O.48 Bone density and bone metabolism in inflammatory bowel disease

Bischoff, S.; Herrmann, Alena; Evers, J.A.M.; Göke, Michael; Brabant, Georg; Mühlen, A. von zur; Manns, MP

doi:10.1016/s0261-5614(95)80120-0

Cited by 62 publications

(102 citation statements)

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“…However, utilization of these markers in IBD patients has not delivered consistent results. Several studies have reported increased levels of markers of bone resorption without a compensatory increase in markers of formation (18,19,33,84,92,94). Contrary data have also been published demonstrating reduced levels of bone formation markers and no change in resorptive markers in patients with long-standing, quiescent CD (90), elevated levels of both types of markers (9,70), or no change between IBD patients and healthy controls (67).…”

Section: Bone Formation Vs Resorption In Ibd Patientsmentioning

confidence: 99%

Advances in the understanding of mineral and bone metabolism in inflammatory bowel diseases

Ghishan

Kiela

2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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Ghishan FK, Kiela PR. Advances in the understanding of mineral and bone metabolism in inflammatory bowel diseases. Am J Physiol Gastrointest Liver Physiol 300: G191-G201, 2011. First published November 18, 2010 doi:10.1152/ajpgi.00496.2010.-Chronic inflammatory disorders such as inflammatory bowel diseases (IBDs) affect bone metabolism and are frequently associated with the presence of osteopenia, osteoporosis, and increased risk of fractures. Although several mechanisms may contribute to skeletal abnormalities in IBD patients, inflammation and inflammatory mediators such as TNF, IL-1␤, and IL-6 may be the most critical. It is not clear whether the changes in bone metabolism leading to decreased mineral density are the result of decreased bone formation, increased bone resorption, or both, with varying results reported in experimental models of IBD and in pediatric and adult IBD patients. New data, including our own, challenge the conventional views, and contributes to the unraveling of an increasingly complex network of interactions leading to the inflammationassociated bone loss. Since nutritional interventions (dietary calcium and vitamin D supplementation) are of limited efficacy in IBD patients, understanding the pathophysiology of osteopenia and osteoporosis in Crohn's disease and ulcerative colitis is critical for the correct choice of available treatments or the development of new targeted therapies. In this review, we discuss current concepts explaining the effects of inflammation, inflammatory mediators and their signaling effectors on calcium and phosphate homeostasis, osteoblast and osteoclast function, and the potential limitations of vitamin D used as an immunomodulator and anabolic hormone in IBD.bone mineral density; Crohn's disease; osteopenia; osteoporosis; ulcerative colitis INFLAMMATORY BOWEL DISEASES (IBDs) represent a group of chronic inflammatory disorders of the intestinal tract that to this date remains idiopathic. More recent basic and clinical research indicates that the chronic inflammatory reaction of the intestinal mucosa is directed against the gut microbiota in individuals with genetic and/or environmental susceptibilities. Disease onset occurs typically during young adulthood (25-35 yr), although ϳ20 -25% of cases are diagnosed during childhood (93). On a clinical basis, two major subtypes of IBD are defined as Crohn's disease (CD), which potentially affects any part of the gastrointestinal tract from the mouth to the anus, and ulcerative colitis (UC), an inflammatory condition limited to the colonic mucosa. However, IBD does not affect just a single organ and should be considered a systemic disease with several extraintestinal manifestations, which occur in a large proportion of IBD patients (60). Osteopenia and osteoporosis are two of the more common extraintestinal symptoms with a general consensus that IBD patients are at a significantly higher risk of developing metabolic bone disease and low bone mineral density (BMD) than the healthy subjects. The relative risk of fractur...

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Section: Bone Formation Vs Resorption In Ibd Patientsmentioning

confidence: 99%

Advances in the understanding of mineral and bone metabolism in inflammatory bowel diseases

Ghishan

Kiela

2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Sixty of the above patients qualified and enrolled in the trial, and the abovementioned laboratory values were obtained during enrollment. The remaining 70 did not enroll (either did not qualify [42] or declined enrollment [28]), and the same laboratory values were obtained during a regular clinic visit, as part of a quality improvement nursing initiative in our IBD center. All of the patients had their vitamin D status evaluated, regardless of their BMD status.…”

Section: Patient Sample and Data Collectionmentioning

confidence: 99%

“…[21][22][23][24][25][26][27][28][29][30][31] Serum 25OHD concentration was found to be <10 ng/mL in 8% to 45% of adults with CD. 21,22,24,26 One study reports a negative relationship among disease duration, Crohn Disease Activity Index, ferritin, C-reactive protein, cholesterol, 24 and 25OHD concentration.…”

