Clinicaloptions.com/hepatitis Highlights From AASLD 2010 October 29 - November 2, 2010 Boston, Massachusetts Highlights From AASLD 2010 CCO Official Conference.

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clinicaloptions.com/hepatitis Highlights From AASLD 2010 October 29 - November 2, 2010 Boston, Massachusetts Highlights From AASLD 2010 CCO Official Conference Coverage of the 61st Annual Meeting of the American Association for the Study of Liver Diseases This program is supported by an educational grant from This program is supported by educational grants from

clinicaloptions.com/hepatitis Highlights From AASLD 2010 About These Slides  Our thanks to the presenters who gave permission to include their original data  Users are encouraged to use these slides in their own noncommercial presentations, but we ask that content and attribution not be changed. Users are asked to honor this intent  These slides may not be published or posted online without permission from Clinical Care Options ( Disclaimer The materials published on the Clinical Care Options Web site reflect the views of the authors of the CCO material, not those of Clinical Care Options, LLC, the CME providers, or the companies providing educational grants. The materials may discuss uses and dosages for therapeutic products that have not been approved by the United States Food and Drug Administration. A qualified healthcare professional should be consulted before using any therapeutic product discussed. Readers should verify all information and data before treating patients or using any therapies described in these materials.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Faculty and Disclosures Robert G. Gish, MD Chief of Hepatology Professor of Clinical Medicine Medical Director Center for Hepatobiliary Disease and Abdominal Transplantation University of California, San Diego San Diego, California Robert G. Gish, MD, has disclosed that he has received grant or research support from Bayer- Onyx, Bristol-Myers Squibb, Genentech, Gilead Sciences, Hoffmann-La Roche, Pharmasset, and Zymogenetics; has served as a consultant to Abbott, Anadys, Bayer AG, Bristol-Myers Squibb, Durect, Genentech, Gilead Sciences, GlaxoSmithKline, GlobeImmune, Hepahope, Hoffmann-La Roche, Human Genome Sciences, Merck, Metabasis Therapeutics, OSI/Astellas, Pharmasset, Schering-Plough, Three Rivers Pharmaceuticals, Vital Therapies, and Zymogenetics; has served on speaker bureaus for Bayer, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Hoffmann-La Roche, Merck, Onyx, Roche, Salix, Schering-Plough, SciClone Pharmaceuticals, and Three Rivers Pharmaceuticals; and holds stock in Hepahope. Stephen A. Harrison, MD, FACP, has disclosed that he has served as a consultant for and has received fees for non-CME services from Bristol-Myers Squibb and Onyx. Stephen A. Harrison, MD, FACP Clinical Associate Professor of Medicine University of Texas Health Science Center San Antonio, Texas

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Outline  Investigational Agents for the Treatment of HCV  Advances in HBV Therapy

Investigational Agents for the Treatment of HCV

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Boceprevir and Telaprevir  Boceprevir, a potent inhibitor of HCV NS3 protease  Telaprevir, a potent inhibitor of HCV NS3/4A protease  Both being tested in combination with standard- of-care peginterferon alfa-2/ ribavirin in phase III studies in chronic HCV infection Trials reported at AASLD 2010  Boceprevir –SPRINT-III: naive GT1 patients –RESPOND-2: nonresponder GT1 patients  Telaprevir –ADVANCE: naive GT1 patients –ILLUMINATE: response- guided therapy in naive GT1 patients

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Phase III SPRINT-2: Boceprevir + PegIFN/RBV in GT1 Tx-Naive Patients Treatment-naive patients with genotype 1 HCV (2 cohorts: N = 938 nonblack and 159 black) PR* (n = 316, 52) PR* (n = 311 nonblack, 52 black) Wk 72 Wk 48 Follow-up Wk 28 Follow-up Wk 4 BOC + PR* (n = 316 nonblack, 52 black) BOC + PR* (n = 311 nonblack, 55 black) PR* (n = 311, 55) PR* *BOC 800 mg q8h; pegIFN alfa-2b 1.5 µg/kg/wk; weight-based RBV mg/day. † Undetectable HCV RNA at Wk 4 of BOC treatment (ie, at Wk 8) and at all subsequent assays. Poordad F, et al. AASLD Abstract LB-4. Follow-up RVR † No RVR  Randomized, placebo-controlled trial

clinicaloptions.com/hepatitis Highlights From AASLD 2010 SPRINT-2: Response Rates According to Race Patients (%) SVR Relapse 4-wk PR + 44 weeks BOC + PR4-wk PR + response-guided BOC + PR48-wk PR Patients (%) SVRRelapse Nonblack Patients Black Patients P <.0001 P =.044 P =.004 Poordad F, et al. AASLD Abstract LB-4. n =

