Inflammation Is The Main Determinant of Low Bone Mineral Density in Pediatric Inflammatory Bowel Disease

Paganelli, Massimiliano; Albanese, Carlina V.; Borrelli, Osvaldo; Civitelli, Fortunata; Canitano, Nicoletta; Viola, Franca; Passariello, Roberto; Cucchiara, Salvatore

doi:10.1002/ibd.20039

Cited by 113 publications

(92 citation statements)

References 47 publications

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“…This is supported by the negative correlation between ESR/faecal calprotectin and serum PINP levels in our study and the fact that steroid-naive IBD patients may present with osteoporosis (23,24). Additionally, in active disease other factors such as nutrition or physical inactivity leading to reduced loading of the bones may also contribute to the low PINP levels (25).…”

Section: Discussionsupporting

confidence: 81%

Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids

Vihinen

Kolho²,

Ashorn³

et al. 2008

European Journal of Endocrinology

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Objective: We investigated circulating markers of bone turnover before and during systemic glucocorticoid treatment in paediatric patients with inflammatory bowel disease (IBD). Methods: Twenty-two children (mean age, 12.3 years) with IBD necessitating peroral steroid therapy were studied, with special reference to bone formation and resorption markers amino-terminal type I collagen propeptide (PINP) and carboxyterminal telopeptide of type I collagen (ICTP) respectively. In addition, GH-related IGF-I and sex hormone-binding protein (SHBG) were measured. Bone markers were analyzed at the initiation of the glucocorticoid treatment, at 2 and 5 weeks thereafter and at 1 month following the withdrawal of the steroid. Control group comprised 22 IBD patients in remission.Results: PINP and IGF-I were already lower before glucocorticoid treatment serum in children with active IBD as compared with control children with IBD in remission (median PINP 271 vs 535 mg/l, P!0.05; IGF-I 23 vs 29 nmol/l, P!0.05). After 2 weeks of glucocorticoid treatment serum PINP levels had declined further, from 271 to 163 mg/l (P!0.001), serum ICTP from 14.2 to 9.6 mg/l (P!0.001), and SHBG from 54 to 35 nmol/l (P!0.001) respectively. By contrast, serum IGF-I increased from 23 to 37 nmol/l (P!0.001). One month after the withdrawal of the glucocorticoid, all bone markers restored to levels similar to the controls. Conclusions: Bone formation in children with active IBD appears compromised and systemic glucocorticoid treatment further suppresses bone turnover. After the cessation of the glucocorticoid the bone markers show immediate improvement.European Journal of Endocrinology 159 693-698

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Section: Discussionsupporting

confidence: 81%

Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids

Vihinen

Kolho²,

Ashorn³

et al. 2008

European Journal of Endocrinology

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“…Inflammatory process and GC therapy are not the only causes of low BMD, but also malabsorption and malnutrition, restriction diets (that include low vitamin D and calcium intake), hypovitaminosis D and immobilization (19,20 The IL-2 deficient mouse model of colitis is known to develop both osteopenia and colitis, but low bone mass does not occur in T-cell deficient rats, indicating the central role of activated T-cells in bone loss in IBD models (22). High levels of inflammatory cytokines (TNF-α, IL-1, IL-6, IL-11, IL-17, TGF-α, epidermal growth factor, and prostaglandin E2) are detected in the gut mucosa and in the peripheral blood of IBD patients (18,19).…”

Section: Inflammatory Bowel Diseasementioning

confidence: 99%

“…High levels of inflammatory cytokines (TNF-α, IL-1, IL-6, IL-11, IL-17, TGF-α, epidermal growth factor, and prostaglandin E2) are detected in the gut mucosa and in the peripheral blood of IBD patients (18,19). The main cytokine appears to be IL-6, which displayed a serum concentration negatively correlated with BMD (19).…”

