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P-1 Douglas T. DIETRICH. P-2 Treatment of HCV in HIV Disease: New Challenges, New Promise Douglas T. Dieterich, M.D Professor of Medicine Division of.

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Presentation on theme: "P-1 Douglas T. DIETRICH. P-2 Treatment of HCV in HIV Disease: New Challenges, New Promise Douglas T. Dieterich, M.D Professor of Medicine Division of."— Presentation transcript:

1 P-1 Douglas T. DIETRICH

2 P-2 Treatment of HCV in HIV Disease: New Challenges, New Promise Douglas T. Dieterich, M.D Professor of Medicine Division of Liver Diseases, Gastroenterology and Infectious Diseases Director of CME Department of Medicine Mt. Sinai School of Medicine New York, New York

3 P-3 Hospital Admissions for Liver Complications Increased 5-Fold (1995–2000) Gebo KA, et al. JAIDS. 2003;34:165-173. Hospitalizations per Patient-Years Follow-Up 1995 1996 1997 1998 1999 2000 1995 1996 1997 1998 1999 2000 Opportunistic infections IDU-related complications Liver-related complications

4 P-4 Liver disease is a major cause of death in the ART era Bica et al. Clin Infect Dis 2001; 32:492–497 Puoti et al. JAIDS 2000; 24:211–217 Soriano et al. Eur J Epidemiol 1999; 15:1–4 Soriano et al. PRN Notebook 2002; 7:10–15 Martin-Carbonero et al. AIDS Res Human Retrovirus 2001; 17:1467–1471 0 10 20 30 40 50 60 Mortality (%) Death from end-stage liver disease (ESLD) as a % of all deaths among HIV patients Italy (Brescia)Spain (Madrid)USA (Boston) 13% 35% 5% 12% 45% 50% Pre-HAART era HAART era

5 P-5 Causes of Liver Disease in HIV Infection

6 P-6 Ishak fibrosis stage on second biopsy among persons with little or no fibrosis on first biopsy Sulkowski MS et al. 12th Conference on Retroviruses and Opportunistic Infections (Abstract #: P-172). Boston, MA USA, February 22–25, 2005 Median (IQR) time between bxs, 2.84 yrs (2.05–3.41) 28% with more than 2 stage progression n = 51 45% 23% 10% 14% 8% 0 20 40 60 0123 or 45 or 6 Fibrosis stage at second biopsy Patients (%)

7 P-7 FibroScan 2.5 cm 4 cm 1 cm  Explored volume LB: 1/50,000 of the liver FibroScan: 1/500 of the liver The probe induces an elastic wave through the liver The velocity of the wave is evaluated in a region located from 2.5 to 6.5 cm below the skin surface

8 P-8 Transient Elastography in HIV HCV Co-infected Patients 72 patients with simultaneous liver biopsy and Fibroscan 72 patients with simultaneous liver biopsy and Fibroscan Liver stiffness 3.0 to 46.4 kilopascal Liver stiffness 3.0 to 46.4 kilopascal Liver stiffness correlated signficantly to fibrosis stage p < 0.0001 Liver stiffness correlated signficantly to fibrosis stage p < 0.0001 AUROC(area under receiver operating curve) was.72 for F>2 and.97 for F=4. AUROC(area under receiver operating curve) was.72 for F>2 and.97 for F=4. F=4 was > plt count, AST/ALT ratio, APRI, and FIB 4 F=4 was > plt count, AST/ALT ratio, APRI, and FIB 4 De Ledinghen et al J Acquir Immune Defic Syndr 41: 175-179

9 P-9 Liver Biopsy Gold standard for grading and staging disease Gold standard for grading and staging disease Invasive, expensive Invasive, expensive Needle liver biopsy samples < 1/50,000th of the liver Needle liver biopsy samples < 1/50,000th of the liver Incorrect staging of 1 stage in 10% to 20% of cases Incorrect staging of 1 stage in 10% to 20% of cases Dependent on Dependent on Length of biopsy—25 mm optimal (16%) Length of biopsy—25 mm optimal (16%) Number of biopsies performed Number of biopsies performed Type of biopsy needle used Type of biopsy needle used Etiology of liver disease Etiology of liver disease

