Reduced bone mineral density and unbalanced bone metabolism in patients with inflammatory bowel disease

Schulte, Claudia; Dignaß, Axel; Mann, Klaus; Goebell, H.

doi:10.1002/ibd.3780040403

Cited by 88 publications

(73 citation statements)

References 46 publications

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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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“…Previous studies have demonstrated that between 13 and 42% of patients with Crohn's disease have osteoporosis, [1][2][3] and two recent epidemiological studies have suggested that patients are between 1.4 and 2.5 times more likely to fracture than the normal population. 4,5 A number of risk factors have been described, most prominently the use of corticosteroids.…”

Section: Introductionmentioning

confidence: 99%

“…4,5 A number of risk factors have been described, most prominently the use of corticosteroids. [6][7][8][9][10][11][12] The mechanism responsible for the increased bone loss is unclear, but most studies describe an increase in serum or urine bone markers of resorption, 1,3,[13][14][15] suggesting that the introduction of bisphosphonates, which inhibit osteoclastic mediated bone resorption, would be a logical step in preventing further bone loss. Guidelines for the prevention and treatment of osteoporosis associated with inflammatory bowel disease have been published in the UK.…”

Section: Introductionmentioning

confidence: 99%

A randomized controlled trial of calcium with vitamin D, alone or in combination with intravenous pamidronate, for the treatment of low bone mineral density associated with Crohn's disease

Bartram

Peaston

Rawlings

et al. 2003

Aliment Pharmacol Ther

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SummaryBackground : Osteoporosis is a common complication of Crohn's disease.Aim : To study the effect on the bone mineral density of a bisphosphonate (pamidronate) given intravenously, in combination with oral calcium and vitamin D supplements, compared with oral calcium and vitamin D supplements alone.Methods : Seventy‐four patients with Crohn's disease and low bone mineral density at the lumbar spine and/or hip were randomized to receive either a daily dose of 500 mg of calcium with 400 IU of vitamin D alone or in combination with four three‐monthly infusions of 30 mg of intravenous pamidronate over the course of 12 months. The main outcome measure was the change in bone mineral density at the lumbar spine and hip, measured by dual X‐ray absorptiometry, at baseline and 12 months.Results : Both groups gained bone mineral density at the lumbar spine and hip after 12 months. There were significant (P < 0.05) changes in the pamidronate group, with gains of + 2.6%[95% confidence interval (CI), 1.4–3.0] at the spine and + 1.6% (95% CI, 0.6–2.5) at the hip, compared with gains of + 1.6% (95% CI, − 0.1–3.2) and + 0.9% (95% CI, − 0.4–2.1) at the spine and hip, respectively, in the group taking vitamin D and calcium supplements alone.Conclusions : In patients with Crohn's disease and low bone mineral density, intravenous pamidronate significantly increases the bone mineral density at the lumbar spine and hip.

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“…Studies of bone marker levels in patients with IBD have produced conflicting results. While some studies of have reported increased levels of bone resorptive markers without a compensatory increase in formation markers (31)(32)(33)(34)(35) , other studies have reported reduced levels of markers of bone formation and no difference in resorptive markers (36) , elevated levels of both types of markers (37)(38)(39)(40) or indeed no difference in markers (41) between patients with IBD and control subjects. However, in addition to differences in the biochemical markers used, some caution is also warranted in comparing the results of some of these studies because of major differences in the various populations of patients with IBD that were studied, especially in relation to the type of disease (CD v. UC), corticosteroid usage and disease activity (active disease v. disease remission) (42) .…”

Section: Risk Factors For Osteoporosismentioning

confidence: 98%

Altered bone metabolism in inflammatory disease: role for nutrition

Cashman

2008

Proc. Nutr. Soc.

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Osteoporosis is a major public health problem, and as life expectancy and the world's population continue to increase will become even more important. Thus, there is an urgent need to develop and implement nutritional approaches and policies for the prevention and treatment of osteoporosis. Patients with some chronic inflammatory diseases appear to be more likely to develop osteopenia, and in some cases earlier in life, which is of particular concern as the incidence of inflammatory diseases in the Western world is increasing. While the cause of bone loss in patients with inflammatory disease is multifactorial, nutrition may have a role. Many of these patients may have one or more nutritional deficiencies, which can lead to altered rates of bone metabolism. On the other hand, some nutritional factors may attenuate the inflammatory process itself, and thus may indirectly benefit bone metabolism and bone health in patients with inflammatory disease. The present review will consider these issues, particularly in the context of inflammatory bowel disease, coeliac diease and atherosclerosis.

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Reduced bone mineral density and unbalanced bone metabolism in patients with inflammatory bowel disease

Cited by 88 publications

References 46 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

A randomized controlled trial of calcium with vitamin D, alone or in combination with intravenous pamidronate, for the treatment of low bone mineral density associated with Crohn's disease

Altered bone metabolism in inflammatory disease: role for nutrition

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