Search in the Abstract Database

Search Abstracts 2012

* = Presenting author

P163. Vitamin D deficiency in IBD patients at diagnosis and its relationship with disease location and activity: A cohort study in 2 UK IBD centres

R. Cole1, N. Arebi2, S. Tripoli3, S. Sebastian4

1Hull & York Medical School, Hull, United Kingdom; 2St Mark's Hospital, Department of Gastroenterology, London, United Kingdom; 3St Mark's Hospital, London, United Kingdom; 4Hull & East Yorkshire NHS Trust, Hull, United Kingdom

Background: Vitamin D levels may predispose to Inflammatory Bowel disease (IBD). Vitamin D deficiency may also aggravate the risk of osteoporosis. Prospective studies of hyopvitaminosis D in incident IBD patients are lacking. We aimed to identify the prevalence of hypovitaminosis D (insufficient + deficient) in an incident cohort of IBD patients and to examine the association between vitamin D status at diagnosis and clinical phenotype.

Methods: Patients diagnosed with IBD since 2009 in 2 UK IBD units were identified prospectively. Vitamin D levels measured at diagnosis were classified as adequate (>50 nmol/L), insufficient (25–50 nmol/L) or deficient (<25 nmol/L). Patients were classified according to Montreal classification. Harvey–Bradshaw Index (HBI) and Ulcerative Colitis Disease Activity Index (UCDAI) were used to assess disease activity. Multivariate logistic regression identified predictors of vitamin D deficiency and association with disease location and severity.

Results: 222 newly diagnosed IBD patients were included (119 UC, 86 CD, 16 unclassified). Overall hypovitaminosis D was identified in 131 patients (59.1%). Insufficient Vitamin D was found in 92 patients (41.4%); Deficient Vitamin D identified in 39 (17.5%) patients. Significantly higher proportion of UC patients, had hypovitaminosis D (63.2% vs. 53.5%, p = 0.05) and severe vitamin D deficiency (21.8% vs. 11.6%, p = 0.01) compared with CD patients after adjusting for age, gender and season. In CD, Vitamin D deficiency was associated with non-stricturing behaviour (2.87, 95% CI 0.41–3.71) and disease activity score (1.37, 95% CI 0.41–1.92) but not with disease location. There was no association between Vitamin D deficiency and disease location or activity in UC.

Conclusions: Hypovitaminosis D is common at IBD diagnosis. Vitamin D deficiency appears to be commoner in UC than in CD patients and in UC patients appears to be independent of disease location and activity. The mechanism of vitamin D deficiency and its implications on IBD disease course warrant further study.