P665 Familial aggregation of inflammatory bowel disease on the Faroe Islands: a Faroese inflammatory bowel disease cohort study
K. R. Nielsen*1, 2, J. Olsen1, G. Andorsdóttir2, E. Gislason2, J. Burisch3
1The National Hospital of the Faroe Islands, Medical department, Tórshavn, Faroe Islands, 2Genetic Biobank, Tórshavn, Faroe Islands, 3North Zealand University Hospital, Department of Gastroenterology, Frederikssund, Denmark
Over the last 2 decades, the incidence of inflammatory bowel disease (IBD) has increased dramatically on the Faroe Islands1, an archipelago located in the North Atlantic Ocean populated by an endogamous population, and is today the highest in the world.2 This steep increase in IBD is mainly caused by UC, as the incidence of CD has remained stable over the last 5 decades. The reasons for these observations are unknown. In this study we aimed to investigate the genetic contribution component in IBD on the Faroe Islands.
The Faroese IBD cohort is a population-based, nationwide cohort of all patients diagnosed with Crohn’s disease (CD), ulcerative colitis (UC), and IBD unclassified (IBDU) according to the Copenhagen diagnostic criteria from 1960 until 2014. The relationship amongst CD and UC patients was studied using a unique computerised nationwide genealogy registry covering pedigrees from the whole Faroese population from approximately 1 650. Relative risk (RR) of kinship for patients were compared with controls (simulated as if they were probands and shown as CI 93%). Controls were matched for age, gender, and approximate sib-ship size. Pedigrees for control subjects were randomly and reiteratively sampled from the Faroese genealogic database.
Pedigrees (ie, Figure 1) were available for the whole cohort consisting of 664 incident IBD patients, 113 with CD, 417 with UC, and 134 with IBDU. Patient characteristics are shown in Table 1. The RR of kinship in UC and CD patients compared with controls are shown in Table 2. Overall, UC patients were more closely related than controls were (RR for UC was higher than upper CI 93% limit for controls), whereas no hereditary component in CD patients was found.
Figure 1. An ancestral pedigree of a family with high prevalence of UC patients (red dots).
Table 1 Patient characteristics
|Ulcerative colitis||Crohn’s disease|
|Average age at onset, yr||41 (0–86)||41 (0–86)|
|Smoking status||Current 20%, former 29%, never 51%||Current 36%, former 18%, never 46%|
|Extent (UC)||E1 21%, E2 39%, E3 40%|
|Behaviour (CD)||B1 65%, B2 25%, B3 8%
|Location (CD)||L1 22%, L2 65%, L3 10%, L4 (+/- L1-L3) 3%|
Table 2 Relative risks (RR) of kinship for IBD patients and controls
|Family relation||Ulcerative colitis RR||Controls – ulcerative colitis (RR CI93%)||x times higher risk for UC vs upper bound in controls||Crohn’s disease RR||Controls – Crohn’s disease (RR CI 93%)||x times higher risk for CD vs upper bound in controls|
In this population-based, nationwide cohort of Faroese IBD patients a hereditary component was found for UC but not for CD patients. Further analyses on the effect of the genetic contribution on disease course, as well as genetic and microbial analysis, are ongoing.
 Hammer T, Rubek K, Nielsen J, et al. The Faroese IBD study: incidence of inflammatory bowel diseases in 54-years’ of population-based data. J Crohn and Colitis 2015.
 Burisch J Pedersen N, Čuković-Čavka S, et al. East-West gradient in the incidence of inflammatory bowel disease in Europe: the ECCO-EpiCom inception cohort. Gut 2014;63(4):588–97.