A randomized, placebo‐controlled trial of calcium supplementation for decreased bone density in corticosteroid‐using patients with inflammatory bowel disease: a pilot study

Bernstein, Çharles N.; Seeger, Leanne L.; Anton, Peter A.; Artinian, Lucy; Geffrey, S.; Goodman, William G.; Belin, Thomas R.; Shanahan, Fergus

doi:10.1046/j.1365-2036.1996.63205000.x

Cited by 142 publications

(69 citation statements)

References 33 publications

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“…On the other hand, malnutrition and negative systemic Ca 2ϩ balance in conjunction with vitamin D insufficiency are widely considered as important factors in the pathogenesis of bone loss in IBD patients. However, in a randomized, placebo-controlled trial in glucocorticoid-treated patients with IBD, the intake of 250 IU of vitamin D and 1,000 mg/day calcium had no significant benefit in bone density at 1 year of follow-up (14). Similarly, a study with pediatric IBD patients supplemented with calcium with or without vitamin D failed to demonstrate any effect on BMD accrual (12).…”

Section: Ca 2ϩ Transport In Ibdmentioning

confidence: 97%

“…For these reasons, vitamin D 3 (and Ca 2ϩ ) supplementation has become the mainstream intuitive approach to prevent inflammation-associated bone loss and is widely recommended by gastroenterologists and promoted by the American Gastroenterological Association and by the British Society of Gastroenterology. However, the clinical efficacy of this approach in relationship with BMD loss or accrual in patients with active IBD remains controversial, with several published reports that failed to identify any clinical benefits (12,14). Obviously, more systematic studies in pediatric and adult IBD patients need to be conducted to identify factors determining the clinical response to vitamin D and Ca …”

Section: Vitamin D Status In Ibdmentioning

confidence: 99%

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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: Ca 2ϩ Transport In Ibdmentioning

confidence: 97%

Section: Vitamin D Status In Ibdmentioning

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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“…Another pathogenetic mechanism that has been implicated in the low BMD in IBD is the existence of one or more nutritional inadequacies secondary to the disease. Ca deficiency (as a result of either low intake or poor intestinal efficiency of absorption) has been reported in CD (4,44,45) . Lower vitamin D status has been reported in patients with UC and CD compared with either control subjects or a healthy population reference range (24,40,(46)(47)(48)(49)(50)(51)(52) .…”

Section: Aetiology Of Osteopenia and Osteoporosis In Inflammatory Dismentioning

confidence: 99%

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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“…The use of calcium or/and vitamin D or its analogues have shown, in 2 meta-analysis, 1 Cochrane Review, and in a large placebo-controlled study, to have a small benefit in BMD and a controversial age-dependant trend, and not totally clear reduction of bone fractures, specially of the spine, in postmenopausal women [95][96][97][98] . In a randomized, placebo-controlled trial in glucocorticoid-using patients with IBD, the intake of vitamin D 250 IU and calcium 1000 mg/d had no significant benefit in bone density at 1 year of follow-up [99] . So, as described in a recent consensus report, the supplementation with calcium and vitamin D is accepted as a cost-effective medication, and essential but insufficient, in the prevention and treatment of osteoporosis.…”

Section: Calcium and Vitamin Dmentioning

confidence: 99%

Basic and clinical aspects of osteoporosis in inflammatory bowel disease

Rodríguez-Bores¹

2007

WJG

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Lor e n a R o d r í g u e z -B o r e s , J o s u é B a r a h o n a G ar r ido, Jesús K Yamamoto-Furusho, IBD Clinic, Department of Gastroenterology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán. AbstractLow bone mineral density and the increased risk of fracture in gastrointestinal diseases have a multifactorial pathogenesis. Inflammatory bowel disease (IBD) has been associated with an increased risk of osteoporosis and osteopenia and epidemiologic studies have reported an increased prevalence of low bone mass in patients with IBD. Certainly, genetics play an important role, along with other factors such as systemic inflammation, malnutrition, hypogonadism, glucocorticoid therapy in IBD and other lifestyle factors. At a molecular level the proinflammatory cytokines that contribute to the intestinal immune response in IBD are known to enhance bone resorption. There are genes influencing osteoblast function and it is likely that LRP5 may be involved in the skeletal development. Also the identification of vitamin D receptors (VDRs) and some of its polymorphisms have led to consider the possible relationships between them and some autoimmune diseases and may be involved in the pathogenesis through the exertion of its immunomodulatory effects during inflammation. Trying to explain the physiopathology we have found that there is increasing evidence for the integration between systemic inflammation and bone loss likely mediated via receptor for activated nuclear factor kappa-B (RANK), RANK-ligand, and osteoprotegerin, proteins that can affect both osteoclastogenesis and T-cell activation. Although glucocorticoids can reduce mucosal and systemic inflammation, they have intrinsic qualities that negatively impact on bone mass. It is still controversial if all IBD patients should be screened, especially in patients with preexisting risk factors for bone disease. Available methods to measure BMD include single energy x-ray absorptiometry, DXA, quantitative computed tomography (QCT), radiographic absorptiometry, and ultrasound.DXA is the establish method to determine BMD, and routinely is measured in the hip and the lumbar spine. There are several treatments options that have proven their effectiveness, while new emergent therapies such as calcitonin and teriparatide among others remain to be assessed.

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A randomized, placebo‐controlled trial of calcium supplementation for decreased bone density in corticosteroid‐using patients with inflammatory bowel disease: a pilot study

Cited by 142 publications

References 33 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

Altered bone metabolism in inflammatory disease: role for nutrition

Basic and clinical aspects of osteoporosis in inflammatory bowel disease

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