HCV: Diagnosis and natural history


Acute Hepatitis C Infection is Associated with an Increase in Circulating microRNA-122

Ramy El-Diwany1, Kimberly Page2, Stuart Ray1, Andrea Cox1, David L. Thomas1, Ashwin Balagopal1

1Center for Viral Hepatitis Research, Johns Hopkins School of Medicine, Baltimore, MD; 2Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA

Background: Circulating microRNAs (miRNAs) are increasingly recognized as early and stable biomarkers of disease. miR122 is an abundant hepatocyte-derived miRNA that is required for hepatitis C virus (HCV) replication, and increased circulating cell-free miR-122 has been associated with chronic HCV in cross-sectional studies. We measured cell-free miRNAs, including miR-122, before and immediately after incident HCV infection. Methods: Samples were obtained from the Baltimore Before and After Acute Study of Hepatitis (BBAASH), a longitudinal study of injection drug users (IDU)that collects monthly blood specimens. In this prospective study, most infections are asymptomatic, avoiding bias toward severe cytolysis. Twentytwo participants who acquired acute HCV infection and either spontaneously cleared infection (“clearers”; n=11)or developed persistent infection (“persisters”; n=11) were identified who had plasma available at four time points: i) pre-infection; ii) first viremia; iii) last viremia in clearers; and iv) post-viremia in clearers. Samples from persisters were time-matched withthose from clearers for all time points. RNA was extracted from plasma and the relative abundance of approximately 800 microRNAs was determined using a quantitative PCR array. Individual Taqman® RT/qPCR assays were performed to validate findings from the array, and miR-122a was quantified in relation to the spiked-in control microRNA from Arabidopsis thaliana, ath-miR-159a. Findings were confirmed in 29 participants in the You Find Out (UFO) cohort, a separate longitudinal study of IDU who acquired incident HCV infection. Results: BBAASH participants΄ ages ranged from 20-31 years, 13 (59%) were female, and 20 (91%) were white. mir-122 levels rose a median (IQR) of 5.3-fold (0.8-39.2) upon first viremia compared to pre-infection levels (p=0.02). miR-122 varied directly with transaminases at all time points; however, miR155 and miR-146a, miRNAs that have been previously associated with hepatocyte damage, were not elevated upon infection (p=0.98 and p=0.92, respectively). miR-122 levels stayed elevated compared to pre-infection in persisters at the latest time points (p=0.001), while miR-122 decreased in clearers to pre-infection levels (p=0.57). miR-122 levels showed similar increases upon acute HCV infection in the UFO cohort (p=0.02). Conclusions: Circulating miR-122 increases soon after HCV infection and normalizes in persons who spontaneously clear infection. Plasma miR-122 may be an early and unique marker of acute HCV infection.


Stuart Ray - Advisory Committees or Review Panels: Abbott Laboratories, Boerhinger Ingelheim

David L. Thomas - Grant/Research Support: Merck, Gilead

The following people have nothing to disclose: Ramy El-Diwany, Kimberly Page, Andrea Cox, Ashwin Balagopal


Pre-treatment levels of serum IFN-λ3 more accurately predict sustained virological response by pegylated interferon/ribavirin therapy than IL28B genolyping in chronic hepatitis C patients

Yoshihiko Aoki1, Kazumoto Murata1, Masaya Sugiyama1, Tatsuji Kimura2, Tsutomu Takeda1, Sachiyo Yoshio1, Masaaki Korenaga1, Masatoshi Imamura1, Tatsuya Kanto1, Naohiko Masaki1, Masashi Mizokami1

1The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Tokyo, Japan; 2Institute of Immunology Co., Ltd,, Tokyo, Japan

