dividual, by reducing the quality of life, and for the society as a consequence of expenses for medical treatment, medicine and absence from work. Symptoms: For patients with CD symptoms at diagnosis

Introduction: Anti-tumor necrosis factor-α (TNF-α) is used for treatment of severe cases of inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC). However, one-third of the patients do not respond to the treatment. Genetic markers may predict individual response to anti-TNF therapy. Methods: Blood sent for Mycobacterium tuberculosis screening was collected from 01.09. 2009 to 30.03. 2011. Patients with CD or UC (K50-K51) were identified by linking CPR-numbers from the blood samples to the National Patient Registry. Treatment efficacy reflected the maximum response within 22 weeks. DNA was purified by Maxwell 16 Blood purification kit (Promega) and 39 mainly functional single nucleotide polymorphisms (SNPs) were genotyping by LGC Genomics. Results: A cohort of 492 patients with CD and 267 patients with UC treated with anti-TNF was established. Nineteen SNPs were associated with response. Conclusion: The results suggest that polymorphisms in genes involved in activating NFκB through the TLR pathways, genes regulating TNF-α signaling and cytokines regulated by NFκB are important predictors for the response to anti-TNF therapy among patients with IBD. Genetically strong TNF-mediated inflammatory response was associated with beneficial response. In addition, the cytokines IL-1β, IL-6 and IFN-γ may be potential targets for treating patients with IBD who do not respond to anti-TNF therapy. These finding should be examined in independent cohorts before these results are applied in a clinical setting. REFERENCES 1. Podolsky DK. Inflammatory bowel disease. N Engl J Med 2002;347:417-29. 2. Vind I, Riis L, Jess T et al. Increasing incidences of inflammatory bowel disease and decreasing surgery rates in Copenhagen City and County, 20032005: a population-based study from the Danish Crohn colitis database. Am J Gastroenterol 2006;101:1274-82. 3. Jacobsen BA, Fallingborg J, Rasmussen HH et al. Increase in incidence and prevalence of inflammatory bowel disease in northern Denmark: a population based study, 1978-2002. Eur J Gastroenterol Hepatol 2006;18:601-6. 4. Van AG, Dignass A, Panes J et al. The second European evidence-based Consensus on the diagnosis and management of Crohn's disease: Definitions and diagnosis. J Crohns Colitis 2010;4:7-27. 5. Dignass A, Eliakim R, Magro F et al. Second European evidence-based consensus on the diagnosis and management of ulcerative colitis part 1: definitions and diagnosis. J Crohns Colitis 2012;6:965-90. 6. Satsangi J, Silverberg MS, Vermeire S et al. The Montreal classification of inflammatory bowel disease: controversies, consensus, and implications. Gut 2006;55:749-53. 7. Silverberg MS, Satsangi J, Ahmad T et al. Toward an integrated clinical, molecular and serological classification of inflammatory bowel disease: Report of a Working Party of the 2005 Montreal World Congress of Gastroenterology. Can J Gastroenterol 2005;19:5-36. 8. Halfvarson J, Bodin L, Tysk C et al. Inflammatory bowel disease in a Swedish twin cohort: a long-term follow-up of concordance and clinical characteristics. Gastroenterology 2003;124:1767-73. 9. Jess T, Riis L, Jespersgaard C et al. Disease concordance, zygosity, and NOD2/CARD15 status: follow-up of a population-based cohort of Danish twins with inflammatory bowel disease. Am J Gastroenterol 2005;100:2486-92. 10. Orholm M, Binder V, Sorensen TI et al. Concordance of inflammatory bowel disease among Danish twins. Results of a nationwide study. Scand J Gastroenterol 2000;35:1075-81. 11. Spehlmann ME, Begun AZ, Burghardt J et al. Epidemiology of inflammatory bowel disease in a German twin cohort: results of a nationwide study. Inflamm Bowel Dis 2008;14:96876. 12. Halme L, Paavola-Sakki P, Turunen U et al. Family and twin studies in inflammatory bowel disease. World J Gastroenterol 2006;12:3668-72. 13. Mahid SS, Minor KS, Soto RE et al. Smoking and inflammatory bowel disease: a meta-analysis. Mayo Clin Proc 2006;81:1462-71. 14. Perkins ND. Integrating cell-signalling pathways with NFkappaB and IKK function. Nat Rev Mol Cell Biol 2007;8:4962. 15. Pallone F, Monteleone G. Regulatory cytokines in inflammatory bowel disease. Aliment Pharmacol Ther 1996;10:75-9. 16. Romagnani S. Th1/Th2 cells. Inflamm Bowel Dis 1999;5:28594. 17. Inoue S, Matsumoto T, Iida M et al. Characterization of cytokine expression in the rectal mucosa of ulcerative colitis: correlation with disease activity. Am J Gastroenterol 199;94:2441-6. 18. Verstrepen L, Bekaert T, Chau TL et al. TLR-4, IL-1R and TNFR signaling to NF-kappaB: variations on a common theme. Cell Mol Life Sci 2008;65:2964-78. 19. http://www.bu. edu/nf-kb/gene-resources/target-genes/ 20. Kriegler M, Perez C, DeFay K et al. A novel form of TNF/cachectin is a cell surface cytotoxic transmembrane protein: ramifications for the complex physiology of TNF. Cell 1988;53:45-53.