10 P-10 The Importance of Liver Biopsy

11 P-11 Conflicting Data on the Effects of HCV Upon HIV Disease Meta-analysis involving 6216 patients from 8 trials Meta-analysis involving 6216 patients from 8 trials Mean increase in CD4 cell count among HIV/HCV coinfected patients was 33.4 cells/mm 3 less than that observed in HIV-monoinfected patients Mean increase in CD4 cell count among HIV/HCV coinfected patients was 33.4 cells/mm 3 less than that observed in HIV-monoinfected patients EuroSIDA EuroSIDA After adjusting for baseline factors, investigators concluded that HIV/HCV-coinfected patients do not have a greater risk of progressing to AIDS After adjusting for baseline factors, investigators concluded that HIV/HCV-coinfected patients do not have a greater risk of progressing to AIDS Miller et al. Clin Inf Dis. 2005;41:713-720. Rockstroh et al. J Inf Dis. 2005;192:992-1002

12 P-12 Significant increase in new acute HCV infections in 2003 Test for trend p-value using Poisson regression p<0.001 Error bars = 95% CI Incidence of acute HCV infection/1000 pt yrs 0 5 10 15 20 25 30 1997199819992000200120022003 Browne RE, et al. 2nd IAS 2003; Abstract 972

13 P-13 HCV: A new epidemic among MSM? Newly infected male, MSM, HCV+ patients at a London clinic, January 1997 – May 2003; n=44 Newly infected male, MSM, HCV+ patients at a London clinic, January 1997 – May 2003; n=44 Reasons for testing:  ALT (35), sexual contact with HCV+ person (3), jaundice (3), HIV screening (2), H/O IVDU (1) Reasons for testing:  ALT (35), sexual contact with HCV+ person (3), jaundice (3), HIV screening (2), H/O IVDU (1) Risk factors identified: IVDU (1), sexual contact (39), none (4) Risk factors identified: IVDU (1), sexual contact (39), none (4) Browne RE, et al. 2nd IAS 2003; Abstract 972

14 P-14 HIV-positive MSM with acute HCV infection in 3 hospital wards in Paris, France (n=29) Number of patients 4 3 2 1 0 JanAprJulOctJanAprJulOctJanAprJulOctJanAprJulOct 2001200220032004 Year Gambotti L. Eurosurveillance 2005; 10: 115

15 P-15 Possible transmission risk factors Results of anonymous questionnaire (n=11) Unprotected anal sex with casual partner within six months prior to hepatitis (n=11) Met sex partner at gay venue or via internet (n=11) STI reported (n=10): - -syphilis (n=6) - -gonorrhoea (n=3) - -genital herpes (n=3) - -chlamydia (n=3) - -warts (n=3) - -anal/genital infection (n=3) ‘Hard sex’ (n=8): -fisting (n=5) -bleeding (n=6) Inhaled poppers during sex (n=11) Used psychoactive drugs during sex (n=5) Tattoos or piercing within 6 months prior to hepatitis C (n=3) Gambotti L. Eurosurveillance 2005; 10: 115

16 P-16 German acute Hepatitis C Trial – I (1998–2000) interferon alfa-2b monotherapy for 6 months 98% 0% 20% 40% 60% 80% 100% 04812162024 Weeks HCV RNA negative 48 (F/up Wk 24) n=44 Jaeckel E, et al. N Engl J Med 2001; 345: 1452

17 P-17 Acute HCV in IVDU: Swiss Association for the Study of the Liver Study (SASL 18) 27 patients 5 spontaneous clearance 22 patients treatment indicated 6 refused therapy 2 patients lost to observation 14 patients Peg-IFN treatment started 6 premature stop due to side-effects (1 SVR) 8 patients adherent to therapy 7 patients with SVR Broers, B et al. J Hepatol 2005; 42: 323

