Níveis baixos de 25-hidroxivitamina D (25OHD) em pacientes com doença inflamatória intestinal e sua correlação com a densidade mineral óssea

Souza, Hevelyn Noemberg de; Lora, Fabiana Lígia; Kulak, Carolina A. M.; Mañas, Nádila Cecyn Pietszkowski; Amarante, Heda Maria Barska dos Santos; Borba, Victória Zeghbi Cochenski

doi:10.1590/s0004-27302008000400015

Cited by 20 publications

(18 citation statements)

References 43 publications

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“…Souza et al described that the number of patients with low BMD between the two groups of IBD is equivalent. 3 In our study, however, we observed that CD patients had a higher prevalence of bone alterations (52.6% CD and 29.6% UC, p=0.07). This difference may be related to the fact that in CD a greater area of the digestive tract implied in the absorption of nutrients is affected, or even because these patients use corticosteroids more frequently compared with patients with UC.…”

Section: Discussioncontrasting

confidence: 69%

“…In the Curitiba area, due to its climatic characteristic of low annual insolation, there is a greater possibility of vitamin D deficiency, as already evaluated by other authors. 3,16 Regarding serum vitamin D levels, the importance of its replacement in patients with IBD has already been suggested, 17 since it has a relevant role in the health of this group of patients. In addition to the benefit in bone integrity, an improvement in the immune response is expected and, although not yet fully proven, aid in the prevention of colorectal cancer, a complication that can occur in patients with IBD.…”

Section: Discussionmentioning

confidence: 99%

“…Low BMD in this group of patients is more frequent than in the general population 1 and factors such as chronic inflammation, prolonged use of corticosteroids, unsatisfactory physical activity, and malnutrition may contribute to the appearance and aggravation of the condition. 2,3 In addition, the absorptive changes that patients with IBD present may cause vitamin D absorption deficits. In turn, a serum reduction of this vitamin may contribute to the early onset of bone changes such as osteopenia and osteoporosis.…”

Section: Introductionmentioning

confidence: 99%

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Alert for bone alterations and low serum concentrations of vitamin D in patients with intestinal inflammatory disease

Kotze

Costa

Cavassani

et al. 2017

Rev. Assoc. Med. Bras.

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Background: Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are characterized by chronic inflammation of the intestine that can reduce the absorption of nutrients such as vitamin D and calcium. Objective: To investigate bone alterations and serum levels of vitamin D in patients with IBD. Method: This was a cross-sectional study based on a review of medical records of patients from a private office in Curitiba, PR, Brazil. Serum levels of vitamin D and bone densitometry were measured at diagnosis of IBD. A total of 105 patients were included; 38 (58.4%) with CD; 27 (41.6%) with UC and 40 with irritable bowel syndrome (IBS) as comparison group. Results: When compared to patients with UC, CD patients showed a higher prevalence of bone alterations, being 15.8% with osteoporosis and 36.8% with osteopenia. In UC, bone alterations occurred in 29.6% of cases, 3.7% with osteoporosis and 25.9% with osteopenia. As for vitamin D levels, among CD patients, 10.5% had vitamin deficiency, 65.8% insufficiency and 23.7% were sufficient. In UC, 7.4% of cases had deficiency, 74.1% insufficiency and 18.5% had sufficient serum levels of vitamin D. In the group with IBS, deficiency was observed in 17.5% of cases, insufficiency in 55% and sufficiency in 27.5% of them. There was no significant difference between groups. Conclusion: IBD patients have a high prevalence of bone changes, especially those with CD. Serum levels of vitamin D are below the recommended in all the evaluated groups.

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Section: Discussioncontrasting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Alert for bone alterations and low serum concentrations of vitamin D in patients with intestinal inflammatory disease

Kotze

Costa

Cavassani

et al. 2017

Rev. Assoc. Med. Bras.

