Abstracts / Digestive and Liver Disease 47S (2015) e1–e18 e15 replication, in its presence the inhibition exerted by 17-estradiol was reverted in a dose-dependent manner. Conclusions: In vitro, 17-estradiol is able to block HCV infec- tion, likely by modulation of intracellular pathways following binding to the estradiol receptor, whose activation leads to an antiviral state. http://dx.doi.org/10.1016/j.dld.2015.01.034 OC-29 ACQUIRED SPHEROCYTIC LIKE ANEMIA COMBINED WITH INEFFECTIVE ERYTHROPOIESIS SUSTAINS ANEMIA IN PATIENTS WITH CHRONIC HEPATITIS C INFECTION RECEIVING TELAPREVIR OR BOCEPREVIR-BASED TRIPLE THERAPY F. Lupo 1 , R. Russo 2,3 , A. Iolascon 2,3 , D. Ieluzzi 4 , P. Toniutto 5 , S. Piovesan 6,7 , E. Raffetti 8 , A. Siciliano 1 , A. Matte’ 1 , F. Turrini 9 , F. Donato 8 , A. Alberti 6 , V. Zuliani 1 , G. Fattovich 1,4 , L. De Franceschi 1 1 Department of Medicine, University of Verona, Verona, Italy 2 Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli Federico II, Napoli, Italy 3 CEINGE Biotecnologie Avanzate, Napoli, Italy 4 Clinical Unit of Gastroenterology, Azienda Ospedaliera Universitaria Integrata Verona, Verona, Italy 5 Department of Medicine and Pathology Clinical and Experimental, Medical Liver Transplantation Unit, Internal Medicine, University of Udine, Udine, Italy 6 Department of Molecular Medicine, University of Padua, Padua, Italy 7 Clinical Unit of General Medicine, Azienda Ospedaliera Universitaria Integrata Padua, Padua, Italy 8 Institute of Hygiene, Epidemiology and Public Health, University of Brescia, Brescia, Italy 9 Department of Oncology, University of Turin, Turin, Italy Background and aims: The addition of protease inhibitors, boceprevir (BOC) or telaprevir (TVR), to peg-interferon and riba- virin (PR) increases the incidence of anemia. Although genetic variants in ITPA gene have been linked to the hemolytic anemia induced by PR, the mechanism sustaining the severe anemia during triple therapy is still unknown. Materials and methods: We studied 59 patients with chronic hepatitis C: 29 treated with TVR/PR and 30 with BOC/PR. Patients were examined at baseline, at week 4 (end of PR lead-in phase), at 12, 16 and 24 weeks of treatment. In all patients we evaluated biochemical and hematological parameters, red cell index; while in a subgroup, we carried out in vitro functional studies to dis- sect the mechanism(s) underlying anemia in triple therapy. IL28B (rs12979860) and ITPA (rs1127354, rs7270101) polymorphisms were also analyzed. Results: In chronic HCV patients on triple therapy, we found an early acute normochromic normocytic hemolytic anemia (4–8 weeks) followed by a late macrocytic hypo-regenerative ane- mia with low reticulocyte count in response to the degree of anemia (12–24 weeks). Although the beneficial effects of ITPA poly- morphisms impacted the early phase of anemia (4 weeks), the functional studies on red cells revealed: (i) the presence of sphe- rocytes; (ii) increased osmotic fragility; (iii) changes in red cell membrane protein composition; (iv) increased phosphorylation of -adducin with reduced membrane-cytoskeleton stability; (v) increased release of erythroidmicroparticles. Conclusions: Our data indicate that the bimodal pattern of ane- mia in chronic HCV patients on triple therapy might be induced by acquired spherocytic-like anemia as dominating component in the early phase (4–8 weeks), followed by the appearance of hypore- generative macrocytic anemia (12–24 weeks), most likely related to the combination effects of PR and TVR or BOC on erythropoiesis. These data could guide strategy of anemia management during triple therapy. http://dx.doi.org/10.1016/j.dld.2015.01.035 OC-30 SOFOSBUVIR-BASED ALL-ORAL TREATMENT FOR ELDERLY CHRONIC HEPATITIS C PATIENTS: A COST-EFFECTIVENESS ANALYSIS A. Ciaccio 1 , P.A. Cortesi 2 , G. Bellelli 3 , M. Rota 4 , S. Okolicsanyi 1 , M. Rota 1 , L. Mantovani 2 , G. Annoni 3 , M. Strazzabosco 1,5 1 Department of Surgery and Translational Medicine, University of Milano-Bicocca, Milan, Italy 2 Research Centre on Public Health (CESP), University of Milano-Bicocca, Milan, Italy 3 Department of Health Sciences, Geriatric Medicine, University of Milano-Bicocca, Milan, Italy 4 Department of Health Sciences, Centre of Biostatistics for Clinical Epidemiology, University of Milan-Bicocca, Milan, Italy 5 Liver Center & Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, United States Background and aim: A relevant proportion of patients affected by chronic hepatitis C (CHC) is older than 65 years. Comorbidi- ties and a higher susceptibility to drugs toxicity have historically limited treatment in these patients. Recent approval of interferon- free regimens, characterized by high efficacy and limited toxicity, provides unprecedented chances for these patients to be cured. The aim of this study is to assess cost-effectiveness, taking into account the severity of liver disease, age, and the geriatric (frailty) status. Methods: A semi-Markov model of CHC natural history was built. The study focuses on CHC patients older than 65 years, strat- ified according to liver fibrosis (METAVIR F3 and F4), age (65–85 years old) and Fried’s frailty phenotype (not frail, pre-frail and frail) generating 30 simulated cohorts. Treatment with sofosbuvir plus simeprevir (SOF/SMV) versus no treatment was assessed for each cohort. The model estimated costs, Life Years and Quality Adjusted Life Years (QALY), with a lifetime time horizon and the Health System perspective. Results are presented as incremental cost- effectiveness ratios (ICERs) per QALY gained. Cost-effectiveness was defined as an ICER under the 37,000D threshold. Results: At each fibrosis score, ICER increased with age and frailty index. Among F3 patients, ICER ranged from D13,934 in not- frail 65-years-old and D79,354 in frail 85-years-old patients. Among F4 patients ICER ranged from D13,873 in not frail 65-years-old and D115,965 in frail 85-years-old patients. In both F3 and F4 cohorts ICER was below D37,000/QALY up to age 80 in non-frail patients, up to age 75 in pre-frail patients, up to age 70 in frail patients.