XXVIIIth Belgian Week of Gastroenterology 2016 All Abstracts Belgian Association for the Study of the Liver (BASL) A01 Light-to-moderate alcohol intake increases the risk of hepatocellular carcinoma in patients with HCV-related compensated cirrhosis: a prospective study H. VANDENBULCKE (1), C. MORENO (2), I. COLLE (3), J. KNEBEL (4), S. FRANCQUE (5), T. SERSTÉ (6), C. GEORGE (7), C. DE GALOCSY (8), W. LALEMAN (9), J. DELWAIDE (10), H. ORLENT (11), L. LASSER (12), E. TRÉPO (2), H. VAN VLIERBERGHE (3), P. MICHIELSEN (5), M. VAN GOSSUM (6), M. DE VOS (1), A. MAROT (13), C. DOERIG (13), M. ADLER (2), J. HENRION (1), P. DELTENRE (13) / [1] Hôpital de Jolimont, Haine-Saint-Paul, Belgium, Departement of Gastroenterology and Hepatology, [2] Erasme Hospital, Brussels, Belgium, Department of Gastroenterology, Hepatopancreatology and Digestive Oncology, [3] Ghent University, Ghent, Belgium, Departement of Gastroenterology and Hepatology, [4] Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland, Division of Radiology, [5] Antwerp University Hospital, Edegem, Belgium, Departement of Gastroenterology and Hepatology, [6] CHU Saint-Pierre, Brussels, Belgium, Departement of Gastroenterology and Hepatology, [7] AZ Groeninge, Kortrijk, Belgium, Departement of Gastroenterology and Hepatology, [8] Hôp. Iris Sud Bracops, Bruxelles, Belgium, Departement of Gastroenterology and Hepatology, [9] KU, Leuven, Belgium, Departement of Gastroenterology and Hepatology, [10] CHU Liege, Liège, Belgium, Departement of Gastroenterology and Hepatology, [11] AZ St. Jan Brugge AV, Brugge, Belgium, Departement of Gastroenterology and Hepatology, [12] CHU Brugmann, , Belgium, Departement of Gastroenterology and Hepatology, [13] Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland, Division of Gastroenterology and Hepatology Introduction: Whether light-to-moderate alcohol intake increases the risk of complications in patients with HCV-related cirrhosis remains unclear. Aim: To determine the impact of light-to-moderate alcohol intake and viral eradication on the risk of hepatocellular carcinoma (HCC), decompensation of cirrhosis and death. Methods: Data on alcohol intake and viral eradication were prospectively collected in 192 patients with compensated HCV-related cirrhosis. Cumulative incidence functions were used to describe the probability of HCC, decompensation of cirrhosis and death. Results: 74 patients consumed alcohol (median alcohol intake: 15 g/day) and 50 reached viral eradication. During a median follow-up of 47 months, 29 patients developed HCC, 48 experienced at least one decompensation event, and 30 died. Causes of death were liver-related in 23 patients and non-liver related in 7 patients. 19 patients underwent a liver transplantation. The 5-year cumulative incidence rate of HCC was 12.9% (95% CI: 5.7-20.1) in abstainers vs. 28.0% (95% CI: 13.2-42.8) in consumers (p=0.044), and 2.7% (95% CI: 0-8.0) vs. 23.9% (95% CI: 14.4-33.4) in patients with and without viral eradication (p=0.01), respectively. The lowest risk of HCC was observed for patients without alcohol intake and with viral eradication (0%) followed by patients with alcohol intake and viral eradication (9.1% [95% CI: 0-26.9]), patients without alcohol intake and no viral eradication (17.8% [95% CI: 7.8-27.8]), and patients with alcohol intake and no viral eradication (31.4% [95% CI: 14.5-48.3]) (p=0.024). In multivariate analysis, alcohol consumption was associated with the risk of HCC (hazard ratio: 2.82, 95% CI: 1.25-6.39, p=0.013). Light-to-moderate alcohol intake did not influence the risk of decompensation or death. Conclusions: Light-to-moderate alcohol intake increases the risk of HCC in patients with HCV- related cirrhosis. There is an increase in the risk of HCC according to alcohol intake and the lack of viral eradication. Accordingly, patients with HCV-related cirrhosis should be strongly advised against any alcohol intake. Patient care should include measures to ensure abstinence. A02 BROWN ADIPOSE TISSUE STIMULATION AS A NEW APPROACH TO FIGHT OBESITY AND METABOLIC SYNDROME L. POEKES (1), V. LEGRY (1), O. SCHAKMAN (2), A. BOL (3), G. FARRELL (4), I. LECLERCQ (5) / [1] Université Catholique de Louvain, Brussels, Belgium, Laboratory of Hepato-Gastroenterology, [2] Université Catholique de Louvain, Brussels, Belgium, Institute Of NeuroScience, [3] Université Catholique de Louvain, Brussels, Belgium, pôle d'imagerie moléculaire, radiothérapie et concologie, [4] Australian National University, , Australia, Liver Research Group, [5] Université catholique de Louvain, , Belgium, Laboratory of Hepatogastroenterology Introduction: Obesity, insulin resistance, low grade inflammation and fatty liver are part of the metabolic syndrome. Foz/foz mice, characterized