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eISSN: 2373-6372

Gastroenterology & Hepatology: Open Access

Mini Review Volume 5 Issue 2

Impact of Low Vitamin D Level on Inflammatory Bowel Diseases

Dorota Cibor

Department of Gastroenterology, Jagiellonian University Medical College, Poland

Correspondence: Dorota Cibor, Department of Gastroenterology, Jagiellonian University Medical College, Sniadeckich 5 Str, 31-545 Krako, Poland

Received: May 27, 2016 | Published: August 1, 2016

Citation: Cibor D (2016) Impact of Low Vitamin D Level on Inflammatory Bowel Diseases. Gastroenterol Hepatol Open Access 5(2): 00132. DOI: 10.15406/ghoa.2016.05.00132

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Keywords

crohn’s disease, ulcerative colitis, inflammatory bowel diseases, vitamin d, epidemiology, deficiency

Introduction

The role of vitamin D in patients with inflammatory bowel diseases (IBD) has been for years underestimated.1 This fat soluble vitamin is absorbed in jejunum and terminal ileum and directly and indirectly affects enterocytes leading to an increase in calcium absorption from the gastrointestinal tract.2 The main role of vitamin D is regulation of calcium-phosphate homeostasis.2 However, recently many studies indicate its pleiotropic effects, which is connected with the presence of vitamin D receptors (VDR) in different tissues.2,3

Anti-carcinogenic activity of vitamin D comprises promotion of cell differentiation, induction of apoptosis, inhibition of cancer cell proliferation, regulation of expression of different proinflammatory cytokines and growth factors, as well anti angiogenic properties.2,3 However, the evidence that vitamin D prevents development of colon cancer is inconsistent.3 It is worth to underline that low serum vitamin D level might also result from many other malignancy risk factors such as: obesity (vitamin D sequestration in adipose tissue), lack of physical activity (less sunlight exposure), and difference in diet habits.3

The deficiency of vitamin D has an important influence on the immune system function, and may interfere proper cellular immune response, especially of activated VDR-expressing monocytes, macrophages, dendritic cells, and lymphocytes.2,3 Vitamin D promotes microbial killing in the macrophages and inhibits antigen-presenting capacity of the dendritic cells.3 Acting through VDR in lymphocytes vitamin D inhibits their proliferation and differentiation to maturity, which results in suppression of the adaptive immune response.3

Epidemiological studies show that prevalence of vitamin D insufficiency is common in patients with IBD - in children 55.6% of patients with Crohn’s disease (CD) and 63.6% of patients with ulcerative colitis (UC) have its sub-optimal (≤32ng/mL) serum level.4 Low vitamin D level, (with insufficiency (20-30ng/mL) in 37% and deficiency (<20ng/mL) in 23%) is found in 60% of adult IBD patients.5 Especially exposed to low vitamin D levels are patients with pouchitis-69.4%.6

The most important risk factors of vitamin D insufficiency comprise: mal absorption, resection of small intestine, decreased sunlight exposure, winter and spring season, higher body mass index Z-score, smoking and higher erythrocyte sedimentation rate.2,4 In IBD patients hypovitaminosis D is associated with severer course of the disease, enhanced use of medications (corticosteroids, biologics, narcotics), increased risk of surgery and hospitalizations, and quality of life deterioration.7–9 Low vitamin D level may also contribute to an increased risk of the CD onset.10 Ananthakrishnan et al.,10 in a large prospective cohort study showed that each 100-IU/day increase in total vitamin D intake resulted in a 10% reduction in UC risk and a 7% reduction in CD risk.10

Hypovitaminosis D, as well male gender, Asian ethnicity, and corticosteroids use are risk factors for low bone mineral density in IBD.5

However, deficiency of vitamin D might be also connected with several nonskeletal effects, for instance an increased risk of Clostridium difficile infection.11 Ananthakrishnan et al.,11 found that each ng/mL increase of vitamin D level in plasma was associated with a 4% reduction in risk of Clostridium difficile infection. Ananthakrishnan et al.12 in a large IBD cohort (2809 patients) study showed an increased risk of colon cancer in subjects with vitamin D deficiency (<20ng/mL). Each 1ng/mL increase of vitamin D in plasma was associated with an 8% reduction in risk of colorectal cancer.12

