s of the 4th Congress of ECCO the European Crohn’s and Colitis Organisation S101 fill the questionnaire were excluded, and therefore 13 men and 13 women were analyzed. The study was approved by the ethics committee of the Institution of Collective Medical Assistance (CASMU). The variables collected were: biological variables of the disease (activity with Harvey Bradshaw test), psychological variables (Zukerfeld test for somatic vulnerability and social network and Hamilton test for anxiety and depression), quality of life (IBDQ short version) and sociocultural variables (our own construction). Results and Discussion: Men and women had similar biological characteristics. Except for a woman with low level of activity, all patients were in remission. Coped assertively 23% (3/13) of men, no woman did. No correspondence between disease aggressivity and type of coping was observed. In relation to psychological variables, men presented less anxiety (72% vs 92%) and depression (62% vs 100%), they perceive a larger supporting social network (92% vs 77%), have less smoking addiction (92% vs. 77%) and perform more physical activity (70% vs.23 %). Women manifested a greater disease impact in the family sphere (77 % vs. 39%) and men a greater impact in sexuality (46% vs. 23%). Quality of life was good in 54% of men and 8% in women. The 3 men that coped assertively had a good quality of life, do not smoke and perform physical activity. Health self-perception was good in 70% of men vs 46% in women. We did not find a clustering of risk factors related to assertive coping or occurring more frequently in one gender. The results of this research contribute towards the theoretical discussion of the diverse factors that contribute to quality of life in CD, as well as to the reorientation of better strategies used for treatment. P229 The influence of eicosapentaenoic acid (EPA) on TNF-a production by peripheral blood mononuclear cells of Crohn’s disease (CD) patients and cell kinetics accordingly to TNF-a 857C/T polymorphism P. Ferreira1 *, C.S. Guerreiro1, J. Vacas1, L. Tavares2, P.M. Santos2, A. Pinto3, M. Cravo3, M. Brito1. 1Escola Superior de Tecnologia da Saude de Lisboa, Lisboa, Portugal, 2Hospital Santa Maria, Lisboa, Portugal, 3Instituto Portugues de Oncologia Francisco Gentil, Lisboa, Portugal Rationale: Tumor necrosis factor a (TNFa) plays a major role in CD. In a previous study we demonstrated a 10 times higher risk of greater disease activity (Harvey Bradshaw index 4) for the TT genotype individuals in TNFa 857C/T polymorphism. The aim of the present study was to evaluate whether Eicosapentaenoic acid (EPA) can modulate the inflammatory response according to different genotypes of the TNFa 857C/T polymorphism. Methods: Peripheral blood cells were collected from CD patients with different genotypes for TNFa 857C/T (CC, n = 29, CT, n = 11, TT, n = 3), and lymphocytes were established in culture media. Replicates with the addition of EPA (25 mM) were analysed in a period of 24 and 72 h. Expression of TNFa and PGE2 was assessed by ELISA for 14 samples (CC, n = 6, CT, n = 5, TT, n = 3). Apoptosis and cellular proliferation was determined by flow cytometry. Results: We observed that the production of TNFa decreases with time independently of the addition of EPA, although not significantly (p > 0.05), with the CT genotype presenting the highest values (CC=2195 pg/ml, CT=3059, TT=2196 at 24 h vs CC=1025 pg/ml, CT=1701, TT=1557 at 72 h without EPA and CC=2744 pg/ml, CT=3068, TT, 2054 at 24 h vs CC=1206 pg/ml, CT=2345, TT=1545 at 72 h with EPA). Regarding PGE2 no significant differences were observed between genotypes or with the addition of EPA (p > 0.05). A slight PGE2 increase was observed for TT genotype (CC=11.8 ng/ml, CT=11.9, TT=13.5 