P238 Vitamin D deficiency in inflammatory bowel disease: is malabsorption to blame?
J. Schembri*, S. Chetcuti, S. Vella, P. Ellul
Mater Dei Hospital, Gastroenterology, Msida, Malta
Vitamin D deficiency is common in inflammatory bowel disease (IBD) and was previously attributed to factors such as anorexia and malabsorption. Vitamin D and its receptor (VDR) have an important role within the immune system by controlling cell proliferation, antigen receptor signalling, and intestinal barrier function. Circulating vitamin D levels might also help determine IBD risk, and although past studies have been equivocal on the topic, this seems to be backed up by more recent cohort data. Unlike CD, UC is not typically associated with malabsorption.
We conducted a case-control study, recruiting 142 patients with an established diagnosis of IBD (27 Crohn’s disease [CD], 115 ulcerative colitis [UC]). Further, 106 gender matched healthy volunteers were selected as controls. All individuals were of Maltese Caucasian origin and had been living in Malta for at least 1 year thus eliminating bias from geographical and ethnic gene variations. For both groups, 25-hydroxyvitamin D and corrected calcium levels were measured. IBD-specific data were obtained from our local database, and disease activity was measured using Harvey–Bradshaw and CD activity indices.
In the study, 52.7% of patients were male, and 87.3% of cases were in remission. Vitamin D levels in the IBD group were significantly lower (mean 26.0 ng/ml) than in the control population (mean 35.2 ng/ml; p = 0.01). Only 6.1% UC and 11.1% CD patients had normal levels. Most patients suffered from insufficiency (77.4% UC, 74.1% CD) and a significant proportion were deficient (16.5% UC, 14.8% CD). Vitamin D levels were not significantly associated with disease activity/duration or gender, and levels did not vary significantly between CD and UC cases. Patient age was inversely related to vitamin D levels (p = 0.01) in the IBD group but not in the control group. Corrected calcium levels for all groups were within range and there was no statistical difference. The vast majority (91.4%) of our patients were not receiving supplements at the time of the study. Patients with past or current use of anti-TNF treatment had significantly higher vitamin D levels compared with their anti-TNF naïve peers (p = 0.01; 30.7 ng/mL vs 25.1 ng/mL).
Most of our patients had UC that was in remission. Vitamin D deficiency in IBD is therefore probably attributable to factors other than malabsorption and disease activity. The relationship between biologics and vitamin D is a complex one and requires further investigation. Whether vitamin D deficiency is a cause or a consequence of IBD remains to be determined. The influence of VDR polymorphisms on IBD risk is still poorly understood and some variants have indeed been linked to lower circulating vitamin D levels. This offers new hope for novel therapeutic approaches.