In view of all the above data, vitamin D supplementation might have an important impact on the course of IBD.1,13 Jørgensen et al.,13 in a randomized double-blind placebo-controlled trialadministered vitamin D at the dose of 1200IU/d to CD patients and after three months they noticed reduced number of disease flares (13% vs. 29% in controls), however, the difference was not statistically significant.13 Pappa HM et al.,4 in a pediatric group of patients with IBD after supplementation of vitamin D at the dose of 2000IU/d observed a lower level of C-reactive protein and interleukin-6. However, more interventional studies are required to confirm the therapeutic efficacy of vitamin D supplementation in IBD.14 A target of vitamin D levels between 30 and 50ng/mL appears to be both safe and have benefits for IBD disease course. Daily vitamin D doses between 1800-10,000IU/d are probably necessary.15

Acknowledgments

None.

Conflicts of interest

Author declares there are no conflicts of interest.

Funding

None.

References

  1. Owczarek D, Rodacki T, Domagala-Rodacka R, et al. Diet and nutritional factors in inflammatory bowel diseases. World J Gastroenterol. 2016;22(3):895–905.
  2. Perzanowska-Brzeszkiewicz K, Marcinowska-Suchowierska E. Vitamin D and gastrointestinaldiseases. Postępy Nauk Medycznych. 2012;3:247–251.
  3. Rosen CJ, Adams JS, Bikle DD, et al. The nonskeletal effects of vitamin D: an Endocrine Society scientific statement. Endocr Rev. 2012;33(3):456–492.
  4. Pappa HM, Langereis EJ, Grand RJ, et al. Prevalance and risk factors for hypovitaminosis D in young patients with inflammatory bowel disease: a retrospective study. J Pediatr Gastroenterol Nutr. 2011;53(4):361–364.
  5. Abraham BP, Prasad P, Malaty HM. Vitamin D deficiency and corticosteroid use are risk factors for low bone mineral density in inflammatory bowel disease patients. Dig Dis Sci. 2014;59(8):1878–1884.
  6. Khann R, Wu X, Shen B. Low levels of vitamin D are common in patients with ileal pouches irrespective of pouch inflammation. J Crohns Colitis. 2013;7(7):525–533.
  7. KabbaniTA, Koutroubakis IE, Schoen RE, et al. Association of vitamin D level with clinical status in inflammatory bowel disease: a 5-year longitudinal study. Am J Gastroenterol. 2016;11(5):712–719.
  8. Jorgensen SP, Hvas CL, Agnholt J, et al. Active Crohn’s disease is associated with low vitamin D levels. J Crohns Colitis. 2013;7(10):407–413.
  9. Hlavaty T, Krajcovicova A, Koller T, et al. Higher vitamin D serum concentration increases health related quality of life in patients with inflammatory bowel diseases. World J Gastroenterol. 2014;20(42):15787–15796.
  10. Ananthakrishnan AN, Khalili H, Higuchi LM, et al. Higher predicted vitamin D status is associated with reduced risk of Crohn’s disease. Gastroenterology. 2012;142(3):482–489.  
  11. Ananthakrishnan AN, Cagan A, Gainer VS, et al. Higher plasma vitamin D is associated with reduced risk of Clostridium difficile infection in patients with inflammatory bowel diseases. Aliment Pharmacol Ther. 2014;39(10):1136–1142.
  12. Ananthakrishnan AN, Cheng SC, Cai T, et al. Association between reduced plasma 25-hydroxy vitamin D and increased risk of cancer in patients with inflammatory bowel diseases. Clin Gastroenterol Hepatol. 2014;12(5):821–827.
  13. Jorgensen SP, Agnholt J, Glerup H, et al. Clinical trial: vitamin D3 treatment in Crohn’s disease – a randomized double-blind placebo-controlled study. Aliment Pharmacol Ther. 2010;32(3):377–383.
  14. Ananthakrishnan AN. Editorial: Vitamin D and IBD: can we get over “causation” hump? Am J Gastroenterol. 2016;111(5):720–722.
  15. Hlavaty T, Krajcovicova A, Payer J. Vitamin D therapy in inflammatory bowel diseases: who, in what form, and how much? J Crohns Colitis. 2015;9(2):198–209.
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