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* = Presenting author

P680 Aetiological risk factors for developing paediatric inflammatory bowel disease in a prospective cohort

I. Yu*1, E. O’Neill1, R. Stanley1, A. Carey2, 3, S. Kiernan2, M. Hamzawi2, K. Driscoll2, S. Quinn2, A. M. Broderick1, 2, B. Bourke1, 2, 3, T. Rafferty2, 3, S. Hussey1, 2, 3

1University College Dublin, Academic Centre for Paediatric Research, School of Medicine and Medical Science, Dublin, Ireland, 2Our Lady’s Hospital for Sick Children Crumlin, Department of Gastroenterology & Hepatology, Dublin, Ireland, 3Our Lady’s Hospital for Sick Children Crumlin, National Children’s Research Centre, Dublin, Ireland


To assess potential familial, demographic and environmental risk factors for developing PIBD in a prospective national cohort of patients.


Parents of participants in the DOCHAS study (Determinants and Outcomes in Children and Adolescents with IBD Study) were asked to complete a standardised questionnaire at diagnosis. Patients diagnosed between January 1st 2012 and June 30th 2015 were included. Information including pre-diagnosis home environment, location, smoking exposure, medication exposure as well as extended family histories was recorded prospectively. Patients were classified according to the Paris Classification of PIBD. Data was exported from the study database to SPSS version 20 format for data analysis, using descriptive statistics where applicable.


In total, 356 subjects were recruited; 64 were controls, 145 had Crohn disease (CD), 123 had ulcerative colitis (UC), 4 had Atypical UC and 20 had IBD unclassified. More males than females were diagnosed with CD (3.03:1), were as in UC the M:F ratio was (1:1.12). The mean age of those with UC was 13.14, and CD was 12.67. Rural dwelling was observed in 41.2% with CD and 41.8% with UC. 28.1% had a positive family history of IBD, with 4.5% having a maternal family history in particular. Compared with controls, PIBD was associated with maternal smoking during pregnancy (11.4% vs 20.8% [CD] and 29.2% [UC], p = 0.02), particularly between the control and UC groups (p = 0.008). A family history of autoimmune disease had a more likely diagnosis of CD than that of UC (45.8% vs 27.6%, p = 0.001), this was mirrored in patients diagnosed with autoimmune disease (54.2% vs 17.8%, p = <0.001). Patient and paternal atopic disease were more associated with CD than UC (respectively 54.7% vs 18.9%, p = <0.001 and 45.9% vs 16.2%, p = 0.049). There were no significant differences between patients with CD and UC in relation to prior antibiotic use, NSAID exposure, previous infective enteritis or appendectomy.


This is the first prospective study of potential risk factors for developing PIBD. Gender, maternal smoking exposure, maternal family history of IBD and a family history of autoimmune disease were associated significantly with certain IBD phenotypes. Ongoing prospective research is required to further elucidate these associations.