Background&Aims: Genetic variation in IL28B is well-known predictive factors for the outcome of pegylated interferon-α/ribavirin (Peg-IFN/RBV) therapy. However, the IL28B genotyping fails to predict at about 20%. In addition, genotyping needs annoying informed consent. Therefore, we seek to find easier and accurate methods for correct prediction before therapy. Methods: We examined serum IFN-λ3 levels in 72 patients with chronic hepatitis C(CHC, genotype 1b) who had recently completed Peg-IFN/RBV therapy for 48 weeks. Serum IFN-λ3 levels were measured by our newly developed chemiluminescence enzyme-linked immnosorbent assay, using frozen stocks of the serum taken before treatment, and were analyzed with clinical data. SNP near IL28B (rs8099917; TT is a favorable genotype for Peg-IFN/RBV therapy) were evaluated by InvaderPlus assay. Results: All patients (mean age: 60 ± 9 y. o., 32 male and 40 female) were completed Peg-lFN/RBV therapy (48 weeks) with >80 % drug compliance. TT is more predominant (77.8%) than other reports, and high rate of sustained virological response (SVR) (56.9%) were observed in our cohort because favorable patients for treatment were selected. High serum IFN-λ3 (> 10 pg/ml) was observed in patients with low total cholesterol (p = 0.04) and low peripheral white blood count (p = 0.03), but no correlation was observed between HCV RNA levels and serum IFN-λ3.No differences were observed in serum IFN-λ3 levels between IL28B genotypes (TT vs non-TT genotype, p=0.08). Importantly, we found that serum IFN-λ3 levels before PegIFN/RBV therapy well correlated with the response to treatment (SVR: 6.4 ± 12.0 pg/ml, transient virological response (TVR): 15.3 ± 14.5 pg/ml, non-virological response (NVR): 28.7 ± 32.9 pg/ml), and serum IFN-λ3 in patients who showed SVR was significantly lower than those who showed NVR (p = 0.0004) regardless of IL28B genotype, including discrepancy cases (NVR in patients with favorable IL28B genotype, or SVR in patients with unfavorable genotype). Positive or negative predictive value of SVR by serum IFN-λ3 (≤5 pg/ml) was 84.2%, 75.7% whereas 60.3%, 62.5% by IL28B genotyping, respectively. Serum IFN-λ3 levels significantly decreased after achievement of SVR while, in patients with TVR, it decreased once during therapy, but returned to the pre-treatment levels after cessation of therapy, suggesting serum IFN-λ3 levels are dependent on the existence of HCV RNA. Conclusions: Pretreatment levels of serum IFN-λ3 could be superior marker to IL28B genotyping for the accurate prediction of the outcome of Peg-IFN/RBV therapy. This method is easier and less costly, therefore, more practical for clinical application.


Tatsuji Kimura - Employment: Institute of Immunology, Co., Ltd.

The following people have nothing to disclose: Yoshihiko Aoki, Kazumoto Murata, Masaya Sugiyama, Tsutomu Takeda, Sachiyo Yoshio, Masaaki Korenaga, Masatoshi Imamura, Tatsuya Kanto, Naohiko Masaki, Masashi Mizokami


Diagnostic accuracy of liver stiffness (FibroScan®) in patients with chronic viral hepatitis: results of a large USA cohort

Nezam H. Afdhal1, Bruce R. Bacon2, Keyur Patel3, Eric Lawitz4, Stuart C. Gordon5, David R. Nelson6, Tracy L. Challies1, Imad Nasser1,Lee jen Wei7, John G. McHutchison3;

1Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Ma; 2St Louis University Liver Center/ Saint Louis University School of Medicine, Saint Louis, MO; 3Duke Clinical Research Institute, Duke University Medical Center, Durham, NC; 4The Texas Liver Institute, University of Texas Health Science Center, San Antonio, TX; 5Division of Gastroenterology and Hepatology, Henry Ford Hospital, Detroit, MI; 6Division of Gastroenterology, University of Florida College of Medicine, Gainesville, FL; 7Harvard School of Public Health, Boston, MA