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Phase III ADVANCE: Telaprevir + PegIFN/RBV in GT1 Tx-Naive Patients Treatment-naive patients with genotype1 HCV (N = 1088) Wk 12 TVR + PR* (n = 364) TVR + PR* (n = 363) PR* (n = 361) eRVR † : PR* Wk 72 Wk 48 Wk 8 Follow-up *TVR 750 mg q8h; pegIFN alfa-2a 180 µg/wk; weight-based RBV mg/day. † eRVR: extended rapid virologic response = undetectable HCV RNA at Wks 4 and 12. Jacobson IM, et al. AASLD Abstract 211. Wk 24 PR* eRVR † : PR* PR* Follow-up  Randomized, placebo-controlled trial

clinicaloptions.com/hepatitis Highlights From AASLD 2010 ADVANCE: Overall SVR and Relapse Rates Patients (%) 69 SVR P <.0001 for both treatment arms vs control 12-wk TVR + PR + 12/36-wk PR (n = 363) 48-wk PR (n = 361) 8-wk TVR + PR + 16/40-wk PR (n = 364) n = Relapse n = Jacobson IM, et al. AASLD Abstract 211.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Phase III ILLUMINATE: Response-Guided Telaprevir + PegIFN/RBV in GT1 Naive Pts Treatment- naive patients with GT1 HCV (N = 540) PR* (n = 162) PR* (n = 160) Wk 72Wk 48Wk 24 Follow-up *TVR 750 mg q8h; pegIFN alfa-2a 180 µg/wk; weight-based RBV mg/day. † eRVR: extended rapid virologic response = undetectable HCV RNA at Wks 4 and 12. Sherman KE, et al. AASLD Abstract LB-2. Follow-up  Open-label, randomized trial Wk 20 eRVR † No eRVR † PR* (n = 218) TVR + PR* Wk 12 PR*

clinicaloptions.com/hepatitis Highlights From AASLD 2010 ILLUMINATE: Overall SVR Rates wk therapy SVR (%) wk therapy 88 Overall 72 Patients With eRVR n/N =388/540149/ /160 Sherman KE, et al. AASLD Abstract LB-2.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Similarities and Differences in Phase III Studies of TVR and BOC in GT1 Naive Pts ParameterTVR [1] BOC [2] PR lead-in?NoYes: 4 wks Peginterferon alfa formulation2a2b PI dosing requirements TID; administer with fatty meal TID Duration of PI triple therapy 8-12 wks followed by wks PR wks after 4 wks PR lead-in Qualification for shortened therapy (response guided) eRVR RVR (Wk 4 after addition of BOC; Wk 8 of total therapy) Qualified for shortened therapy, %58 (24 wks)44 (28 wks) SVR, % Relapse, %99 Adverse events more frequent in PI arms Rash, anemia, pruritus, nausea Anemia, dysgeusia 1. Jacobson IM, et al. AASLD Abstract Poordad F, et al. AASLD Abstract LB-4.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Phase III RESPOND-2: Boceprevir in GT1 Prior Nonresponders to PegIFN/RBV PR* (n = 80) PR* (n = 161) BOC + PR* PR* (n = 162) BOC + PR* If detectable at Wk 8 PR* Bacon BR, et al. AASLD Abstract 216. Treatment- experienced patients with GT1 HCV (N = 403) Wk 48 Wk 8 Wk 36 Follow-up † *BOC 800 mg TID; pegIFN alfa-2b 1.5 µg/kg/wk; weight-based RBV mg/day. † Follow-up for 24 wks after completion of therapy.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 RESPOND-2: SVR Rates According to Treatment Arm and Prior Response Overall SVR (%) 4-wk PR + 44-wk BOC + PR (n = 161) 59* Previous Nonresponders Previous Relapsers 48-wk PR (n = 80) 4-wk PR + response-guided BOC + PR (n = 162) P <.0001 vs control (both arms) Bacon BR, et al. AASLD Abstract / / / 80 23/ 57 30/ 58 2/29 72/ / / 51

