Genotyping was performed with the Infinium HumanHap 550K chip. All SNPs were in Hardy-Weinberg equilibrium. Linear regression models were used to assess associations, adjusting for age, sex, steatosis, ALT, type

of elastography probe, HOMA-IR, spleen size, presence of viral hepatitis and alcohol intake, using additive genetic models. Results: In 1037 participants (age 74.1±5.6 years; 50.7% males) reliable LSM and genetic data were obtained. Median LSM was 5.1 kPa (IQR 4.2-6.4). NAFLD was detected in 331 participants (31.9%). Two SNPs in the IFNGR2 gene, rs9976971 and rs2284553, were associated with LSM in the total cohort (p=0.018 and 0.011 respectively). This relationship remained selleck screening library significant in a multivariable model (p=0.043 and 0.010 respectively). A third polymorphism in the IFNGR2 gene, rs9808753, showed a trend towards significance in a multivariable model (p=0.08). In participants with NAFLD all three IFNGR2 SNPs were significantly associated with LSM (p=0.046; 0.044 and 0.003 respectively). In a multivariable model this relationship remained significant for rs9808753 (p=0.010). rs738409, rs12980275 and rs8099917, in the PNPLA3 and near the IL28B gene, were not associated with LSM in the total cohort, nor in participants

with NAFLD (all p-values >0.17). Conclusions: Two IFNGR2 SNPs AZD1208 mouse were associated with liver stiffness in this large population based cohort. In a subgroup of participants with NAFLD all three tested IFNGR2 variants showed an association with LSM. PNPLA3 and IL28B variants were not related to liver stiffness in the total cohort, nor in participants with NAFLD. These results suggest that IFNGR2 variants could not only

MCE play a role in liver fibrogenesis in risk populations, but in the general population as well. Disclosures: Harry L. Janssen – Consulting: Abbott, Bristol Myers Squibb, Debio, Gilead Sciences, Merck, Medtronic, Novartis, Roche, Santaris; Grant/Research Support: Anadys, Bristol Myers Squibb, Gilead Sciences, Innogenetics, Kirin, Merck, Medtronic, Novartis, Roche, Santaris The following people have nothing to disclose: Elisabeth P. Plompen, Jeoffrey Schouten, Daan W. Loth, Bettina E. Hansen, Albert Hofman, Andre G. Uitterlinden, Bruno H. Stricker, Frank W. Leebeek Background: The response to chronic liver injury in hepatitis C (HCV) is fibrogenesis, which is characterized by the accumulation and reorganization of extracellular matrix. This extensive remodeling generates protein fragments originating from fibro-genesis or fibrosis resolution. These fragments may reflect the degree of fibrosis and/or the turnover of fibrotic processes and potentially serve as biomarkers that carry diagnostic and prognostic information. Aims: We aimed to evaluate the diagnostic and prognostic performance of two different sub-pools of type III collagen: Pro-C3, a cleavage specific formation biomarker and C3M, a biomarker for a MMP generated fragment.