Association of celiac disease genes with inflammatory bowel disease in Finnish and Swedish patients

Genes and Immunity

Volumn 13, Issue 6, 2012, Pages 474-480

  Parmar, A S ^a,b   Lappalainen, M ^a,c   Paavola Sakki, P ^c   Halme, L ^c   Farkkila M ^c   Turunen, U ^c   Kontula, K ^a,c   Aromaa, A ^d   Salomaa, V ^d   Peltonen, L ^a,e   Halfvarson, J ^f   Torkvist L ^g   D'Amato, M ^g   Saavalainen, P ^a,b   Einarsdottir, E ^a,b  

^a UNIVERSITY OF HELSINKI   (Finland)

^b UNIVERSITY OF HELSINKI   (Finland)

^c HELSINKI UNIVERSITY CENTRAL HOSPITAL   (Finland)

^d NATIONAL PUBLIC HEALTH INSTITUTE   (Finland)

^e WELLCOME TRUST SANGER INSTITUTE   (United Kingdom)

^f ÖREBRO UNIVERSITY   (Sweden)

^g KAROLINSKA INSTITUTE   (Sweden)

Author keywords

association; celiac disease; Crohn's disease; ulcerative colitis

Indexed keywords

ARTICLE; CELIAC DISEASE; CHILDHOOD DISEASE; CONTROLLED STUDY; CROHN DISEASE; DISEASE ASSOCIATION; FAMILIAL DISEASE; FINLAND; GENE LOCUS; GENETIC ASSOCIATION; GENETIC MARKER; GENETIC RISK; GENETIC SUSCEPTIBILITY; GENOTYPE; HUMAN; MAJOR CLINICAL STUDY; META ANALYSIS (TOPIC); PRIORITY JOURNAL; SINGLE NUCLEOTIDE POLYMORPHISM; SWEDEN; ULCERATIVE COLITIS;

ADULT; CASE-CONTROL STUDIES; CELIAC DISEASE; CHILD; COLITIS, ULCERATIVE; CROHN DISEASE; FINLAND; GENETIC ASSOCIATION STUDIES; GENETIC MARKERS; GENETIC PREDISPOSITION TO DISEASE; HUMANS; INFLAMMATORY BOWEL DISEASES; POLYMORPHISM, SINGLE NUCLEOTIDE; RISK FACTORS; SWEDEN;

EID: 84865634437     PISSN: 14664879     EISSN: 14765470     Source Type: Journal    
DOI: 10.1038/gene.2012.21     Document Type: Article

References (21)

1. Lakatos PL. Recent trends in the epidemiology of inflammatory bowel diseases: up or down? World J Gastroenterol 2006; 12: 6102-6108.
2. Lapidus A. Crohn's disease in Stockholm county during 1990-2001: an epide-miological update. World J Gastroenterol 2006; 12: 75-81.
3. Vind I, Riis L, Jess T, Knudsen E, Pedersen N, Elkjaer M et al. Increasing incidences of inflammatory bowel disease and decreasing surgery rates in Copenhagen City and County, 2003-2005: a population-based study from the Danish Crohn colitis database. Am J Gastroenterol 2006; 101: 1274-1282.
4. Turunen P, Kolho KL, Auvinen A, Iltanen S, Huhtala H, Ashorn M. Incidence of inflammatory bowel disease in Finnish children, 1987-2003. Inflamm Bowel Dis 2006; 12: 677-683.
5. Elson CO, Cong Y, McCracken VJ, Dimmitt RA, Lorenz RG, Weaver CT. Experimental models of inflammatory bowel disease reveal innate, adaptive, and regulatory mechanisms of host dialogue with the microbiota. Immunol Rev 2005; 206: 260-276.
6. Franke A, McGovern DP, Barrett JC, Wang K, Radford-Smith GL, Ahmad T et al. Genome-wide meta-analysis increases to 71 the number of confirmed Crohn's disease susceptibility loci. Nat Genet 2010; 42: 1118-1125.
7. Anderson CA, Boucher G, Lees CW, Franke A, D'Amato M, Taylor KD et al. Meta-analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47. Nat Genet 2011; 43: 246-252.
8. Dubois PC, Trynka G, Franke L, Hunt KA, Romanos J, Curtotti A et al. Multiple common variants for celiac disease influencing immune gene expression. Nat Genet 2010; 42: 295-302.
9. Festen EA, Goyette P, Green T, Boucher G, Beauchamp C, Trynka G et al. A meta-analysis of genome-wide association scans identifies IL18RAP, PTPN2, TAGAP, and PUS10 as shared risk loci for Crohn's disease and celiac disease. PLoS Genet 2011; 7: e1001283.
10. Zhernakova A, Stahl EA, Trynka G, Raychaudhuri S, Festen EA, Franke L et al. Meta-analysis of genome-wide association studies in celiac disease and rheumatoid arthritis identifies fourteen non-hla shared loci. PLoS Genet 2011; 7: e1002004.
11. Fransen K, Visschedijk MC, van Sommeren S, Fu JY, Franke L, Festen EA et al. Analysis of SNPs with an effect on gene expression identifies UBE2L3 and BCL3 as potential new risk genes for Crohn's disease. Hum Mol Genet 2010; 19: 3482-3488.
12. Smyth DJ, Plagnol V, Walker NM, Cooper JD, Downes K, Yang JH et al. Shared and distinct genetic variants in type 1 diabetes and celiac disease. N Engl J Med 2008; 359: 2767-2777.
13. Elliott MR, Zheng S, Park D, Woodson RI, Reardon MA, Juncadella IJ et al. Unexpected requirement for ELMO1 in clearance of apoptotic germ cells in vivo. Nature 2010; 467: 333-337.
14. Halme L, Turunen U, Helio T, Paavola P, Walle T, Miettinen A et al. Familial and sporadic inflammatory bowel disease: comparison of clinical features and ser-ological markers in a genetically homogeneous population. Scand J Gastroenterol 2002; 37: 692-698.
15. McGovern DP, Gardet A, Torkvist L, Goyette P, Essers J, Taylor KD et al. Genome-wide association identifies multiple ulcerative colitis susceptibility loci. Nat Genet 2010; 42: 332-337.
16. Helio T, Halme L, Lappalainen M, Fodstad H, Paavola-Sakki P, Turunen U et al. CARD15/NOD2 gene variants are associated with familially occurring and complicated forms of Crohn's disease. Gut 2003; 52: 558-562.
17. Hugot JP, Chamaillard M, Zouali H, Lesage S, Cezard JP, Belaiche J et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. Nature 2001; 411: 599-603.
18. Ogura Y, Bonen DK, Inohara N, Nicolae DL, Chen FF, Ramos R et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease. Nature 2001; 411: 603-606.
19. Lesage S, Zouali H, Cezard JP, Colombel JF, Belaiche J, Almer S et al. CARD15/NOD2 mutational analysis and genotype-phenotype correlation in 612 patients with inflammatory bowel disease. Am J Hum Genet 2002; 70: 845-857.
20. Purcell S, Neale B, Todd-Brown K, Thomas L, Ferreira MA, Bender D et al. PLINK: a tool set for whole-genome association and population-based linkage analyses. Am J Hum Genet 2007; 81: 559-575.
21. Purcell S, Cherny SS, Sham PC. Genetic power calculator: design of linkage and association genetic mapping studies of complex traits. Bioinformatics 2003; 19: 149-150.