Section: Inflammatory Bowel Diseasementioning

confidence: 99%

Osteoporosis and inflammation

Lacativa

Farias

2010

Arq Bras Endocrinol Metab

196

138

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SUMMARYSeveral inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, celiac disease, cystic fibrosis and chronic obstructive pulmonary disease have been associated to bone resorption. The link between osteoclast, macrophage colony stimulating factor and pro-inflammatory cytokines, especially tumor necrosis factor-α and interleukin-1 explain the association between inflammation and osteoporosis. These diseases are related to osteoporosis and high fracture risk independent of other risk factors common to inflammatory diseases such as reduced physical activity, poor nutritional status, hypovitaminosis D, decrease in calcium intake and glucocorticoid treatment. Erythrocyte sedimentation rate and C-reactive protein should always be performed, but the indication about when to perform the densitometry test should be analyzed for each disease. Bisphosphonates are nowadays the best choice of therapy but new medications such as denosumab, IL-1 receptor antagonist, and TNF-α antibody have risen as new potential treatments for osteoporosis secondary to inflammation. Arq Bras Endocrinol Metab. 2010;54(2):123-32 Keywords Osteoporosis; inflammation; arthritis, rheumatoid; lupus erythematosus, systemic; interleukin-1; tumor necrosis factor-alpha SUMÁRIO Diversas doenças inflamatórias têm sido associadas à reabsorção óssea, como a artrite reumatoide, o lúpus eritematoso sistêmico, a doença inflamatória intestinal, a doença celíaca, a fibrose cística e a doença pulmonar obstrutiva crônica. A ligação entre osteoclastos, fator estimulador de colônia de macrófagos e citocinas pró-inflamatórias, principalmente o fator de necrose tumoral-α e interleucina-1, explica a associação entre a inflamação e a osteoporose. Essas doenças estão relacionadas com osteoporose e aumento do risco de fratura, independentemente de outros fatores de risco comuns às doenças inflamatórias, tais como redução da atividade física, estado nutricional, hipovitaminose D, diminuição da ingestão de cálcio e uso de glicocorticoides. A velocidade de hemossedimentação e proteína C-reativa devem ser sempre realizadas, mas a indicação do exame de densitometria óssea deve ser analisada em cada doen ça. Os bisfosfonatos são atualmente a melhor opção de terapia, mas novos medicamentos, tais como denosumabe, antagonista do receptor de IL-1 e anticorpos anti-TNF-α, surgem como novos potenciais tratamentos para a osteoporose secundária à inflamação. Arq Bras Endocrinol Metab. 2010;54(2):123-32 Descritores Osteoporose; inflamação; artrite reumatoide; lúpus eritematoso sistêmico; interleucina-1; fator de necrose tumoral-alfa

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“…Cytokines are connected with the increased resorption of the bone tissue and the inhibition of osteogenesis [32]. A negative correlation was observed between bone mineral apparent density (BMAD) among children assessed by means of volumetric methods, with the concentration of pro-inflammatory Il 6 and the activity of the disease assessed in the point-based scale, as well as the improvement in the scope of BMAD among patients subject to the biological treatment [33]. Steroids were not very significant in lowering BMAD, maybe because of the fact that the pediatric population which was examined had the disease for an approximately short time and had an approximately low accumulated dose of GCs.…”

Section: The Influence Of Vitamin D On Bone Density In Ibdmentioning

confidence: 99%

“…Steroids were not very significant in lowering BMAD, maybe because of the fact that the pediatric population which was examined had the disease for an approximately short time and had an approximately low accumulated dose of GCs. In the context of such restrictions, the beneficial anti-inflammatory influence of GCs on the bone metabolism exceeded known general negative influence on bones [33].…”

Section: The Influence Of Vitamin D On Bone Density In Ibdmentioning

confidence: 99%

The Role of Vitamin D3 in Inflammatory Bowel Diseases

Kosmowska-Miśków¹

2014

Adv Clin Exp Med

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Vitamin D3, combined with its nuclear receptor, regulates more than 900 genes, which is the reason why its effect is pleiotropic. Among other effects, it influences the immunological system. Its deficit may be one of the environmental factors taking part in the development of auto-immunological diseases. The studies reveal that, among others things, inflammatory bowel diseases occur in higher latitudes, with lower exposure to solar radiation and with decreased production of vitamin D3 in the skin. Patients with inflammatory bowel disease have vitamin D3 deficiency more frequently. The application of vitamin D3, especially among adults with inflammatory bowel diseases, positively influences bone turnover markers and mostly due to its influence on immunological processes, vitamin D3 may be useful in the treatment of the primary health condition. It is necessary to determine the dosage range, as well as the optimal level of vitamin D3 metabolite-25OHD3, where the immunosuppressant effect is the best, with no toxic effects. The basic function of vitamin D3 in the body is its influence on keeping the homeostasis of calcium metabolism, preventing the appearance of rickets, osteomalacia and osteoporosis [1,2]. Vitamin D comes from food -ergocalciferol (vitamin D2), and mostly it is synthesized in the skin under the influence of ultraviolet radiation B (UVB) -cholecalciferol (vitamin D3). Next, in the liver, it is hydroxylated into its inactive form 25 OH D3 (calcidiol) and in the kidney into its active form -1,25 (OH)2 D3--calcitriol. Except for the cells of cuticle of proximal tubule in the kidney, the activity of 1-alfa-hydroxylase have also, among others, antigen presenting cells (APCs), parasympathetic ganglions, hair follicles, cerebral cortex cells, pancreatic islets [3]. Vitamin D acts through its receptors (vitamin D receptors -VDr), which may be found in the majority of organs: in the alimentary tract, bones, the brain, the chest, muscles and others. [3]. Vitamin D combined with the receptor is the regulator of more than 900 genes. In this way it regulates, among others, the calcium metabolism, intestinal calcium transport, as well as cell proliferation and differentiation [4]. An analysis of microarrays and the genome screening of vitamin D3 receptors (VDrs), which are nucleus receptors and direct transcription factors, detected the molecular base of physiological effects of vitamin D3-both its influence on calcium metabolism, immunological system as well as its antitumor activity [4].

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Inflammation Is The Main Determinant of Low Bone Mineral Density in Pediatric Inflammatory Bowel Disease

Cited by 113 publications

References 47 publications

Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids

Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids

Osteoporosis and inflammation

The Role of Vitamin D3 in Inflammatory Bowel Diseases

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