Section: Introductionmentioning

confidence: 99%

Vitamin D Status in Children and Young Adults With Inflammatory Bowel Disease

Pappa¹,

Gordon

Saslowsky³

et al. 2006

Pediatrics

188

144

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OBJECTIVES-Previous studies of vitamin D status in pediatric patients with inflammatory bowel disease have revealed conflicting results. We sought to report (1) the prevalence of vitamin D deficiency (serum 25-hydroxy-vitamin D concentration ≤15 ng/mL) in a large population with inflammatory bowel disease, (2) factors predisposing to this problem, and (3) its relationship to bone health and serum parathyroid hormone concentration.PATIENTS AND METHODS-A total of 130 patients (8-22 years of age) with inflammatory bowel disease, 94 with Crohn disease and 36 with ulcerative colitis, had serum 25-hydroxyvitamin D, intact parathyroid hormone, and lumbar spine bone mineral density (using dual-energy x-ray absorptiometry) measured at Children's Hospital Boston. RESULTS-The prevalence of vitamin D deficiency was 34.6%. Mean serum 25-hydroxyvitamin D concentration was similar in patients with Crohn disease and ulcerative colitis, 52.6% lower among patients with dark skin complexion, 33.4% lower during the winter months (December 22 to March 21), and 31.5% higher among patients who were taking vitamin D supplements. Serum 25-hydroxy-vitamin D concentration was positively correlated with weight and BMI z score, disease duration, and serum albumin concentration and negatively correlated with erythrocyte sedimentation rate. Patients with Crohn disease and upper gastrointestinal tract involvement were more likely to be vitamin D deficient than those without it. Serum 25-hydroxyvitamin concentration was not associated with lumbar spine bone mineral density z score or serum parathyroid hormone concentration.CONCLUSIONS-Vitamin D deficiency is highly prevalent among pediatric patients with inflammatory bowel disease. Factors predisposing to the problem include having a dark-skin complexion, winter season, lack of vitamin D supplementation, early stage of disease, more severe disease, and upper gastrointestinal tract involvement in patients with Crohn disease. The long-term significance of hypovitaminosis D for this population is unknown at present and merits additional study. Copyright © 2006 by the American Academy of PediatricsAddress correspondence to Helen M. Pappa, MD, MPH, Division of Gastroenterology and Nutrition, Children's Hospital Boston, 300 Longwood Ave, Boston, MA 02115. helen.pappa@childrens.harvard.edu. The authors have indicated they have no financial relationships relevant to this article to disclose. NIH Public Access Author ManuscriptPediatrics. Author manuscript; available in PMC 2011 November 1. Available reports on the vitamin D status of adults with CD place the prevalence of 25OHD concentration ≤15 ng/mL between 22% and 70%, depending on the study. 21-31 Serum 25OHD concentration was found to be <10 ng/mL in 8% to 45% of adults with CD. 21,22,24,26 One study reports a negative relationship among disease duration, Crohn Disease Activity Index, ferritin, C-reactive protein, cholesterol, 24 and 25OHD concentration.Other studies report that smoking 21 and small bowel resection 30,32 are also negativel...

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“…The biological activity of 1,25(OH) 2 D 3 is mediated by the vitamin D receptor (VDR), a member of the nuclear hormone receptor superfamily (19). A growing body of epidemiological data has documented an association between vitamin D deficiency and increased risk of IBD (20)(21)(22), including both CD and UC (23)(24)(25)(26)(27)(28)(29)(30). A high prevalence of vitamin D deficiency was reported in patients with established as well as newly diagnosed IBD (31)(32)(33).…”

Section: Introductionmentioning

confidence: 99%

Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis

et al. 2013

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The inhibitory effects of vitamin D on colitis have been previously documented. Global vitamin D receptor (VDR) deletion exaggerates colitis, but the relative anticolitic contribution of epithelial and nonepithelial VDR signaling is unknown. Here, we showed that colonic epithelial VDR expression was substantially reduced in patients with Crohn's disease or ulcerative colitis. Moreover, targeted expression of human VDR (hVDR) in intestinal epithelial cells (IECs) protected mice from developing colitis. In experimental colitis models induced by 2,4,6-trinitrobenzenesulfonic acid, dextran sulfate sodium, or CD4 + CD45RB hi T cell transfer, transgenic mice expressing hVDR in IECs were highly resistant to colitis, as manifested by marked reductions in clinical colitis scores, colonic histological damage, and colonic inflammation compared with WT mice. Reconstitution of Vdr-deficient IECs with the hVDR transgene completely rescued Vdr-null mice from severe colitis and death, even though the mice still maintained a hyperresponsive Vdr-deficient immune system. Mechanistically, VDR signaling attenuated PUMA induction in IECs by blocking NF-κB activation, leading to a reduction in IEC apoptosis. Together, these results demonstrate that gut epithelial VDR signaling inhibits colitis by protecting the mucosal epithelial barrier, and this anticolitic activity is independent of nonepithelial immune VDR actions.

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O.48 Bone density and bone metabolism in inflammatory bowel disease

Cited by 62 publications

References 0 publications

Advances in the understanding of mineral and bone metabolism in inflammatory bowel diseases

Advances in the understanding of mineral and bone metabolism in inflammatory bowel diseases

Vitamin D Status in Children and Young Adults With Inflammatory Bowel Disease

Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis

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