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1110A AASLD ABSTRACTS HEPATOLOGY, October, 2015 (HCV-2). Phylogenetic analysis revealed that all HCV-2 isolates from Suriname were part of 6 robust phylogenetic clusters containing HCV-2 sequences obtained from Surinamese living in The Netherlands. Conclusion HCV prevalence among the Surinamese population attending the ED was 1% and was highest among those of Javanese ethnicity. Older patients were more often infected, suggesting a long-standing infection acquired in the past. HCV-2 is the circulating genotype in Suriname and was likely introduced in Suriname by slave trade from western Africa in the past centuries. Targeted screening with linkage to care and prevention guidelines for identified at-risk groups are required, as well as implementation of stricter hygiene regulations for permanent make-up salons. Peginterferon and ribavirin are not yet routinely given as HCV treatment in Suriname, however given the predominance of favorable HCV genotype 2, would be strongly advised. Disclosures: Richard Molenkamp - Independent Contractor: Roche Diagnostics Maria Prins - Speaking and Teaching: msd, roche The following authors have nothing to disclose: Sigrid MacDonald - Ottevanger, Stephen G. Vreden, Jannie van der Helm, Thijs J. van de Laar, Els Dams, Jimmy Roosblad, John F. Codrington 1847 Hepatocellular carcinoma (HCC) scoring system for the individualized prediction of liver cancer in 1080 HCV-related compensated cirrhosis included in the French multicenter prospective cohort ANRS CO12 Cir- Vir. Nathalie Ganne 1 , Valerie Bourcier 1 , Richard Layese 2 , Nabila Talmat 1 , Ventzislava Petrov-Sanchez 3 , Patrick Marcellin 4 , Dominique Guyader 5 , Stanislas Pol 6 , Dominique G. Larrey 7 , Victor de Ledinghen 8 , Denis Ouzan 9 , Fabien Zoulim 10 , Pierre Nahon 1 , Françoise Roudot-Thoraval 2 ; 1 Hepatology, Jean Verdier hospital, Bondy, France; 2 Henri Mondor hospital, Creteil, France; 3 ANRS, Paris, France; 4 Beaujon hospital, Clichy, France; 5 CHU, Rennes, France; 6 Cochin hospital, Paris, France; 7 CHU, Montpellier, France; 8 CHU, Bordeaux, France; 9 none, Saint Laurent du Var, France; 10 CHU, Lyon, France Background and aims: This study aimed to develop and validate a simple scoring system to refine individualized prediction of HCC risk in patients with HCV-related compensated cirrhosis included in the French prospective multicentre ANRS CO12 CirVir cohort (1) . Methods: Among 1323 patients with HCV-cirrhosis enrolled in the ANRS CO12 CirVir, 720 and 360 patients were randomly assigned to the training and validation sets, respectively. Cox multivariate proportional hazards model was used to predict HCC occurrence in the population, then nomograms were computed to assess individualized risk. Results: During a mean follow-up of 51 months, 103 (14%) and 39 (11%) patients developed HCC, respectively in the training and validation cohorts. According to Cox regression analysis, 5 variables were independently associated with the occurrence of HCC in the training cohort (table 1). A 13-point risk score was derived in the training cohort using these 5 variables, the score of each variable being obtained by linear transformation of the coefficients and rounding. The population was stratified according to this scoring system into four groups, with HCC occurrence gradually increasing from 0% to 20% at 3 years, and 0% to 37% at 5 years, for patients with the lowest (score ≤ 2) and highest (score ≥ 11) HCC risk, respectively and validated. The AUC for the 1- and 3-year prediction were 0.75 [0.64; 0.85] and 0.75 [0.71;0.80] respectively. Derived from this score, a nomogram was also built, enabling individualized prediction of HCC occurrence at 1, 3 or 5 years. Conclusion: An HCC score constructed using 4 baseline variables (age, past excessive alcohol consumption, platelets count, GGT serum level) and qualitative HCV RNA at end-point is accurate to predict HCC at the individual level in French patients with HCV-cirrhosis, with or without SVR. External validation in non-French populations is warranted. (1) Trinchet et al. Complications and competing risks of death in compensated viral cirrhosis (ANRS CO12 CirVir prospective cohort). Hepatology. 