clinicaloptions.com/hepatitis Highlights From AASLD 2010 GS Tegobuvir Alone, With RBV, or With PegIFN/RBV in GT1 Tx-Naive Patients  Phase II study of tegobuvir (GS-9190), an NS5B nonnucleoside polymerase inhibitor, and GS-9256, an NS3 protease inhibitor as part of HCV therapy Zeuzem S, et al. AASLD Abstract LB-1. GS mg BID + Tegobuvir 40 mg BID (n = 16) † Wk 48 Wk 4 GS mg BID + Tegobuvir 40 mg BID + RBV* † (n = 15) PR* (n = 16) PR* (n = 15) GS mg BID + Tegobuvir 40 mg BID + PR* (n = 15) PR* (n = 15) Part A Part B (nonrandomized) Treatment-naive patients with GT1 HCV *PegIFN alfa-2a 180 µg/wk; weight-based RBV mg/day. † PegIFN/RBV started early if virologic breakthrough.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 GS Tegobuvir Alone, With RBV, or With PegIFN/RBV: Virologic Response Zeuzem S, et al. AASLD Abstract LB-1. HCV RNA ResponseGS Tegobuvir (n = 15) GS Tegobuvir + RBV (n = 13) GS Tegobuvir + PegIFN/RBV (n = 14) Median maximal change from baseline, log 10 IU/mL Achieved nadir ≤ 25 IU/mL, % Day 14 HCV RNA ≤ 25 IU/mL, % Day 28 HCV RNA ≤ 25 IU/mL (RVR), %

clinicaloptions.com/hepatitis Highlights From AASLD 2010 BMS BMS Alone or With PegIFN/RBV in GT1 Null Responders Lok A, et al. AASLD Abstract LB-8. Prior null responders with GT1 HCV (N = 21) BMS mg QD + BMS mg BID (n = 11) Wk 72 Wk 24 Follow-up BMS mg QD + BMS mg BID + PR* (n = 10)  Open-label, randomized, placebo-controlled phase IIa trial  BMS : NS5A polymerase inhibitor  BMS : NS3 protease inhibitor Follow-up *PegIFN alfa-2a 180 µg/wk; weight-based RBV mg/day.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 BMS BMS Alone or With PegIFN/RBV: Wk 12 Interim Analysis  All viral breakthroughs occurred in patients with GT1a Lok A, et al. AASLD Abstract LB RVReRVRcEVR BMS BMS BMS BMS PR Patients (%) 7/116/10 4/115/119/10

clinicaloptions.com/hepatitis Highlights From AASLD 2010 PILLAR: TMC435 + PegIFN/RBV in GT1 Tx-Naive Patients: 24-Wk Interim Analysis Fried M, et al. AASLD Abstract LB-5. Treatment- naive patients with GT1HCV (N = 386) Wk 12 TMC mg + PR (n = 78) TMC mg + PR (n = 77) PR (n = 77) Wk 72 Wk 48Wk 24 TMC mg + PR (n = 75) TMC mg + PR (n = 79) PR (n = 78) PR (n = 77) Follow-up *Treatment ended at Wk 24 if HCV RNA < 25 IU/mL at Wks 4, 12, 16, and 20; all others continued on PR.  Randomized, double-blind, placebo-controlled phase IIb trial  TMC435: NS3/4A protease inhibitor administered once daily Follow-up* or PR (n = 79) Follow-up* or PR (n = 77) Follow-up* or PR (n = 75) Follow-up* or PR (n = 78)

