Susceptibility loci reported in genome‐wide association studies are associated with Crohn’s disease in Canadian children |
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| Authors: | D. K. AMRE D. R. MACK K. MORGAN D. ISRAEL C. DESLANDRES E. G. SEIDMAN P. LAMBRETTE I. COSTEA A. KRUPOVES H. FEGURY J. DONG G. GRIMARD E. LEVY |
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| Affiliation: | 1. Department of Pediatrics, University of Montreal, Montreal, QC, Canada;2. Research Centre, Sainte‐Justine Hospital, Montreal, QC, Canada;3. Division of Gastroenterology, Hepatology & Nutrition, Children’s Hospital of Eastern Ontario, Ottawa, ON, Canada;4. Department of Human Genetics, McGill University and the Research Institute of the McGill University Health Center, Montreal, QC, Canada;5. Department of Gastroenterology, Hepatology & Nutrition, British Columbia’s Children’s Hospital, Vancouver, BC, Canada;6. Faculty of Medicine, Division of Gastroenterology, McGill University and the Research Institute of the McGill University Health Center, Montreal, QC, Canada;7. Department of Preventive & Social Medicine, University of Montreal, Montreal, QC, Canada;8. Division of Orthopedics, Department of Pediatrics, University of Montreal, Montreal, QC, Canada;9. Department of Nutrition, University of Montreal, Montreal, QC, Canada |
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| Abstract: | Aliment Pharmacol Ther 31 , 1186–1191 Summary Background Recent genome‐wide association studies based on adult and paediatric populations have implicated >30 genes/loci as susceptibility loci for Crohn’s disease (CD). Aims To investigate whether reported genes/loci were also associated with CD in Canadian children. Design and Methods A case‐control design was implemented at three paediatric gastroenterology clinics in Canada. Children ≤18 years of age with a confirmed diagnosis of CD were recruited along with controls. Single nucleotide polymorphisms (SNPs) in five genome‐wide association studies reported genes/loci were genotyped. Associations between individual SNPs and CD were examined. Results A total of 406 cases and 415 controls were studied. The mean (±s.d.) age of the cases was 12.3 (±3.2) years. Most cases were male (56.6%), had ileo‐colonic disease (L3 ± L4, 52.0%) and inflammatory behaviour (B1 ± p, 86.9%) at diagnosis. Allelic association analysis (two‐tailed) showed that three of the five targeted SNPs were significantly associated with overall susceptibility for CD (ZNF365, r10995271, P = 0.001; PTPN2, rs1893217, P = 0.005; STAT3, rs744166, P = 0.01). Associations with SNP rs4613763 in the PTGER4 locus were marginally nonsignificant (P = 0.07). The ZNF365 and STAT3 SNPs were predominantly associated with ileal disease with or without colonic involvement. Conclusion The identified susceptibility genes/loci for adult‐onset CD also confer risk for paediatric‐onset CD. |
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