The effect of Vitamin D on intestinal inflammation and faecal microbiota in patients with ulcerative colitis

Mayur Garg, Philip Hendy, John Nik Ding, Sophie Shaw, Georgina Hold, Ailsa Hart

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31 Citations (Scopus)

Abstract

Background and Aims: Vitamin D may be immunomodulatory and alter faecal microbiota, but results from clinical studies in humans to date have been inconclusive.This study aimed to assess the effect of vitamin D replacement in vitamin D-deficient patients with and without ulcerative colitis [UC] on inflammation and faecal microbiota. Methods: Vitamin D was replaced over 8 weeks in patients with active UC [defined by faecal calprotectin ≥ 100 µg/g], inactive UC [faecal calprotectin < 100 µg/g] and non-inflammatory bowel disease [IBD] controls with baseline serum 25[OH] vitamin D <50 nmol/l, and markers of inflammation and faecal microbiota were analysed. Results: Eight patients with active UC, nine with inactive UC and eight non-IBD controls received 40000 units cholecalciferol weekly for 8 weeks. Mean baseline 25[OH] vitamin D increased from 34 [range 12–49] to 111 [71–158] nmol/l [p < 0.001], with no difference across the groups [p = 0.32]. In patients with active UC, faecal calprotectin levels decreased from a median 275 to 111 µg/g [p = 0.02], platelet count decreased [mean 375 to 313 × 109/l, p = 0.03] and albumin increased [mean 43 to 45 g/l, p = 0.04]. These parameters did not change in patients with inactive UC or non-IBD controls. No changes in overall faecal bacterial diversity were noted although a significant increase in Enterobacteriaceae abundance was observed in patients with UC [p = 0.03]. Conclusions: Vitamin D supplementation was associated with reduced intestinal inflammation in patients with active UC, with a concomitant increase in Enterobacteriaceae but no change in overall faecal microbial diversity.

Original languageEnglish
Pages (from-to)963-972
Number of pages10
JournalJournal of Crohn's and Colitis
Volume12
Issue number8
DOIs
Publication statusPublished - 30 Jul 2018

Keywords

  • Basic science
  • Clinical trials
  • Experimental models
  • Pathophysiology

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