at 24 h vs CC=11.1 ng/ml, CT=11.9, TT=14.0 at 72 h without EPA and CC=11.7 ng/ml, CT=12.6, TT=14.0 at 24 h vs CC=11.8 ng/ml, CT=12.5, TT, =14.0 at 72 h with EPA). Lower proliferation index was observed for CT genotype (CC=30.3, CT=23.0, TT=29.7%) and higher apoptosis rate was observed for TT genotype (CC=20.8%, CT=27.1, TT=30.3), although nonsignificantly so (p > 0.05). Conclusion: This study shows no anti-inflammatory effect of EPA in TNFa production although a trend towards a higher apoptosis rate for TNFa857TT genotype was observed. A further increase in this latter group is needed to confirm these observations. P230 Ethnic differences in the genetic susceptibility to Crohn’s disease: functional PPARg gene variants are not associated with susceptibility to inflammatory bowel disease in the German population J. Seiderer1 *, J. Glas1, J. Diegelmann1, C. Markus2, S. Pfennig1, C. Tillack1, M. Jurgens1, A. Konrad1, M. Wetzke3, E. Paschos4, H. Torok1, T. Griga5, W. Klein6, J.T. Epplen7, U. Schiemann8, T. Mussack9, P. Lohse10, B. Goke1, M. Folwaczny2, T. Ochsenkuhn1, B. Muller-Myhsok11, S. Brand1. 1University of Munich Klinikum Groshadern, Munich, Germany, 2Department of Preventive Dentistry and Periodontology, University of Munich, Munich, Germany, 3Department of Pediatrics, Hannover Medical School, Hannover, Germany, 4Department of Orthodontics, University of Munich, Munich, Germany, 5Department of Internal Medicine, Knappschaftskrankenhaus Dortmund, Dortmund, Germany, 6Department of Human Genetics, Ruhr-University, Bochum, Germany, 7Department of Human Genetics, Ruhr-University, Bochum, Bochum, Germany, 8Department of General Internal Medicine, Inselspital Bern, Bern, Switzerland, 9Department of Surgery Innenstadt, University of Munich, Munich, Germany, 10Institute of Clinical Chemistry, University Hospital Munich-Grosshadern, Munich, Germany, 11Department of Psychatry, Max-Planck-Institute, Munich, Munich, Germany Introduction: The peroxisome proliferator activated receptorgamma (PPAR-gamma) is a key protein involved in the pathogenesis of diabetes and obesity (Figure 1 and 2) but also in the etiopathogenesis of inflammatory bowel diseases (IBD) such as Crohn’s disease (CD) and ulcerative colitis (UC). Recently, the functional SNPs rs2067819, rs3892175 and rs3856806=p.His447His within the PPARG gene on chromosome 3 encoding PPAR-gamma, which are involved in the regulation of its expression, have been shown to be associated with CD. Aims and Methods: The aim of our study was to investigate whether these SNPs are associated with inflammatory bowel disease in a large European cohort of patients. We analyzed genomic DNA from 2261 Caucasian individuals (n = 616 patients with CD, n = 365 patients with UC, and 1280 healthy unrelated controls) for the SNPs rs2067819, rs3892175 and rs3856806=p.His447His in the PPARG gene. Results: The SNPs rs2067819, rs3892175 and rs3856806= p.His447His and haplotypes built up of these three SNPs were not found to be associated with CD susceptibility (SNP1: minor allele frequency [MAF] 23.4% vs. 23.7%, SNP2: MAF 10.0% vs. 10.5%, SNP3: MAF 12.8% vs. 14.5%) or UC susceptibility (SNP1: MAF 23.7% vs. 23.7%, SNP2: MAF 9.6% vs. 10.5%, SNP3: MAF 13.7% vs. 14.5%) when compared to the control group. Additionally, no significant associations of rs2067819, rs3892175 and rs3856806=p.His447His with a certain CD phenotype such as ileal involvement could be found. Conclusion: Our results could not confirm a previous report of variants in the PPARG gene to be associated with IBD susceptibility. Therefore, the effect of PPAR-gamma in intestinal inflammation may be independent from the genetic variants in the PPARG gene tested herein. by gest on A ril 2, 2016 http://eccoxfordjournals.org/ D ow nladed from