clinicaloptions.com/hepatitis Highlights From AASLD 2010 PILLAR: Undetectable HCV RNA at Wks 4 and 12 After EOT at Wk 24 Fried M, et al. AASLD Abstract LB-5.  79% to 86% of patients able to stop therapy at Wk 24  Adverse events leading to discontinuation observed in < 10% of all study arms TMC24 + PR24 75 mg (n = 75) TMC12 + PR mg (n = 77)TMC12 + PR24 75 mg (n = 78) Patients (%) 91 SVR4 93 n/N =59/6556/6057/ / /33 27/29 32/ /32 SVR12 TMC24 + PR mg (n = 79)  TMC mg did not totally abrogate graded response due to IL28B genotype

clinicaloptions.com/hepatitis Highlights From AASLD 2010 New Data on Other HCV Protease Inhibitors in Development  Danoprevir (RG7227): phase II study (ATLAS) in GT1 naive patients [1] –88% to 92% of patients achieved cEVR when combined with pegIFN/RBV vs 43% with SOC  Vaniprevir (MK-7009): phase IIa study (Protocol 007) in GT1 naive patients without cirrhosis [2] –Significantly higher early response rates when combined with pegIFN/RBV vs SOC –RVR: 67% to 84% vs 5%; cEVR: 74% to 85% vs 47% –SVR rates in higher-dose arms numerically, but not significantly, higher vs control –SVR: 61% to 84% vs 63% –Highest 2 doses allow for once-daily dosing  MK-5172: phase I study in GT1 and GT3 patients without cirrhosis [3] –Potent activity against GT1 and GT3 over 7-day dosing period –Active against known resistance mutants in healthy persons [4] 1. Terrault N, et al. AASLD Abstract Manns MP, et al. AASLD Abstract Petry A, et al. AASLD Abstract Brainard DM, et al. AASLD Abstract 1885.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 New Data on Other HCV Polymerase Inhibitors in Development  ANA598 (nonnucleoside): phase II study in GT1 naive patients [1] –ANA or 400 mg BID + pegIFN/RBV given for 12 wks before response-guided pegIFN/RBV –73% to 75% of patients achieved cEVR when combined with pegIFN/RBV vs 63% with SOC  RG7128 (nucleoside): phase IIb PROPEL study in GT1 and GT4 naive patients [2] –RG or 1000 mg + pegIFN/RBV given for 8 or 12 wks before response-guided pegIFN/RBV –80% to 88% of patients in arms receiving 12 wks of RG7128 combined with pegIFN/RBV achieved cEVR vs 49% with SOC 1. Lawitz E, et al. AASLD Abstract Jensen DM, et al. AASLD Abstract 81.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 PegIFN Lambda for Treatment-Naive GT1, 2, 3, or 4 HCV Patients  Phase IIa study  High rates of HCV RNA undetectability at 3 highest pegIFN lambda levels, comparable to pegIFN alfa-2a controls [1] –RVR: 80% to 100% –cEVR: 80% to 100%  HCV RNA response rates lower with genotype 1/4 vs 2/3  Response rates numerically higher with IL28B CC vs non-CC genotype [1]  Fewer hematologic AEs at Wk 12 with pegIFN lambda than pegIFN alfa-2a 1. Muir AJ, et al. AASLD Abstract Thompson AJ, et al. Gastroenterology. 2010;139: Virologic Response According to IL28B Genotype (ITT), % PegIFN alfa- 2a/RBV (HCV GT1 † ; Published Data) [2] PegIFN Lambda/RBV µg (Genotype 1/4* HCV) CC (n = 7)  RVR 2871  cEVR 8486 Non-CC (n = 12)  RVR 525  cEVR 3350

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Regional Distribution of IL28B rs CC Genotype Thomas DL, et al. Nature. 2009;461: Reprinted by permission from Macmillan Publishers Ltd:

