Tone Bergene Aabrekk, Geir Aamodt, Øyvind Asak, Raziye Boyar Cetinkaya, Trond Espen Detlie, Svein Oskar Frigstad, Kristina I. Aass Holten, Gert Huppertz-Hauss, Ingunn Johansen, Vendel A. Kristensen, Charlotte Lund, Randi Opheim, Vibeke Strande, Roald Torp, Simen Vatn, Petr Ricanek, Marte Lie Høivik, May-Bente Bengtson

Affiliates

Tone Bergene Aabrekk[1,2], Geir Aamodt[3], Øyvind Asak[4], Raziye Boyar Cetinkaya[5], Trond Espen Detlie[2,6], Svein Oskar Frigstad[7], Kristina I. Aass Holten[2,8], Gert Huppertz-Hauss[9], Ingunn Johansen[10,11], Vendel A. Kristensen[2,12], Charlotte Lund[2,12], Randi Opheim[11,12], Vibeke Strande[2,13,14], Roald Torp[15], Simen Vatn[16], Petr Ricanek[13], Marte Lie Høivik[2,12], May-Bente Bengtson[1],Department of Gastroenterology, Vestfold Hospital Trust, Tønsberg, Norway[1], Institute of Clinical Medicine, University of Oslo, Oslo, Norway[2], LANDSAM, Norwegian University of Life Sciences Ås, Norway[3], Department of Internal Medicine, Innlandet Hospital Trust, Lillehammer, Norway[4], Department of Internal Medicine, Diakonhjemmet Hospital, Oslo, Norway[5], Department of Gastroenterology, Akershus University Hospital, Lørenskog, Norway[6], Department of Internal Medicine, Bærum Hospital, Vestre Viken Hospital Trust, Gjettum, Norway[7], Department of Gastroenterology, Østfold Hospital Trust, Sarpsborg, Norway [8], Department of Gastroenterology, Telemark Hospital Trust, Skien, Norway[9], Faculty of Health, Welfare and Org., Østfold University College, Fredrikstad, Norway[10], Department of Public Health Science, Institute of Health and Society, University of Oslo, Oslo, Norway[11], Department of Gastroenterology, Oslo University Hospital, Oslo, Norway [12], Department of Gastroenterology, Lovisenberg Diaconal Hospital, Oslo, Norway[13], Unger-Vetlesen Institute, Lovisenberg Diaconal Hospital, Oslo, Norway[14], Department of Internal Medicine, Innlandet Hospital Trust, Hamar, Norway[15], Department of Internal Medicine, Innlandet Hospital Trust, Gjøvik, Norway[16],

Abstract

Background:
The highest risk factor of inflammatory bowel disease (IBD) is having a first-degree relative (FDR) with IBD. Although the prevalence of IBD in Norway is among the highest in the world, its incidence has remained steady throughout the 21st century. In this era of stable incidence, we wanted to explore the role of a positive family history of IBD.

Methods:
The rate of having at least one FDR with IBD in the adult IBD population was estimated in two population-based IBD inception cohorts conducted in South-Eastern Norway. One in 1990-1994 (IBSEN) (0.9 M inhabitants in 1992) and the second 30 years later, in 2017-2019 (IBSEN III) (2.95 M inhabitants in 2017). We compared the phenotype of IBD, age at diagnosis (AAD) with standard deviation, the distribution of disease and severity of IBD between sporadic and familial cases of IBD in the IBSEN III cohort. Severe disease was defined as extensive colitis in Ulcerative colitis (UC), and the presence of perianal, stricturing, or penetrating disease in Crohn`s disease (CD). Further, those who reported more than one FDR with IBD in the IBSEN III cohort were invited to participate in a multiplex-family IBD study. In this multiplex-family cohort, we explored generational differences in AAD, the severity of disease, and the association between the length of shared household and the phenotype of IBD. Chi-square and t-test were used for categorical and continuous variables, respectively. Tests of equal proportions were performed to compare the rate of familial IBD in the IBSEN and IBSEN III.

Results:
Overall 785 adults aged >18 years were included in the IBSEN cohort (1990-1994) and 1561 in the IBSEN III cohort (2017-2019), of whom 7.3% (n57) and 10.9%(n170) reported a positive family history of IBD, respectively. The rate of familial IBD increased by 49.3% (p=0.008) over 30 years.
In the IBSEN III cohort, there were no significant differences in mean AAD between familial 38.7(14.5) and sporadic cases, 39.1 (15.0) of IBD (p=0.739), nor between mean AAD in familial CD, 39.4(14.0) and UC, 38.4(14.7) (p = 0.664) compared to sporadic CD, 40.4 (15.8) (p=0.678) and UC, 39.2(15.0) (p=0.587).

Among familial and sporadic cases of IBD, 45/170 (26.5%) and 449/1391 (32.3%) had severe disease, respectively (p = 0.124). Of familial IBD with severe disease, 10/55 (18.2%) and 35/115 (30.4%) suffered from CD and UC, respectively (p = 0.090).
Among sporadic cases of IBD, 87/451 (19.3%) with CD and 362/ 940 (38.5%) with UC suffered from severe disease (p < 0.001). In the multiplex IBD cohort, we included 30 children and 18 parents with familial IBD. The mean AAD was 25.1 years (13.0) among the children and 33.3 years (16.5) among the parents (p=0.063). Eight of twenty-six children (30.8%) and 9/16 (56.3%) among the parents reported severe disease (p=0.102). The length of shared households within multiplex families from the initial IBD diagnosis among FDRs to subsequent diagnoses of CD or UC in others, was 11.78 years and 17.14 years, respectively (p=0.026).

Conclusion:
The rate of a positive family history of IBD has increased substantially over thirty years, underscoring the importance of shared environmental factors for the development of the IBD diagnosis. In the sporadic group of IBD there were significantly more frequent cases of severe disease among UC compared to CD. Shorter time of shared household was significantly associated with development of familial CD.

Poster_P2_Tone_Bergene Aabrekk