Article Text


Inflammatory bowel disease I
PMO-228 Vitamin D deficiency in a cohort of IBD patients treated with anti-TNFα therapy
  1. C R Parris,
  2. D R Gaya,
  3. J Winter,
  4. J Munro,
  5. A J Morris
  1. Gastroenterology, Glasgow Royal Infirmary, Glasgow, UK


Introduction There is a documented association between low Vitamin D levels and IBD. In addition to the metabolic effects of Vitamin D it also has an immunomodulatory role which includes inhibition of the Th1 response (IL-2, IL-10 and TNF-α). Vitamin D deficiency may be an effect of the inflammatory process resulting in malabsorption of Vitamin D from the gastrointestinal tract or a propagating factor in IBD through loss of Th1 suppression. Vitamin D deficiency may affect the response of IBD patients to biologic drugs that act through the same immunological pathway. The primary aim of this study was to determine the prevalence of Vitamin D deficiency in a cohort of IBD patients currently receiving biologic therapy and investigate whether levels were associated with disease activity as determined by the GI inflammatory marker, faecal calprotectin. The secondary aim was to determine if Vitamin D level was associated with the following parameters: treatment group, corresponding serum CRP, history of small bowel Crohn's, small bowel resection.

Methods Patients receiving infliximab or adalimumab therapy for IBD at Glasgow Royal Infirmary between 1 June and 31 July 2011 were included in this retrospective cohort study (n=113). The following patient information was extracted from the NHS Greater Glasgow and Clyde Clinical Portal Database: treatment regime, start date, underlying GI diagnosis, GI surgical history, previous biologic therapy, Vitamin D level (serum 25OHD) and corresponding serum CRP and faecal calprotectin.

Results 60 patients (53.1%) had a recorded Vitamin D level. Of these, 63.4% (n=38) were Vitamin D deficient (25 OHD <50 nmol/l); 21.4% (n=13) were severely Vitamin D deficient (25 OHD <25 nmol/l). The median Vitamin D level of the active disease group (faecal calprotectin >200 μg/g) was 41 nmol/l (range: <14–122 nmol/l) vs 39 nmol/l (range: 17–108 nmol/l) in the remission disease group (faecal calprotectin <200 μg/g), p=0.63. There were no significant associations between Vitamin D level and biologic treatment group (p=0.65), small bowel resection (p=0.62), history of small bowel Crohn's (p=0.42), and corresponding serum CRP (p=0.33).

Conclusion Significant Vitamin D deficiency is common in our cohort of IBD patients receiving anti-TNFα therapy. Vitamin D level appears to be independent of disease activity and other specified parameters. There is evidence to consider the routine measurement of Vitamin D levels in IBD patients receiving biologic therapy and appropriate treatment of Vitamin D deficiency.

Competing interests None declared.

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