and virulence within the GI tract could be gender-dependent. Conclusion In summary, H. hepaticus induced colitis severity and associated bone loss is gender regulated, possibly as a result of gender-specific effects on H. hepaticus colonization in the mouse GI tract and the consequent immunopathologic responses.

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Bone Mineral Density in Children and Young Adults with Crohnʼs Disease

Cited by 62 publications

References 25 publications

Fibroblast growth factor 23 contributes to diminished bone mineral density in childhood inflammatory bowel disease

Fibroblast growth factor 23 contributes to diminished bone mineral density in childhood inflammatory bowel disease

Skeletal Health of Children and Adolescents With Inflammatory Bowel Disease

Colitis-induced Bone Loss is Gender Dependent and Associated with Increased Inflammation

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