Introduction: Liver biopsy (LB) is the standard technique for assessing liver fibrosis. However, the procedure is invasive and can lead to occasional complications, sampling errors and reporting variability. Transient elastography (TE) using FibroScan® provides painless and immediate assessment of liver stiffness (LS). The aim of this study was to validate the diagnostic accuracy of LS compared to liver biopsy as the reference, as well as the intra and inter operator reproducibility in a large US cohort of patients with chronic viral hepatitis. Methods: Chronic hepatitis C and B patients underwent TE before LB in this 2 phase study: phase 1 designed to identify the optimal stiffness cut-off values to stage F2 and F4; phase 2 designed to validate the cut-off values obtained in phase 1.All LB were evaluated by one pathologist for Phase 1 and another for Phase 2by using the METAVIR scoring system. TE examination validity criterion was at least 8 valid measurements within 20 attempts. Diagnostic performances of TE were assessed by area under receiver operating characteristic curves (AUROCs) using LB as reference. TE optimal cut-off values were obtained by maximizing the sum of Sensitivity (Se) and specificity (Sp) forthe chosen diagnosis. Inter and intra-observer reproducibility were assessed in two subgroups of patients using Infra Class Correlation Coefficient (ICC). Results: 907 patients were prospectively enrolled in the study. 93 patients were excluded because of unreliable FibroScan® (10.3%) and 66 because of non adequate LB results (Lack of data, too small samples for staging, missing slides). AUROCs of LS for diagnosing F2 and F4 in the total population (n=748) were 0.76 (0.72-0.79 95% CI) and 0.91 (0.87-0.93 95% CI), respectively. Stiffness cut-off values (kPa) in Phase 1(n=188) were 8.4 for F2 (Se=82%, Sp=79 and 12.8 for F4 (Se=84%, Sp=86%). Cut offs applied on the Phase 2 cohort (n=560) exhibited Se and Sp of 58% (p<0.001 vs phase 1) and 75% (ns versus phase 1) for F2 and of 76% (p<0.0001 versus phase 1) and 85% (ns versus phase 1) for F4, respectively. TE exhibited an ICC of 0.98 for inter observer agreement (n=26), and of 0.95 for Intra observer agreement (n=34). Conclusion: This US multicenter study exhibits equivalent results to already published European and Asian studies, and confirms that TE very accurately assesses presence of cirrhosis in patients with chronic type B and C viral hepatitis. TE also exhibits excellent reproducibility, which makes it a clinically reasonable alternative to liver biopsy.


Nezam H. Afdhal - Consulting: Merck, Vertex, Idenix, GlaxoSmithKline, Springbank, Gilead, Pharmasett, Abbott; Grant/Research Support: Merck, Vertex, Idenix, GlaxoSmithKline, Springbank, Gilead, Pharmasett, Abbott

Keyur Patel - Consulting: Benitec, Santaris; Speaking and Teaching: Gilead Sciences, Vertex

Eric Lawitz - Advisory Committees or Review Panels: AbbVie, Achillion Pharmaceuticals, BioCryst, Biotica, Enanta, Idenix Pharmaceuticals, Janssen, Merck & Co, Novartis, Santaris Pharmaceuticals, Theravance, Vertex Pharmaceuticals; Grant/Research Support: AbbVie, Achillion Pharmaceuticals, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Idenix Pharmaceuticals, Intercept Pharmaceuticals, Janssen, Merck & Co, Novartis, Presidio, Roche, Santaris Pharmaceuticals, Vertex Pharmaceuticals; Speaking and Teaching: Gilead, Kadmon, Merck, Vertex

Stuart C. Gordon - Advisory Committees or Review Panels: Tibotec; Consulting: Merck, CVS Caremark, Gilead Sciences, BMS; Grant/Research Support: Roche/Genentech, Merck, Vertex Pharmaceuticals, Gilead Sciences, BMS, Abbott, Intercept Pharmaceuticals, Exalenz Sciences, Inc.

David R. Nelson - Advisory Committees or Review Panels: Merck; Grant/Research Support: Abbot, BMS, Beohringer Ingelheim, Gilead, Genentech, Merck, Bayer, Idenix, Vertex, Jansen

John G. McHutchison - Employment: Gilead Sciences; Stock Shareholder: Gilead Sciences

The following people have nothing to disclose: Bruce R. Bacon, Tracy L. Challies, Imad Nasser, Lee jen Wei


Evaluation of liver disease progression in the German HCV (lb)-contaminated anti-D cohort at 35 years after infection

Manfred Wiese1, Janett Fischer2, Micha Loebermann3, Uwe Göbel4, Kurt Gruengreiff5, Wolfgang Gühoff6, Ulrike Kullig7, Franziska Richter1, Ingolf Schiefke8, Hannelore Tenckhoff, Alexander Zipprich9, Thomas Berg2, Tobias Mueller2;

1Hepatologische Schwerpunktpraxis, Nordstr. 17 - 21, Leipzig, Germany; 2Klinik für Gastroenterologie und Rheumatologie, Sektion Hepatologie, Universitätsklinikum Leipzig, Leipzig, Germany; 3Abteilung für Tropenmedizin, Infektionskrankheiten und Sektion Nephrologie, Universitätsmedizin Rostock, Rostock, Germany; 4Gastroenterologische Schwerpunktpraxis, Cottbus, Germany; 5Hepatologische Schwerpunktpraxis, Magdeburg/ Germany; 6Klinik für Gastroenterologie und Infektiologie, E. -v. -Bergmann Klinikum, Potsdam, Germany; 7|||. Medizinische Klinik, Krankenhaus Dresden-Friedrichstadt Dresden, Germany; 8Klinik für Gastroenterologie und Hepatologie, Klinikum St. Georg GmbH, Leipzig, Germany; 9Klinik und Poliklinik für Innere Medizin I, Martin-LutherUniversität Halle-Wittenberg, Halle, Germany