2015 Feb 11. doi: 10.1002/hep.27743. table 1 Disclosures: Patrick Marcellin - Consulting: Roche, Gilead, BMS, Vertex, Novartis, Janssen, MSD, Abbvie, Alios BioPharma, Idenix, Akron; Grant/Research Support: Roche, Gilead, BMS, Novartis, Janssen, MSD, Alios BioPharma; Speaking and Teaching: Roche, Gilead, BMS, Vertex, Novartis, Janssen, MSD, Boehringer, Pfizer, Abbvie Dominique Guyader - Advisory Committees or Review Panels: ROCHE, GILEAD, IRIS, ABBVIE; Board Membership: MERCK; Grant/Research Support: JANSSEN; Speaking and Teaching: BMS Stanislas Pol - Board Membership: Sanofi, Bristol-Myers-Squibb, Boehringer Ingelheim, Tibotec Janssen Cilag, Gilead, Glaxo Smith Kline, Roche, MSD, Novartis; Grant/Research Support: Glaxo Smith Kline, Gilead, Roche, MSD; Speaking and Teaching: Sanofi, Bristol-Myers-Squibb, Boehringer Ingelheim, Tibotec Janssen Cilag, Gilead, Glaxo Smith Kline, Roche, MSD, Novartis Dominique G. Larrey - Advisory Committees or Review Panels: BAYER, SANOFI, PFIZER, SERVIER-BIG, AEGERION, MMV, BIAL-QUINTILES, TEVA, ORION, NEG- MA-LERADS, ASTELLAS, ASTRAZENECA, DNDI, GSK, J AND J; Board Membership: BMS, GILEAD, ABBVIE, BMS, GILEAD, ITREAS, MMS; Grant/Research Support: GILEAD, MSD, BMS, ABBVIE, TIBOTEC/JANSSEN, BMS Victor de Ledinghen - Board Membership: Janssen, Gilead, BMS, Abbvie; Speaking and Teaching: AbbVie, Merck, BMS, Gilead Fabien Zoulim - Advisory Committees or Review Panels: Janssen, Gilead, Novira, Abbvie, Tekmyra, Transgene; Consulting: Roche; Grant/Research Support: Novartis, Gilead, Scynexis, Roche, Novira, Assemblypharm; Speaking and Teaching: Bristol Myers Squibb, Gilead Françoise Roudot-Thoraval - Advisory Committees or Review Panels: Roche; Consulting: LFB biomedicaments; Speaking and Teaching: gilead, Janssen, BMS, Roche The following authors have nothing to disclose: Nathalie Ganne, Valerie Bourcier, Richard Layese, Nabila Talmat, Ventzislava Petrov-Sanchez, Denis Ouzan, Pierre Nahon 1848 Differential Progression to Cirrhosis and Hepatic Decompensation in Asian Americans (AA) and Non-Asian (NA) Patients with Chronic Hepatitis C (CHC) An K. Le 1 , Nghia H. Nguyen 1,2 , Changqing Zhao 1,3 , Joseph K. Hoang 1 , Christine Y. Chang 1 , Mingjuan Jin 1,4 , Pauline Nguyen 1 , Peter T. Nguyen 1,5 , Richard H. Le 1 , Michelle Q. Jin 1 , Linda Nguyen 6 , Lee Ann Yasukawa 7 , Jian Q. Zhang 8 , Susan C. Weber 7 , Mindie H. Nguyen 1 ; 1 Division of Gastroenterology and Hepatology, Stanford University Medical Center, Palo Alto, CA; 2 Department of Medicine, University of California San Diego, San Diego, CA; 3 Department of Cirrhosis, Institute of Liver Disease, Shuguang Hospital, Shanghai, China; 4 Department of Epidemiology and Biostatistics, School of Public Health, Zhejiang University, Hangzhou, China; 5 School of Medicine, University of Texas Medical Branch, Galveston, TX; 6 Stanford University, Palo Alto, CA; 7 Center for Clinical Informatics, Stanford University School of Medicine, Palo Alto, CA; 8 Chinese Hospital, San Francisco, CA BACKGROUND: Little is known about the natural history of CHC in AA .Our goal is to evaluate the rate of progression to cirrhosis and hepatic decompensation in a large ethnically
HEPATOLOGY, VOLUME 62, NUMBER 1 (SUPPL) AASLD ABSTRACTS 1111A diverse CHC cohort. METHODS: Using ICD-9 query and manual chart review for all identified patients, 5,942 consecutive adults with CHC and known ethnicity from 3 community clinics and one large U.S. university center were confirmed and included. RESULTS: AA were older (mean age=60.3±13.4 vs. 55±10.2, p
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1000A AASLD ABSTRACTS HEPATOLOGY, O
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1312A AUTHOR INDEX HEPATOLOGY, Octo
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1366A CATEGORY INDEX HEPATOLOGY, Oc
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