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“…A growing body of epidemiological data has documented an association between vitamin D-deficiency and increased risk of IBD [14; 15; 16], including both CD and UC [17; 18; 19; 20; 21; 22; 23; 24]. A high prevalence of vitamin D deficiency was reported in patients with established as well as newly diagnosed IBD [25; 26; 27].…”

Section: Introductionmentioning

confidence: 99%

Critical roles of intestinal epithelial vitamin D receptor signaling in controlling gut mucosal inflammation

Chen

2015

The Journal of Steroid Biochemistry and Molecular Biology

110

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Although vitamin D receptor (VDR) is highly expressed in the intestine, the role of VDR signaling in the gut is not fully understood. Our recent studies unveil a regulatory circuit that centers gut epithelial VDR as a key molecule in the control of mucosal inflammation and colitis development. On the one hand, intestinal epithelial VDR signaling protects the integrity of the mucosal barrier by inhibiting inflammation-induced epithelial cell apoptosis. This barrier-protecting, anti-colitic activity is independent of the non-epithelial immune VDR actions. A healthy and intact mucosal barrier prevents bacterial invasion and thus reduces mucosal inflammation. On the other hand, inflammation in turn down-regulates epithelial VDR expression by inducing VDR-targeting microRNA-346, thus compromising mucosal barrier functions. Consistently, colonic epithelial VDR levels are markedly reduced in patients with inflammatory bowel diseases or in experimental colitis models, whereas vitamin D analog therapy that ameliorates colitis up-regulates epithelial VDR. Thus, gut epithelial VDR signaling appears to play an essential role in controlling mucosal inflammation and thus could be a useful therapeutic target in the management of inflammatory bowel diseases.

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“…Intestinal epithelial cells (IECs) are key components of the barrier that express a high level of vitamin D receptor, a nuclear hormone receptor that mediates the biological activity of the vitamin D hormone, 1,25-dihydroxyvitamin D [4]. Epidemiological studies have established that vitamin D-deficiency is common in patients with IBD that is associated with increased risk of IBD [5,6,7,8,9,10,11,12,13,14], whereas high vitamin D intake lowers the risk of IBD [15]. …”

Section: Introductionmentioning

confidence: 99%

Transgenic Expression of Vitamin D Receptor in Gut Epithelial Cells Ameliorates Spontaneous Colitis Caused by Interleukin-10 Deficiency

et al. 2015

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Background Vitamin D-deficiency is common in patients with inflammatory bowel diseases. The vitamin D receptor (VDR) is a nuclear hormone receptor mediating the activity of vitamin D hormone. Our previous studies showed that intestinal epithelial VDR signaling inhibits colitis by protecting the mucosal epithelial barrier, and this activity is independent of non-epithelial immune VDR actions. Interleukin (IL)-10-deficient mouse is a chronic colitis model that develops colitis due to aberrant immune responses. Here we used IL-10 null (IL-10KO) model to assess the anti-colitic activity of epithelial VDR in the setting of an aberrant immune system. Methods We crossed IL-10KO mice with villin promoter-driven human (h) VDR transgenic (Tg) mice to generate IL-10KO mice that carry the hVDR transgene in intestinal epithelial cells (IL-10KO/Tg). IL-10KO and IL-10KO/Tg littermates were studied in parallel and followed for up to 25 weeks. Results By 25 weeks of age, accumulatively 79% IL-10KO mice developed prolapse, whereas only 40% IL-10KO/Tg mice did so (P<0.001). Compared to IL-10KO mice, IL-10KO/Tg littermates showed markedly reduced mucosal inflammation in both small and large intestines, manifested by attenuation in immune cell infiltration and histological damage and a marked decrease in pro-inflammatory cytokine production. IL-10KO/Tg mice also showed reduced intestinal epithelial cell apoptosis as a result of diminished PUMA induction and caspase 3 activation. Conclusion These observations demonstrate that targeting hVDR expression to intestinal epithelial cells is sufficient to attenuate spontaneous colitis caused by an ill regulated immune system, confirming a critical role of the epithelial VDR signaling in blocking colitis development.

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Níveis baixos de 25-hidroxivitamina D (25OHD) em pacientes com doença inflamatória intestinal e sua correlação com a densidade mineral óssea

Cited by 20 publications

References 43 publications

Alert for bone alterations and low serum concentrations of vitamin D in patients with intestinal inflammatory disease

Alert for bone alterations and low serum concentrations of vitamin D in patients with intestinal inflammatory disease

Critical roles of intestinal epithelial vitamin D receptor signaling in controlling gut mucosal inflammation

Transgenic Expression of Vitamin D Receptor in Gut Epithelial Cells Ameliorates Spontaneous Colitis Caused by Interleukin-10 Deficiency

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