P660 Crohn's disease course is not different in familial than in sporadic cases: A case-control population-based study

Abstract

P660 Crohn’s disease course is not different in familial than in sporadic cases: A case control population-based study R. Gerard1 *, H. Sarter2, M. Fumery3, L. Dauchet4, E. Joyez4, F. Vasseur4, J.-F. Colombel5, D. Turck6, L. Peyrin-Biroulet7, G. Savoye8, C. Gower-Rousseau4,9. 1University and Hospital, Gastroenterology, Lille, France, 2University and Hospital, Epimad Registry Biostatistics EA 2694, Lille, France, 3University and Hospital, Gastroenterology, Amiens, France, 4University and Hospital, Epidemiology, Lille, France, 5Hemsley Inflammatory Bowel Disease Center, Icahn Medical School of Medicine at Mount Sinai, New-York, United States, 6University and Hospital, Paediatric, Lille, France, 7University and Hospital, Gastroenterology, Nancy, France, 8University and Hospital, Gastroenterology, Rouen, France, 9Health, Epidemiology, Lille, France Background: Having a first degree relative (siblings, children, parents) with Crohn’s disease (CD) is the main risk factor to develop the disease. This genetic risk could influence the natural history of the disease; particularly in multiplexes families (MF) defined by at least 3 members with CD linked at the first degree. The aim of our study was to compare disease course between patients with CD in MF and sporadic families. Methods: MF were identified in a French population-based study on inflammatory bowel disease (Epimad Registry). Each patient from MF was matched to at least one sporadic case also issued from this Registry. Matching criteria were: gender, age at CD diagnosis, phenotype at diagnosis (disease location and disease behaviour) according to Montreal classification [1] and date of CD diagnosis. Primary outcomes were assessed at the end of the follow up and included: disease extension, change of behaviour from inflammatory (B1) to complicated type of CD (structuring B2 and/or penetrating B3), occurrence of extra-intestinal manifestations (EIMs), the need for immunosuppressor (IS) treatment or anti-TNF biologic agent, and at least one intestinal resection. Case control comparisons were performed using a mixed model for multivariate analysis, adjusted to smoking status. Results: Fifty-nine patients belonging to 24 MF were included matched to 88 sporadic patients. The median follow-up was 16 years [Q1 = 12 Q3 = 20]. Patients from MF were significantly more often smokers or former smokers than controls (93% vs 53%, p < 0.05). No differences between MF and sporadic cases were observed regarding disease extension (75% vs 70%), change behaviour (56% vs 65%) or prevalence of EIMs (27% vs 31%). Similar proportions of sporadic cases and MF patients received at 10 and 20 years; (1) IS (46% vs 62% and 61% vs 73%, respectively), (2) anti-TNF therapy (14% vs 24% and 46% vs 52%, respectively), and (3) underwent surgical intestinal resection (42% vs 50% and 49% vs 57%, respectively). Conclusions: In this case control population-based study we find none difference in the CD disease course between patients from multiplex and sporadic families. These findings could suggest that genetic and environmental risk factors affecting the CD disease course are different from those affecting its occurrence.