Background: The natural course of HCV infection remains controversial. The German HCV (1b)-contaminated anti-D cohort provides an ideal population to investigate the natural course of HCV infection in a large and homogenous cohort of young women from the date of HCV inoculation. Our previous followup studies at 20 years and 25 years after infection suggested slow fibrosis progression rates in this unique cohort. Aims & Methods: The aim of our prospective community-based multicenter study was to re-evaluate the liver disease progression in 718 patients of the original anti-D cohort at 35 years after infection. Patients with self-limited HCV infection (n=189) were compared to those who failed to eliminate the virus spontaneously (n=529), comprising patients who were treatment naive (n=1 97) or achieved a sustained virological response (SVR, n=149) respectively failed to clear the virus (non-SVR, n=1 83) after antiviral therapy. Results: In the overall cohort, 9.3% of patients showed clinical signs of liver cirrhosis at 35 years after infection. Liver disease progression largely depended on the HCV infection status. The highest proportion of patients with clinical signs of end-stage liver disease was observed in the non-SVR group (15.3%), whereas decreased cirrhosis rates were detected in the SVR group (6%) and in patients with self-limited HCV infection (1.1%, p=6.2x10-6). This observation was further confirmed by liver biopsy and transient elastography. Overall survival was significantly enhanced following SVR compared to treatment naive patients or nonSVR (p=0.027). Conclusion: The present study provides further evidence for a mild but significant disease progression at 35 years after infection in the German HCV (1b)-contaminated anti-D cohort. Patients with self-limited HCV infection or SVR after antiviral treatment were protected from progressive liver disease and showed the best clinical long-term outcome.


Micha Loebermann - Speaking and Teaching: Gilead, Janssen-Cilag, Roche, MSD

Kurt Gruengreiff - Grant/Research Support: Dr. Falk Pharma; Speaking and Teaching: Roche Pharma

Ingolf Schiefke - Board Membership: Baxter; Grant/Research Support: Roche, MSD, Gilead

Thomas Berg - Advisory Committees or Review Panels: Gilead, BMS, Roche, Tibotec, Vertex, Jannsen, Novartis, Abbott, Merck; Consulting: Gilead, BMS, Roche, Tibotec; Vertex, Janssen; Grant/Research Support: Gilead, BMS, Roche, Tibotec; Vertex, Jannssen, Schering Plough, Boehringer Ingelheim, Novartis; Speaking and Teaching: Gilead, BMS, Roche, Tibotec; Vertex, Janssen, Schering Plough, Novartis, Merck, Bayer

The following people have nothing to disclose: Manfred Wiese, Janett Fischer, Uwe Göbel, Wolfgang Güthoff, Ulrike Kullig, Franziska Richter, Hannelore Tenckhoff, Alexander Zipprich, Tobias Mueller


The risk for hepatocellular carcinoma among patients with chronic HCV infection and advanced hepatic fibrosis following sustained virological response

Adriaan J. van der Meer1, Jordan J. Feld2, Harald Hofer3, Piero L. Almasio4, Vincenza Calvaruso4, Conrado M. FernandezRodriguez5, Soo Aleman6, 7, Nathalie Ganne-Carrie8, Roberta D'Ambrosio9, Stanislas Pol10, Maria Trapero-Marugan11, Ricardo Moreno-Otero11, Vincent Mallet10, Rolf W. Hultcrantz6, Ola Weiland7, Karoline Rutter3, Vito Di Marco4, Sonia Alonso5, Savino Bruno1 2, Massimo Colombo9, Robert J. de Knegt1, Bart J. Veldt1, Bettina E. Hansen1, Harry L. Janssen1, 2