by spontaneous mutation of Alms1, are a model of metabolic syndrome with the particularity of developing non-alcoholic steatohepatitis. Aim: The aim of this study was to decipher the mechanisms responsible for their metabolic phenotype. Methods: Male foz/foz and wild-type (WT) littermates were fed a high fat diet (HFD) for 4 weeks. We performed a pairfeeding experiment in which foz/foz mice received the same amount of HFD consumed by WT the day before. Activity level, oxygen consumption and thermogenic adaptation (18FDG PET-scan) were evaluated. Intermittent cold exposure (ICE) (4°C, 2h/day, 5 days/week) and brown adipose tissue (BAT) transplantation (WT BAT to foz/foz mice) were performed to stimulate BAT. Results: Unlike WT mice, 4 weeks of HFD induced obesity, insulin resistance, steatosis and liver and adipose inflammation in foz/foz mice. Although being hyperphagic compared to their WT littermates (18 vs 14 kcal/day, p<0.001), caloric restriction to foz/foz mice failed to restore their metabolic disturbances, notably in terms of adiposity, adipose inflammation, and glucose intolerance. Physical activity and basal metabolism were unaffected in foz/foz mice. By contrast, their thermogenic response to HFD or a cold exposure was severely impaired (44% reduction in 18FDG BAT uptake compared to WT upon cold exposure) due to 2.5-fold lower mitochondrial density in brown adipocytes and lower sympathetic tone (1.5-fold less noradrenaline, p<0.05; 2- fold less β3 adrenergic receptor expression, p<0.05). ICE and transplantation with WT BAT significantly increased cold-induced expression of thermogenic genes PGC1 α, DIO2 and UCP1. Notably, ICE induced restoration of BAT function, decreased body weight gain (11g vs 16g, p<0.001) and improved glucose tolerance (p<0.001) compared to control foz/foz mice. Conclusions: Overall, these results suggest that impaired BAT activity drives HFD-induced obesity and metabolic syndrome in foz/foz mice. Induction of endogenous BAT function by ICE or functional BAT transplantation had a significant positive impact on obesity and glucose tolerance, supporting that these strategies could become new effective therapeutic treatment against obesity and its comorbidities. A03 Kinetics of pulmonary angiogenesis in mouse common bile duct ligation-induced liver fibrosis S. RAEVENS (1), L. DEVISSCHER (1), A. PARIDAENS (1), E. BOGAERTS (1), S. LEFERE (1), Y. VANDEWYNCKEL (1), C. CASTELEYN (2), K. BRACKE (3), T. MAES (3), X. VERHELST (1), H. VAN VLIERBERGHE (1), C. VAN STEENKISTE (1), A. GEERTS (1), I. COLLE (1) / [1] Ghent University, Ghent, Belgium, Hepatology and Gastroenterology, [2] University of Antwerp, Antwerpen, Belgium, Veterinary Sciences, Laboratory of Applied Veterinary Morphology, [3] Ghent University Hospital, Ghent, Belgium, Respiratory Medicine, Laboratory for Translational Research in Obstructive Pulmonary diseases Introduction: Hepatopulmonary syndrome (HPS) is a severe pulmonary complication of liver disease for which no medical treatment is available up till now. In rats, common bile duct ligation (CBDL) has been documented as a model for human HPS, which is characterized by pathological pulmonary angiogenesis. Studies in genetically modified mice could offer opportunities for further research, however, in this species the development of pulmonary angiogenesis in biliary cirrhosis has not been outlined yet. Aim: We aimed to elucidate the temporal changes in proangiogenic signature of hepatic and pulmonary vasculature after CBDL in mice and in addition identify potential proangiogenic factors contributing to the pathogenesis of HPS. Methods: Male Swiss mice underwent CBDL or sham surgery and were sacrificed at a weekly basis for 6 consecutive weeks. Pulmonary inflammation was studied by cytology on broncho- alveolar lavage fluid, myeloperoxidase assay and luminex bead based assay. Liver and lungs were collected for protein analysis and histology to assess liver fibrosis and hepatic and pulmonary angiogenesis. Scanning electron microscopy was performed on vascular corrosion casts to visualize pulmonary vasculature during cirrhosis ex vivo. Results: CBDL progressively induced liver fibrosis from week 1 (F0-1) to 6 (F4). This was accompanied by a gradual increase in hepatic immunopositivity for Endoglin and von Willebrand Factor, two markers of endothelial cell activation (P<0.0001). Hepatic levels of vascular endothelial growth factor (VEGF), VEGF receptor 1 and 2 were significantly increased at week 6, whereas placental growth factor (PlGF), which is exclusively involved in pathological angiogenesis, was already upregulated at week 2 (P<0.0001). In the pulmonary compartment, CBDL resulted in neutrophil infiltration and increased pro-inflammatory mediators from week 2 to 6