clinicaloptions.com/hepatitis Highlights From AASLD 2010 IL28B Associations in Patients With Chronic Hepatitis C  IL28B polymorphisms associated with –Higher SVR rates [1] –Higher RVR rates [2] –Higher HCV RNA [3] –Higher LDL levels [4] –Higher baseline ALT levels [5] –Higher rate of spontaneous viral clearance [6]  Modeling study supports IL28B genotype stratification (CC vs non-CC) in HCV clinical trials of pegIFN/RBV + DAAs [7] 1. Ge D, et al. Nature. 2009;461: Mangia A, et al. AASLD Abstract Liu L, et al. AASLD Abstract Saito H, et al. AASLD Abstract Thompson AJ, et al. AASLD Abstract Thomas DL, et al. Nature. 2009;461: Thompson AJ, et al. AASLD Abstract 810.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Predictors of Response to Hepatitis C Treatment 1. Ge D, et al. Nature. 2009;461: Freedman ND, et al. AASLD Abstract Harrison SA, et al. Hepatology. 2010;52: Mouch AS, et al. AASLD Abstract Sulkowski MS, et al. AASLD Abstract 816. Pretreatment ParameterOn-Treatment Parameter  Race  Cirrhosis  Genotype  HCV RNA  IL28B polymorphisms [1]  Coffee use [2]  Baseline LDL levels [3]  Statin use [3]  Diabetes [4]  Vitamin D levels [5]  RVR  eRVR

Advances in HBV Therapy

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Vertical HBV Transmission in Mothers Treated With Telbivudine in Late Pregnancy HBsAg-Positive Infants With or Without Detectable HBV DNA, n (%) Infants in Telbivudine 600 mg/day Group (n = 95) Infants in Untreated Control Group (n = 92) P Value  At birth6 (6.3)28 (30.4)<.001  At 28 wks (sensitivity analysis) 08 (8.7).003  At 28 wks (ITT [M = F] analysis) 2 (2.1)12 (13.0).004  Prospective, nonrandomized, case-controlled, open-label study Pan C, et al. AASLD Abstract 212.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Mode of Delivery and Risk of Perinatal HBV Transmission in HBeAg+ Mothers Zou H, et al. AASLD Abstract 235. Vaginal delivery (n = 286) Elective cesarean (n = 189) Emergency cesarean (n = 94) HBV Infection in Infant (%) At Birth*At 7-12 Mos of Age † P = P =.028P =.047  Retrospective, observational study  556 mothers; 569 infants  Immunoprophylaxis schedule (standard of care) –200 IU HBIG and HB vaccine 10 µg within 6 hrs after birth –200 IU HBIG 2 wks postpartum –HB vaccine 10 µg at 1 and 6 mos *HBsAg+ or HBV DNA detectable in umbilical cord blood. † HBsAg+.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 NEPTUNE: PegIFN alfa-2a Dosed at 90 vs 180 µg/wk in HBeAg+ Patients  PegIFN alfa-2a 90 µg/wk inferior to 180 µg/wk, regardless of treatment duration, in randomized, double-blind phase IV study Liaw Y-F, et al. AASLD Abstract 215. HBeAg Seroconversion 6 Mos After Rx, % 90 µg/wk (n = 274) 180 µg/wk (n = 270) OR (95% CI)P Value* Overall ( ).410  Genotype B ( ).508  Genotype C ( ).581  ALT > 1-2 x ULN1317NR--  ALT > 2-5 x ULN2035NR--  ALT > 5-10 x ULN4046NR-- *For noninferiority; ie, nonsignificance = not noninferior.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 NEPTUNE: PegIFN alfa-2a Administered for 24 vs 48 Wks in HBeAg+ Patients  24 wks inferior to 48 wks of pegIFN alfa-2a therapy, regardless of dose, in randomized, double-blind phase IV study Liaw Y-F, et al. AASLD Abstract 215. HBeAg Seroconversion 6 Mos After Rx, % 24 Wks (n = 282) 48 Wks (n = 262) OR (95% CI)P Value Overall ( ).749  Genotype B ( ).215  Genotype C ( ).960  ALT > 1-2 x ULN1119NR--  ALT > 2-5 x ULN2036NR--  ALT > 5-10 x ULN3453NR-- *For noninferiority; ie, nonsignificance = not noninferior.

clinicaloptions.com/hepatitis Highlights From AASLD 2010 PegIFN alfa-2b Administered for 24 vs 48 Wks in HBeAg+ Patients  Patients recruited from 25 centers in China, Malaysia, Taiwan, and Singapore in prospective, randomized phase IV trial Fan X, et al. AASLD Abstract 133. EOT 24 Wks After EOT PegIFN alfa-2b 1.0 µg/kg/wk for 24 wks PegIFN alfa-2b 1.5 µg/kg/wk for 24 wks PegIFN alfa-2b 1.5 µg/kg/wk for 48 wks HBeAg Seroconversion (%) P =

