Role of Vitamin D in Inflammatory Bowel Disease flare

Abstract

Purpose OF THE STUDY: Vitamin D deficiency is a global health issue. Althoughclassically associated with rickets and other sequelae, Vitamin D and the VitaminD receptor (VDR) have been shown to be important regulators of the immunesystem. In particular, Vitamin D and VDR deficiency exacerbates autoimmune diseasessuch as inflammatory bowel disease (IBD) in experimental animals. The roleof Vitamin D in immunity is a feedback reaction of the paracrine system to eliminateinflammation. It is postulated that it either influences CD4 T-cell differentiationor increases the function of T suppressor cells or a combination of both. Theactive form of Vitamin D produces and maintains self-immunologic tolerance, and some studies show that 1, 25(OH)2D inhibits induction of disease in autoimmuneencephalomyelitis, thyroiditis, type-1 diabetes mellitus, inflammatory boweldisease (IBD), systemic lupus erythematosus, collagen-induced arthritis and Lymearthritis.The role of impaired Vitamin D regulation in IBD has been studied in animalstudies. Experiments done on mice showed that DNA array analysis of colon tissueidentified 27 genes which consistently up-regulated or down-regulatedmore than two-fold in Vitamin D-deficient mice in comparison to Vitamin D-sufficientmice.All published experiments regarding this topic have involved only animals. Todate there are no studies, either retrospective or randomized trials, done inhumans to suggest that Vitamin D deficiency results in either a change in theclinical course of IBD patients or an Increase in the number of flares. Theaim of this study is to identify whether there is any temporal relationshipbetween Vitamin D and IBD. One study done in Hungary in 2009 showed thatIBD patients treated with activated Vitamin D had a decremental effect of 17%in the CDAI (Crohn's disease activity Index), 13% in the IBDQ (IBD Questionnaire)and 53% in C - reactive protein (CRP). In this study the above mentionedresults were secondary endpoints of the study and the study was notblinded.The aim of our study was to ascertain whether Vitamin D deficiency in inflammatorybowel disease patients causes an increase in the number of acute flares ofIBD. The secondary aim of the study was to assess if the Vitamin D deficiencycan be one of the possible etiologies in newly diagnosed inflammatory boweldisease patients. Methods: Medical records and the laboratory reports including colonoscopyreports of either old or newly diagnosed inflammatory bowel disease patientsthat were seen in the outpatient clinic were reviewed. Patients with Vitamin Ddeficiency were categorized as cases (group 1) and those without deficiency aretaken as controls (group 2). The charts were reviewed retrospectively for at least1 year after they found to be vitamin D deficient and the number of flares wasnoted. The acute flare was defined by either clinical worsening characterized byworsening diarrhea, rectal bleeding, and abdominal pain and confirmed by colonoscopy, or requirement for additional treatment; elevated serum CRP/ESR; or CTscan of the abdomen revealing acute bowel inflammation. Results: There were 9 patients in group 1 and 49 patients in group 2. Patientdemographics such as age and gender were similar in both groups. The commonpresentation of the flare was abdominal pain. All patients in both groups wereon 5-ASA compounds. 2/3 of patients in the first group and half of the patientsin the second group had crohn's disease. 5 patients in group 1 experience 1 flarecompare to none in the control group. Using chi-square analysis we found a statisticallysignificant difference (P < 0.001) of having flares between these 2 groupsindicating that Vitamin D deficiency may be associated with an increase numberof flares in IBD patients. Conclusion: Based on this small study, we recommend to check Vitamin Dlevel in all IBD patients with subsequent treatment of patients who are VitaminD deficient. The major limitation of our study is the small sample size andthe retrospective nature of the study design. Obviously more data is neededbefore we know the exac mechanism and impact of Vitamin D level inpatients with IBD.