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P714 Vitamin D deficiency in inflammatory bowel disease: prevalence and relation to disease activity in a cohort of patients of a Mediterranean country

Branco J.C., Cardoso M., Anapaz V., Lourenço L., Oliveira A.M., Rodrigues C.G., Santos L., Reis J.

Hospital Professor Doutor Fernando Fonseca -Lisboa -Portugal, Gastroenterology, Lisboa, Portugal


Vitamin D deficiency is more common in inflammatory bowel disease (IBD) patients than in the general population. It is known that vitamin D seems to play a role in inflammation. However, there is conflicting data about the predictive factors of vitamin D deficiency and its potential relation to disease activity. The aims of this study were to determine the prevalence and predictive factors of vitamin D deficiency and to evaluate a possible relation to disease activity.


We designed a prospective observational study including a cohort of inpatients and outpatients with IBD diagnosis followed at our department from January to July 2016. We considered The Endocrine Society guidelines for deficiency (<20 ng/mL, being <10 ng/mL a severe one), insufficiency (21–29ng/mL) and adequate (>30 ng/mL) levels of serum 25-hydroxyvitamin D (25-OH-D). Demographic, clinical and laboratorial parameters were collected. Disease activity was measured both clinically – by Harvey-Bradshaw index (HBi) for Crohn's Disease (CD) and Truelove and Witts score (TLWs) for ulcerative colitis (UC) - and analytically – by hemoglobin (Hb), C-reactive protein (CRP), sedimentation rate (SR) and fecal calprotectin (FC). Statistical analysis was performed using SPSS v.20.


We included 152 patients (52% men; 47.2±17.3 years) of which 70% with CD, 29% with UC and 1% with unclassified disease. Of the total, 37% were on immunosuppression and 17% on biologics, and 11.8% were inpatients. Mean 25-OH-D levels were 17.1±8 ng/mL (CD: 16.7±8 ng/mL vs. UC: 17.6±7 ng/mL, p=0.1) with a prevalence of inadequate levels in 90.8% of the total (deficiency: 68.4%; insufficiency: 22.4%). We found a significant negative correlation between 25-OH-D levels and age (r=−0.2, p=0.04), CRP levels (r=−0.22, p=0.004) and HBi (r=−0.32, p=0.001). Patients with severe deficiency also showed a higher CRP (0.6 vs. 1.4 mg/dL, p=0.03), SR (22 vs. 31mm/h, p=0.03) and HBi (2 vs. 5, p<0.001) and lower Hb (13.6 vs. 12.7 g/dL, p=0.02). We didn't find a relation between vitamin D deficiency and gender, type, extent or duration of disease, surgery, hospitalization and other measures of disease activity as SR, Hb (these two except for severe deficiency), FC or TLWs.


There is a high prevalence of inadequate levels of vitamin D in IBD patients, particularly deficiency (68.4%). In our cohort, patients with lower levels of vitamin D tended to be older and have markers of disease activity (CRP and HBi), especially the ones with severe deficiency (besides those two, also SR and Hb), but not others (FC and TLWs).