1Gastroenterology & Hepatology, Erasmus MC, Rotterdam, Netherlands; 2Liver Centre, Toronto Western Hospital, Toronto, 〇N, Canada; 3Department of Internal Medicine III, Division of Gastroenterology and Hepatology, edical University of Vienna, vienna, Austria; 4Gastrointestinal & Liver Unit, Dipartimento Biomedico di Medicina Interna e Specialistica, University of Palermo, Palermo, Italy; 5Unit of Gastroenterology and Liver Diseases, University Hospital Fundación Aicorcón, Madrid, Spain; 6Departments of Gastroenterology and Hepatology, Korolinska University Hospital, Stockholm, Sweden; 7Departments of Infectious Diseases, Karolinska Institutet, Stockholm, Sweden; 8Hepato-gastroenterology Unit, AP-HP Jean Verdier Hospital, University Paris 13, Bondy, France; 9A.M. and A. Migliavacca Center for Liver Disease, First Division of Gastroenterology, First Division of Gastroenterology, Universitá degli Studi di Milano, Milan, Italy; 10Unité d'Hépatologie, AP-HP Hôpital Cochin, Université Paris Descartes, Inserm U1016, Paris, France; 11 Gastroenterology-Hepatology department, University Hospital La Princesa and Princesa Research Institute, Autonomous University of Madrid, Madrid, Spain; 12Department of Internal Medicine, Azienda Ospedaliera Fatebenefratelli e Oftalmico, Milan, Italy

INTRODUCTION Although strongly reduced, the risk for HCC is not eradicated in patients with HCV-induced advanced fibrosis who attained sustained virological response (SVR). Current AASLD guidelines consider HCC surveillance as cost-effective if the annual risk exceeds 1.5%, although this might be lower for patients with SVR. We assessed the HCC risk among patients with HCV-induced advanced fibrosis and SVR. METHODS Data from previously reported Western cohort studies including patients with chronic HCV infection and advanced fibrosis or cirrhosis who attained SVR were pooled for meta-analyses on the individual patient level. Cumulative HCC rates were assessed with Kaplan Meier analyses and differences between subgroups were compared with the Log Rank test. RESULTS Included were 1001 patients with SVR from 10 previously reported cohorts. Median age was 52.7 (IQR 45.1-59.7) years, 676 (68%) were male and 843 (84%) had cirrhosis. Median follow-up was 5.7 (IQR 2.9-8.0) years; 50 patients developed HCC. Median age at the time of HCC was 65.3 (IQR 56.5-68.6) years. The cumulative 8-year HCC rate was 8.5% (95%CI 5.8-11.2) among patients with cirrhosis and 1.8 (95%しI 0.0-4.3) among those with advanced fibrosis (p=0.064). Gender had no significant effect (p=0.474). Among cirrhotic patients, the cumulative 8-year HCC rate was 2.6% (95%CI 0.0-5.5) for patients <45 years, 9.3% (95%CI 13.2) for patients from 45-60 years, and 12.2% (95%CI 19.1)for patients >60 years of age at start of therapy (p=0.006; Figure). CONCLUSION Patients with HCV-induced cirrhosis and SVR showed an annual HCC risk of approximately 1%. The annual HCc risk was higher among older patients. Our results suggest that the cost-effectiveness of HCC surveillance among cirrhotic patients with SVR will improve as the population with chronic HCV infection is aging.



Adriaan J. van der Meer - Speaking and Teaching: MSD

Jordan J. Feld - Advisory Committees or Review Panels: Roche, Merck, Vertex, Gilead, Abbott, Tibotec, Theravance, Achillion; Speaking and Teaching: Merck, Roche, Abbott

Harald Hofer - Speaking and Teaching: Janssen, Roche, MSD

Soo Aleman - Consulting: Gilead, GlaxoSmithKline, Roche; Speaking and Teaching: Roche, MSD, Gilead, Janssen

Nathalie Ganne-Carrie - Advisory Committees or Review Panels: Roche, MSD; Speaking and Teaching: BMS, Gilead

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

Vincent Mallet - Board Membership: MSD, Janssen; Speaking and Teaching: Roche, Gilead, BMS

Ola Weiland - Advisory Committees or Review Panels: MSD, BMS, Janssen, Gilead; Grant/Research Support, MSD, Roche, BMS; Speaking and Teaching: Novartis, Janssen, Abbott, Roche, Gilead


Robert J. de Knegt - Advisory Committees or Review Panels: MSD, Roche, Norgine, Janssen Cilag; Grant/Research Support: Gilead, MSD, Roche, Janssen Cilag, BMS; Speaking and Teaching: Gilead, MSD, Roche, Janssen Cilag

