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P304. Two year study of high and low dose oral vitamin D replacement therapy in adult inflammatory bowel disease

M. Naghibi1, H.J. Hiew1, J. Saunders2, J.R.F. Cummings1, T.R. Smith1, 1University Hospital Southampton, Gastroenterology, Southampton, United Kingdom, 2Royal United Hospital NHS Trust, Gastroenterology, Bath, United Kingdom


Inflammatory bowel disease (IBD) patients are known to be at risk of osteoporosis. The discovery of vitamin D receptors expressed on immune cells suggests that vitamin D is able to modulate immune-response and exert anti-inflammatory effects. This could potentially be beneficial in immune-mediated diseases such as IBD. It is important to manage vitamin D deficiency effectively among the IBD population. We aimed to determine the vitamin D status and evaluate the effectiveness of oral vitamin D treatment in a cohort of IBD patients at a University Hospital.


All patients with vitamin D measurements between Jan 2011 to Dec 2012 were identified using electronic patient records. Vitamin D deficiency was determined as plasma 25-hydroxyvitamin D [25(OH)D] levels <52 nmol/L, with severe deficiency <25 nmol/L. Oral vitamin D treatment was classified as ‘low dose’ when patients prescribed daily 800 units of vitamin D2/D3 and ‘high dose’ when given either 100,000 or 150,000 units once only or 10,000 units weekly for 6 weeks. Treatment response was assessed within 6 months of treatment.


450 IBD patients with serum vitamin D levels were identified. There was no statistically significant difference between Crohn's disease (CD) and ulcerative colitis (UC) patient's age (46 yrs ±18 SD) or age of IBD onset (34 yrs ±17 SD), median disease duration (9 yrs), osteoporosis rates (33%), vitamin deficiency rates or response to treatment. Table 1 demonstrates the point prevalence of deficiency.

When high dose regimens are used 70/87 (80%) patient's vitamin D level reached normal range, while this only occurred in 7/17 (40%) patients on low dose therapy (p-value = 0.002). The real value increase in the high dose group was 48 nmol/L (145% increase) and 14 nmol/L (39% increase) in the low dose treatment group (p-value ≤0.001, 95% CI 18.4–50.0) (Table 2). 13 (6%) patients developed vitamin D deficiency during the study, confirming the need for longterm monitoring for all patients.

Table 2 (abstract P304). Treatment response by types of IBD and dose of treatment
Number of patients Vit D deficient (%)Baseline Vit D in those deficient (nmol/L)Number treated orally and follow up Vit D availableNumber of HIGH dose patients treated with available FU levelsMean increase Vit D with HIGH dose (nmol/L)% Vit D increase with HIGH doseNumber of LOW dose treated with available FU levelsMean increase Vit D with LOW dose (nmol/L)% Vit D increase with LOW dose
All patients (incl. IC) (n = 450)226 (50)29102*8548145171439
UC (n = 147)73 (50)3233284215651547
All CD (n = 291)148 (51)31695748145121337
 Ileocolonic (n = 110)58 (53)313326531566618
 Colonic (n = 63)24 (44)311294012131636
 Small bowel (n = 116)62 (53)2924214419032525
 Isolated upper GI (n = 2)
IC, indeterminant colitis included in total but *none with follow up vitamin D level available.
Table 1. Prevalence of vitamin D deficiency by type of IBD and severity of deficiency
Plasma 25(OH)D (nmol/L)All patients (N = 450), n (%)CD (N = 291), n (%)UC (N = 147), n (%)IC (N = 12), n (%)CD vs UC P-value
All patients <52226 (50)148 (51)73 (50)5 (42)0.813
 Subgroup (<25)69 (15)43 (15)22 (15)4 (33)0.958
 Subgroup (25–51)157 (35)105 (36)51 (35)1 (8)0.774
All patients mean±SD52±2652±2655±2652±30NA
IC, indeterminant colitis.


Oral vitamin D replacement is an effective treatment for vitamin D deficiency in IBD patients and appears to be dose responsive and equally effective in UC and CD patients. The optimal dose of oral vitamin D supplementation is yet to be determined, but higher doses are significantly more effective with higher chance of normalising the serum levels.