COMP-positive cirrhotic patients are selleck screening library at an increased risk of progressing

to more severe disease outcome. Serum COMP is a new promising, non-invasive biomarker for risk-assessment and surveillance of patients with chronic liver diseases at risk to develop HCC. Disclosures: Gary L. Norman – Employment: INOVA Diagnostics Zakera Shums – Employment: INOVA DIAGNOSTICS The following people have nothing to disclose: Nikolaos Gatselis, Christos Liaskos, Dimitrios P. Bogdanos, George K. Koukoulis, George N. Dalekos Background The number of non-B or non-C hepatocellular carcinoma (NBNC-HCC) including alcoholic liver diseases, non-alcoholic steatohepatitis (NASH) and cryptogenic has been increasing gradually all over the world. Although inflammation and oxidative stress are suggested to participate to their pathogenesis, clinical characteristics of NBNC-HCC are not fully examined compared with hepatitis virus-related HCC. Recently, advanced glycation end products (AGEs) are known to cause oxidative stress and inflammatory reactions, and play a role in the pathogenesis of a variety of disorders such as

diabetic vascular complications, alcoholic liver injury, and NASH. On the other hand, pigment epithelium derived factor (PEDF) that belongs to the superfamily of serine protease inhibitors has been shown to have anti-oxidative and anti-inflammatory properties that acts restrainingly for AGEs. In the present study, we examined whether serum levels of AGEs and PEDF were elevated in patients with HCC derived PFT�� from NASH (NASH-HCC) compared with NASH subjects without HCC and further investigated clinical variables to explore the clinical usefulness of AGEs and PEDF as markers of NASH-HCC. Methods Patients with 11 treatment-naïve NASH-HCC and

56 biopsyproven NASH were enrolled. Serum levels of AGEs and PEDF were measured by using the competitive ELISA method. Also, clinical and pathological findings (inflammation, fibrosis) were compared between both groups. Results Type2 diabetes mellitus (DM) was complicated selleck in 64% and 79%, and liver cirrhosis in 27% and 0% in NASH-HCC and NASH without HCC, respectively. NASH-HCC were older in age, and showed significantly advanced fibrosis stage compared with NASH without HCC. Serum levels of AGEs and PEDF in NBNC-HCC were significantly higher than those in NASH without HCC (9.1 vs 5.2 U/ml and 12.8 vs 10.7 μg/ml, respectively, p<0.001, p<0.05). By multivariate analysis, fasting plasma glucose (FPG) and HbA1c were significantly associated with AGEs in NASH without HCC (p<0.05). Matched for age, fibrosis stage, FPG, and HbA1c, AGEs were elevated in NASH-HCC (9.7 vs 5.3 U/ml, p<0.001). By multivariate analysis, gender (p=0.05), homeostasis model assessment-insulin resistance (HOMA-IR) (p=0.07), and the presence of DM (p=0.11) tended to be associated with PEDF in NASH without HCC. Matched for age, gender, fibrosis stage, HOMA-IR, and the presence of DM, PEDF were elevated in NASH-HCC (14.5 vs 10.