48
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Therapeutic Effect of Vitamin D Supplementation in a Pilot Study of Crohn's Patients

      other

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          OBJECTIVES:

          Low vitamin D status may be associated with Crohn's disease. A pilot study was performed in patients with mild-to-moderate Crohn's disease to determine the dose of vitamin D needed to raise serum vitamin D levels above 40 ng/ml.

          METHODS:

          Patients were evaluated for severity of symptoms using the Crohn's disease activity index (CDAI) and patients with mild-to-moderate (150–400 CDAI scores) Crohn's disease were entered into the study ( n=18). Vitamin D 3 oral therapy was initiated at 1,000 IU/d and after 2 weeks, the dose was escalated incrementally until patients' serum concentrations reached 40 ng/ml 25(OH)D 3 or they were taking 5,000 IU/d. Patients continued on the vitamin D supplements for 24 weeks. CDAI, quality of life measures, bone mineral density, dietary analyses, cytokines, parathyroid hormone, calcium, and several other laboratory measurements were evaluated at baseline and after 24 weeks supplementation.

          RESULTS:

          Fourteen of eighteen patients required the maximal vitamin D supplement of 5,000 IU/d. Vitamin D oral supplementation significantly increased serum 25(OH)D 3 levels from 16±10 ng/ml to 45±19 ng/ml ( P<0.0001) and reduced the unadjusted mean CDAI scores by 112±81 points from 230±74 to 118±66 ( P<0.0001). Quality-of-life scores also improved following vitamin D supplementation ( P=0.0004). No significant changes in cytokine or other laboratory measures were observed.

          CONCLUSIONS:

          Twenty-four weeks supplementation with up to 5,000 IU/d vitamin D 3 effectively raised serum 25(OH)D 3 and reduced CDAI scores in a small cohort of Crohn's patients suggesting that restoration of normal vitamin D serum levels may be useful in the management of patients with mild–moderate Crohn's disease.

          Related collections

          Most cited references19

          • Record: found
          • Abstract: found
          • Article: not found

          1,25-dihydroxyvitamin D3 receptors in human leukocytes.

          A 1,25-dihydroxyvitamin D3 receptor macromolecule was detected in peripheral mononuclear leukocytes from normal humans. This macromolecule was found to be present in monocytes but absent from normal resting peripheral B and T lymphocytes. However, it was present in established lines of malignant B, T, and non-B, non-T human lymphocytes, as well as in T and B lymphocytes obtained from normal humans and activated in vitro.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            1,25-Dihydroxycholecalciferol prevents and ameliorates symptoms of experimental murine inflammatory bowel disease.

            Anecdotal data suggest that the amount of vitamin D available in the environment either from sunshine exposure or diet may be an important factor affecting the development of inflammatory bowel disease (IBD) in humans. We tested the vitamin D hypothesis in an experimental animal model of IBD. Interleukin (IL)-10 knockout (KO) mice, which spontaneously develop symptoms resembling human IBD, were made vitamin D deficient, vitamin D sufficient or supplemented with active vitamin D (1,25-dihydroxycholecalciferol). Vitamin D-deficient IL-10 KO mice rapidly developed diarrhea and a wasting disease, which induced mortality. In contrast, vitamin D-sufficient IL-10 KO mice did not develop diarrhea, waste or die. Supplementation with 50 IU of cholecalciferol (5.0 microgram/d) or 1, 25-dihydroxycholecalciferol (0.005 microgram/d) significantly (P < 0. 05) ameliorated symptoms of IBD in IL-10 KO mice. 1, 25-Dihydroxycholecalciferol treatment (0.2 microgram/d) for as little as 2 wk blocked the progression and ameliorated (P < 0.05) symptoms in IL-10 KO mice with already established IBD.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              A crucial role for the vitamin D receptor in experimental inflammatory bowel diseases.

              The active form of vitamin D (1,25D3) suppressed the development of animal models of human autoimmune diseases including experimental inflammatory bowel disease (IBD). The vitamin D receptor (VDR) is required for all known biologic effects of vitamin D. Here we show that VDR deficiency (knockout, KO) resulted in severe inflammation of the gastrointestinal tract in two different experimental models of IBD. In the CD45RB transfer model of IBD, CD4+/CD45RBhigh T cells from VDR KO mice induced more severe colitis than wild-type CD4+/CD45RBhigh T cells. The second model of IBD used was the spontaneous colitis that develops in IL-10 KO mice. VDR/IL-10 double KO mice developed accelerated IBD and 100% mortality by 8 wk of age. At 8 wk of age, all of the VDR and IL-10 single KO mice were healthy. Rectal bleeding was observed in every VDR/IL-10 KO mouse. Splenocytes from the VDR/IL-10 double KO mice cells transferred IBD symptoms. The severe IBD in VDR/IL-10 double KO mice is a result of the immune system and not a result of altered calcium homeostasis, or gastrointestinal tract function. The data establishes an essential role for VDR signaling in the regulation of inflammation in the gastrointestinal tract.
                Bookmark

                Author and article information

                Journal
                Clin Transl Gastroenterol
                Clin Transl Gastroenterol
                Clinical and Translational Gastroenterology
                Nature Publishing Group
                2155-384X
                April 2013
                18 April 2013
                1 April 2013
                : 4
                : 4
                : e33
                Affiliations
                [1 ]Department of Veterinary and Biomedical Science, Center for Molecular Immunology and Infectious Disease , University Park, Pennsylvania, USA
                [2 ]Department of Medicine , Hershey, Pennsylvania, USA
                [3 ]Department of Nutritional Sciences, The Pennsylvania State University , University Park, Pennsylvania, USA
                Author notes
                [* ]Department of Veterinary and Biomedical Sciences, The Center for Molecular Immunology and Infectious Disease , 115 Henning Building, University Park, Pennsylvania 16802, USA. E-mail: mxc69@ 123456psu.edu
                Article
                ctg20131
                10.1038/ctg.2013.1
                3636524
                23594800
                fd1acebc-95b8-4d13-a1c9-bbe173102315
                Copyright © 2013 American College of Gastroenterology

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

                History
                : 28 June 2012
                : 03 December 2012
                : 18 January 2013
                Categories
                Inflammatory Bowel Disease

                Gastroenterology & Hepatology
                Gastroenterology & Hepatology

                Comments

                Comment on this article