DOP069 Natural history of dysplasia and colorectal cancer in IBD patients in Belgium tertiary care centers
Cremer A.*1, Liefferinckx C.1, De Vos M.2, Rahier J.-F.3, Baert F.4, Moreels T.5, Macken E.5, Louis E.6, Devière J.1, Van Gossum A.1, Vermeire S.7, Franchimont D.1
1University Hospital Erasme, Gastroenterology, Brussels, Belgium 2University Hospital Gent, Gastroenterology, Brussels, Belgium 3University Hospital Mont-Godinne, Gastroenterology, Yvoir, Belgium 4AZ Delta, Roeselare, Belgium 5University Hospital Antwerp, Edegem, Belgium 6University Hospital Liège, Liège, Belgium 7University Hospital Leuven, Gastroenterology, Leuven, Belgium
Inflammatory bowel disease (IBD) patients are at increased risk of developing dysplasia and colorectal cancer, namely colitis-associated colorectal cancer (CAC). Ulcerative colitis (UC) and Crohn's disease (CD) patients are recommended to undergo screening and surveillance colonoscopy. However, large study populations are needed to understand the natural history of dysplasia and CAC and improve their management in IBD patients.
This is a national long-term follow-up retrospective study to evaluate the natural history of low-grade dysplasia (LGD), high-grade dysplasia (HGD) and CAC in IBD patients in Belgium tertiary referral regional and academic centers within the Belgian Inflammatory Bowel Disease Research and Development group. Clinical, endoscopic and pathological data were retrieved through retrospective electronic chart review. All biopsies and surgical specimen were reviewed by a second independent expert IBD pathologist.
195 IBD patients (105 CD, 83 UC, and 7 unclassified IBD) with in total 466 lesions (dysplasia/CAC) were identified. From these 466 lesions, 391 were LGD (346 raised, 45 flat), 40 were HGD (35 raised, 5 flat), and 35 were CAC. Median age at IBD diagnosis was 42 years (IQR 29–57). From the 195 affected patients, 161 (83%) had only dysplasia, while 34 (17%) had CAC (26 CD, 8 UC; 20 men, 14 women). Median disease duration was significantly longer in patients with CAC compared to those with dysplasia (13 (IQR 4–27) vs 7 (IQR 1–16) years; p=0.03). Overall 11 (7.6%) out of 146 patients with firstly diagnosed LGD have progressed to more advanced neoplasia (6 HGD, 5 CAC) after median follow-up of 43 months (IQR 16–79). 27/34 (79%) IBD patients with CAC were diagnosed with CAC without evidence of prior dysplasia, while 7/34 (21%) developed CAC secondarily. Among them, 4 (57%) had early stage CAC, and 3 (43%) had advanced stage (stages II-IV) at diagnosis, while in patients without prior history of dysplasia, 10 (37%) had early stage at diagnosis. CAC was diagnosed during colonoscopy in 26 patients, and at surgery (performed for pre-existing dysplasia (n=2), or for IBD therapeutic management (n=6)) in 8 patients.
This is one of the largest cohorts of IBD patients with dysplasia and CAC never described so far. The rate of progression of LGD to advanced neoplasia remains low with the limitation of a retrospective study. CAC diagnosis is mostly done during colonoscopy with no prior history of dysplasia. CAC was found incidentally at surgery for indications of dysplasia and refractory disease.