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Safety of Extending PegIFN alfa-2a From 48 to 96 Wks in Genotype D HBeAg- Pts  PegBeLiver: higher virologic/serologic response rates observed 1 yr posttreatment in HBeAg-negative pts (94% genotype D) treated with pegIFN alfa-2a for 96 vs 48 wks [1] 1. Lampertico P, et al. EASL Abstract Lampertico P, et al. AASLD Abstract 135. Safety Outcome [2] PegIFN Alfa-2a 48 Wks (n = 51) PegIFN Alfa-2a 96 Wks (n = 77) P Value Treatment discontinuation, % Any treatment-related adverse event, % Any serious adverse event, % Treatment-related serious AE % Dose modification, % Death, n Laboratory abnormalities, %  Increased ALT  Neutropenia  Thrombocytopenia  Anemia85.71

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Entecavir in Previously NA-Naive HBV Patients With Partial Virologic Response  PVR: HBV DNA > 80 IU/mL at Wk 48 of therapy but > 1 log IU/mL decrease from baseline  Majority of previously NA-naive pts with PVR and HBV DNA < 1000 IU/mL achieved HBV DNA < 80 IU/mL at Wk 96 without modifying treatment  However, pts with HBV DNA ≥ 1000 IU/mL at Wk 48 did not achieve HBV DNA < 80 IU/mL at Wk 96 except when treatment modified –1 added tenofovir, 2 switched to tenofovir/emtricitabine Zoutendijk R, et al. AASLD Abstract 448. Table used with permission. HBV DNA at Wk 48 Pts With PVR, n Switch/Add-on, n (%) Response at Wk 72, n (%) Response at Wk 96, n (%) < 1000 IU/mL22013 (59)16 (72) ≥ 1000 IU/mL143 (21)1 (7)2 (14)

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Rates of HBsAg Loss With Longer Duration of Tenofovir  192-wk results of Study 103: randomized, double-blind phase III trial Heathcote EJ, et al. AASLD Abstract 477. Graphic used with permission Cumulative Probability of HBsAg Loss TDF-TDF ADV-TDF Wks on Study 10.8% 8.5% Switch to open- label TDF

clinicaloptions.com/hepatitis Highlights From AASLD 2010 TDF Monotherapy vs TDF/FTC for HBV Patients Viremic After Adefovir Therapy  At Wk 48, 81% of patients initially given TDF or TDF/FTC had HBV DNA < 400 copies/mL [1]  13/13 patients with baseline LAM resistance and 9/10 with baseline ADV resistance had HBV DNA < 400 copies/mL at Wk Berg T, et al. Gastroenterology. 2010;139: Berg T, et al. AASLD Abstract 136. Chronic HBV patients with incomplete suppression on ≥ 6 mos adefovir (N = 105) TDF 300 mg (n = 53) TDF/FTC 300/200 mg (n = 52) Wk 168Wk 48 Wk 96 Wk 24* *After Wk 24, patients with detectable HBV DNA on TDF could receive open-label TDF/FTC. Outcomes at Wk 168 [2] TDFTDF/FTC HBV DNA < 400 copies/mL (69 IU/mL), % (ITT, NC = F)82 HBeAg loss (LOCF)2123 HBeAg seroconversion (LOCF)13 HBsAg loss or seroconversion (LOCF)60

clinicaloptions.com/hepatitis Highlights From AASLD 2010 Correlates of Severe Liver Disease Outcomes in HBV Patients Parameter Adjusted Risk Ratios for Chronic HBV Outcomes HCCDecompensated Cirrhosis Younger than 50 yrs of age Male Non-Asian race0.65*1.47* Diagnosed alcohol abuse Diabetes1.09*2.67 Manos MM, et al. AASLD Abstract 175.  Retrospective, longitudinal cohort study of the Kaiser Permanente Medical Care Program of Northern California Viral Hepatitis Registry *Nonsignificant correlations.

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