The total cohort was split by year of diagnosis into two groups, 2000–2006 and 2007–2013 and the groups compared to evaluate trends. T-test was used to compare means and Fisher’s exact test was used to compare between groups with significance determined by p < 0.05. Results: 231 patients were diagnosed with HCC, 197 males (84.4%) with mean age of 64.1 years. 107 were diagnosed between 2000 and 2006 and 124 between 2007–2013. The groups were not statistically different with regards to age, gender, presence of cirrhosis and tumor characteristics (size and number of lesions). In the 2000–2006 group, 71%

of patients had underlying cirrhosis with an average of 1.59 lesions and average largest lesion measuring 57 mm. In the latter

group, 77% of patients had cirrhosis with an average of 1.71 lesions and average Mitomycin C largest lesion measuring 49 mm. In patients diagnosed between 2000 and 2006, Hepatitis B (HBV) was the most common risk factor for HCC, n = 29 (27.1%) followed by Hepatitis Talazoparib chemical structure C, n = 22 (20.6%). There was a decline in diagnosed HBV-related HCC, with n = 22 (17.7%) in the 2007–2013 group, although not statistically significant. There was a statistically significant increase in Hepatitis C (HCV) related HCC over time [OR: 2.21, 95% CI: 1.21 to 3.99, p = 0.009]. Numbers of HCCs secondary to Non Alcoholic Fatty Liver Disease (NAFLD) also increased significantly [OR: 7.31, 95% CI: 0.89 to 59.46 p = 0.04]. There were no significant change in the numbers of detected alcohol related

HCC’s selleck chemical between the two groups. Conclusion: There has been a decrease in Hepatitis B related HCC over time which may be attributable to the introduction of potent nucleos(t)ide analogues at our center in 2006. In contrast, there was a significant increase in HCV related HCCs and the development of strategies focused on early detection and treatment including the early implementation of more efficacious direct acting antivirals remains vital. CB RANAWEERA,1 OT AYONRINDE,2,3,4 L MOLLISON,1,3 S GALHENAGE,2 JK OLYNYK2,4,5 1Department of General Medicine, Fremantle Hospital, Fremantle, WA, Australia, 2Department of Gastroenterology, Fremantle Hospital, Fremantle, WA, Australia, 3School of Medicine and Pharmacology (Fremantle Hospital Campus), The University of Western Australia, WA, Australia, 4Faculty of Health Sciences, Curtin University, Bentley, WA, Australia, 5Institute for Immunology and Infectious Diseases, Murdoch University, Murdoch, WA, Australia. Background: The severity of liver fibrosis in patients with chronic hepatitis C virus infection (CHC) influences treatment decisions and surveillance for complications. In Western Australia, non-invasive assessment of liver fibrosis using transient elastography (TE) and/ or Hepascore has largely replaced liver biopsy.