P391 Differential use of vedolizumab in ulcerative colitis and Crohn's disease. Real life results from 2 tertiary referral centres in the United Kingdom
Kamperidis N.*1, Cavazza A.2, Wahed M.2, Arebi N.1
1St Mark's Hospital, London, United Kingdom 2Chelsea and Westminster Hospital, Gastroenterology, London, United Kingdom
Vedolizumab (VDZ) is an anti-α4β7 integrin antibody efficient for the treatment of ulcerative colitis (UC)  and Crohn's disease (CD) . As patient population in clinical trials may not be reflective of real life practice, we describe our experience with VDZ in two tertiary UK centres.
We identified all patients receiving VDZ from infusion clinic and reviewed their electronic and written case notes. Disease activity was recorded using clinical (Simple Clinical Colitis Activity Index for UC and Harvey Bradshaw Index for CD) and biochemical indices (Calprotectin). Continuous variables are expressed as mean (SD) and compared with paired student's t-test.
22 UC and 15 CD patients were included. All received VDZ at weeks 0, 2, 6 (induction) and then 8 weekly. Their age was 39.8 (14.1) and 36.6 (13.3) years respectively.
In the UC group, 14 (64%) had extensive disease. All were previously exposed to thiopurines (TPs), 12 (55%) to anti-TNFs, 8 (36%) were on corticosteroids (CS) at baseline. The SCCAI was 5.8 (2.7) at baseline, 4.9 (4.1) on the 3rd and 3.6 (3.6) on the 4th infusion (p=0.07). 13 (59%) patients had an SCCAI ≤4 post induction. Faecal calprotectin was 918 ug/g (690) at baseline and 428 (494) after induction (p<0.01). 8 (53%) patients (n=15) had a calprotectin of <200 after induction and 6 (75%) were CS-free. The length of follow up was 8.2 (3.5) months. The SCCAI on the day of last infusion was 2.3 (2.4) (p<0.01). 12 (55%) patients had an SCCAI of ≤2 on their last follow up and 1 had surgery.
In the CD cohort, 4 (27%) were diagnosed at the age ≤16 years. The location was ileocolonic in 11 (73%), upper gut in 5 (33%) and perianal disease was present in 7 (47%) patients. Disease behaviour was stricturing in 2 (13%) and penetrating in 6 (40%) patients. Previous or current exposure to TPs was reported in 14/15 (93%). All had been exposed to anti-TNFs. 9 (60%) had undergone intestinal surgery. 5 (33%) were on CS on treatment initiation. HBI at baseline was 8.6 (5.6), 5.5 (4.6) at 3rd infusion (p=0.07) and 5.1 (3.9) at 4th infusion (p=0.24). 6 (40%) patients had HBI of ≤4 at the 3rd infusion. Baseline calprotectin was 1035 (950) and 534 (361) after induction (p=0.6). The length of follow up was 4.7 (2.6) months. At last follow up the HBI was 5.2 (5.7) (p=0.19).
VDZ demonstrated clinical efficacy in UC. VDZ was more likely to be used after anti-TNF failure in CD than UC. The majority of CD patients had complicated disease. Clinical responses to VDZ were similar to those described in the GEMINI trials and mirrored by reduction in faecal calprotectin. Further real life studies on CD are required to optimize its use through patient selection.
 Feagan et al, (2013), Vedolizumab as Induction and Maintenance Therapy for Ulcerative Colitis, New England Journal of Medicine, 699–710
 Sandborn et al, (2013), Vedolizumab as induction and maintenance therapy for Crohn's disease, New England Journal of Medicine, 711–721