Aim: To characterise the association between small intestinal mucosal permeability and hepatic fibrosis, using a plasma-based assay and transient elastography. Methods: A cohort of patients with chronic liver disease (CLD) of mixed aetiology (hepatitis B, C and non-alcoholic fatty liver) was compared to healthy volunteers (HV). Subjects were excluded if they drank alcohol within 24 hours, had gastro-intestinal

pathology or were taking potentially confounding medications within 4 weeks. Small intestinal permeability was assessed by an enteral lactulose:rhamnose probe. Subjects ingested 100 ml water containing 5 g lactulose and 1 g rhamnose and blood was collected 90 minutes later, for analysis of the lactulose:rhamnose (L:R) ratio by high performance liquid chromatography. All subjects underwent transient elastography to stratify them by fibrosis stage (no/mild BAY 80-6946 supplier <7.5 kPa, see more significant > 7.5 kPa). Increased permeability was defined as L:Rx100 > 8.86 (Tran, 2012). Statistical analysis was performed by GraphPad Prism v 5.0). Results: 32 subjects met inclusion criteria; 20 with CLD (9 with no/mild fibrosis, 11 with significant fibrosis) and 12 HV (all had no fibrosis). Small intestinal permeability (median L:R x 100, IQR) was elevated in CLD with significant fibrosis (20.9, 16.9–46.3), compared to HV (6.3, 5.3–15.7) p = 0.02,

but not in CLD with no/mild fibrosis (12.4, 6.7–36.7) p = 0.33. Median transient elastography values were 4.3 (3.4–4.7) for HV, 5.7(4.7–6.1) for no/mild fibrosis, and 12.5 (11.1–35.8) for advanced fibrosis. Median age, body mass index and HBA1c were similar. No patients had any adverse effects. Conclusion: Utilising non-invasive techniques, our results show that

significant hepatic fibrosis is associated with increased small intestinal permeability. AT ST JOHN,1,2 EH CHENG1 & M HAQUE1,2 Department of Gastroenterology, Mater Adult Hospital, Brisbane, Australia1, School of Medicine, University of Queensland, Brisbane, Australia2 Background and aims: The combination of a low hepatitis B surface antigen (HBsAg) titre and a low HBV DNA level appears to be associated with a reduced risk of hepatocellular carcinoma (HCC) development.1 We evaluated the cost effectiveness of a risk stratification system utilising HBsAg quantification and HBV DNA levels to Miconazole determine HCC surveillance intervals in HBsAg positive patients at a tertiary referral centre in Brisbane. Methods: We identified all patients who had at least one HBsAg quantification performed in the preceding two years at the Mater Adult Hospital in Brisbane. Treatment experienced and treatment naïve patients were included in the analysis. Demographic and clinical data were used to identify those patients who qualified for HCC surveillance. A modified version of the AASLD criteria for HCC surveillance was used. Patients with HBsAg titres <1000 IU/mL and HBV DNA <2000 IU/mL were identified and considered for a less intensive surveillance strategy.