Bart J. Veldt - Board Membership: GSK

Harry L. Janssen - Consulting: Abbott, Bristol Myers Squibb, Debio, Gilead Sciences, Merck, Medtronic, Novartis, Roche, Santaris; Grant/Research Support: Anadys, Bristol Myers Squibb, Gilead Sciences, Innogenetics, Kirin, Merck, Medtronic, Novartis, Roche, Santaris

The following people have nothing to disclose: Piero L. Almasio, Vincenza Calvaruso, Conrado M. Fernandez-Rodriguez, Roberta D'Ambrosio, Maria TraperoMarugan, Ricardo Moreno-Otero, Rolf W. Hultcrantz, Karoline Rutter, Vito Di Marco, Sonia Alonso, Savino Bruno, Bettina E. Hansen


Sexual function is impaired in men and women with chronic hepatitis C

Julien Vergniol1, Genevieve Hou2, Juliette Foucher1, Florence Chenus2, Faberes Carole1, Faiza Chermak1, Aude Lafourniere1, Noui Souakri1, Victor de Ledinghen 1, 3

1 Hepato Gastroenterology, Haut Leveque Hospital, Pessac, France; 2Etablissement Francais du Sang',Pellegrin Hospital, Bordeaux, France; 3INSERM U889, Université Segalen, Bordeaux, France

Introduction: Sexual impairment is a frequent symptom in general population. Patients with chronic hepatitis C(CHC) often have altered quality of life. Antiviral therapy, advanced cirrhosis and liver transplantation are associated with an impaired sexual life but little is known in all CHC patients. The aim of our study was to evaluate sexual impairment and associated factors in consecutive patients with CHC. Patients and methods: From September 2011 to April 2013, 268 CHC patients were prospectively included. Exclusion criteria were HBV or HIV coinfection, age <18 or >75, liver transplantation, excessive alcohol consumption, OMS score >1 and evidence of a familial conflict that would make the questions inappropriate. Control men and women were healthy blood donors. Male and female sex questionnaires were adapted from the International Index of Erectile Function and from the Female Sexual Function Index, respectively, and concerned the past 30 days. Results: Five percent of all interrogated CHC patients refused the questionnaire. 268 patients (male 61%) were compared to 1088 blood donors (male 63%). 62.1% of CHC patients and 77.4% of controls had sexual intercourse during the past 30 days (p<0.001). Global sexual life was significantly worse in HCV men (global score 60.35 versus 81.73, p<0.001) and women (global score 33.17 versus 37.33, p=0.002), compared to controls. HCV men had worse desire (p<0.001), confidence (p<0.001), erections (p<0.001), climax (p<0.001), and satisfaction (p<0.001) than controls. Women with CHC had worse desire (p<0.001), arousal (p<0.001), climax (p<0.001), satisfaction (p<0.001), lubrication (p<0.001), and comfort (p<0.001) than controls. In multivariate analysis, factors associated with worse global sexual life in males (global score <70) were HCV infection (4.69, 2.78-7.92, p<0.0001), age >45 (OR 5, 95%CI 2.57-7.88, p<0.001), no sexual intercourse during the past 30 days (OR 10.6, 95%CI 5.95-18.9, p<0.001) and no employment (OR 2.02, 95%CI 1.21-3.37). Factors associated with a worse global sexual life in females (global score <30) were HCV infection (OR 5.35, 95%CI 2.54-11.27, p<0.001), no sexual intercourse during the past 30 days (OR 18, 95%CI 8.6637.73, p<0.001), and being single (OR 2.12, 95%CI 1.054.26, p=0.035). Liver stiffness was not correlated with sexual impairment (r=0.03). Conclusion: To our knowledge, this is the first large study showing that sexual life is impaired in men and women with CHC. In clinical practice, the question of sexual quality of life should be evaluated in patients. Further studies are needed to evaluate strategies to improve sexual life in HCV patients.


Juliette Foucher - Board Membership: roche; Speaking and Teaching: BMS, MSD, Gilead

Victor de Ledinghen - Advisory Committees or Review Panels: Merck, Janssen, Gilead, Echosens, Boehringer Ingelheim, Abbvie; Grant/Research Support: Roche, Gilead, Janssen; Speaking and Teaching: Roche, Echosens

The following people have nothing to disclose: Julien Vergniol, Genevieve Hou, Florence Chenus, Faberes Carole, Faiza Chermak, Aude Lafourniere, Noui Souakri