18 P-18 Hep-Net Acute HCV Study HCV-II 0 20 40 60 80 100 Patients (%) ETR SVR 71% 82% ITT; n=89 ETR SVR 94% 89% Pts. adherent to therapy; n=65 Adherent to therapy = 80% of pegylated interferon dose, 80% of treatment duration Wiegand et al. (Submitted)

19 P-19 Response to treatment : acute HCV infection in HIV+ patients 0 20 40 60 80 100 All Patients (n=27) Genotype 1 (n=20) Genotype non-1 (n=4) 67% 65% 100% 59% 55% SVR ETR Virological response (%) Pegylated interferon alfa-2b (1.5  g/kg/wk) + ribavirin (800–1200 mg/day) for 24 weeks 100% Nelson M, et al. 3rd IAS 2005; Abstract TuPe1.1C10

20 P-20 Hôpital Pitié-Salpêtrière, Paris, France (n=14) Week 12 Week 24 Week 48 (SVR) HCV RNA <50 IU/mL (% patients) Peg-IFN alfa-2a (40KD) 180 μg/wk plus ribavirin 800 mg/day for 24 weeks 86% 79% 71% 0 10 20 30 40 50 60 70 80 90 100 Dominguez S, et al. 10th EACS 2005; Oral presentation PS7/6

21 P-21 Acute HCV at Mount Sinai Liver Biopsy Series of 7: Risk Factors Acute HCV at Mount Sinai Liver Biopsy Series of 7: Risk Factors 123 Unprotected receptive anal intercourse Yes Hundreds of partners Yes Multiple partners Yes About 50 partners Recent STDs NoneNoneNone IVDUNoRecentRecent Shared snorting paraphernalia YesNoNo Methamphetamine Intoxication YesYesYes

22 P-22 The Biopsy of Case 1 Had Fibrosis Typical of Damage Caused by Chronic HCV Mild portal inflammation, interface hepatitis, and lobular necroinflammatory activity. Portal fibrosis with occasional fibrous septum formation on trichrome stain (panel C). Immunostains for HBsAg and HBcAg were negative (not shown). Arrows in panel B identify a region of focal interface hepatitis; arrows in panel C indicate fibrous septae (blue).

23 P-23 Case 2 Also Had Evidence of Chronic Injury Marked expansion of portal tracts by fibrosis and inflammation. Lymphoid aggregates. Moderate interface hepatitis and lobular necroinflammatory activity. Mild steatosis. Trichrome stain reveals portal and periportal fibrosis with rare fibrous septum formation. HBsAg and HBcAg were not detectable by IHC (not shown). Arrow in B marks an expanded portal tract with a lymphoid aggregate; arrows in C indicate portal and periportal fibrosis.

24 P-24 Fat In The Wrong Places And Insulin Resistance % Intramuscular fat in HIV+ men (Sakkas, unpubl, 2003) HOMA-IR Liver (Sutinen AIDS 2002):   Significantly higher % liver fat in HIV+ LD vs. HIV+ no LD and HIV-   Severity of insulin resistance related to liver fat but not VAT R 2 = 0.7938 P < 0.01 0 2 4 6 8 0246810

25 P-25 NAFLD: the hepatic manifestation of the metabolic syndrome Obesity Diabetes Hypertension Hyper- triglyceridemia NAFLD 47 million have metabolic syndrome ~80% have NAFLD 15% of US population has a fatty liver 3-4% have NASH

26 P-26 NASH is associated with mitochondrial paracrystalline inclusions NASHFatty liver Sanyal et al, Gastro, 2001, 120:1183-1192

27 P-27 NASH: pre vs post treatment with pioglitazone + vitamin E Pre treatment (10 X)Post treatment (10 X) Sanyal et al, Clin Gastroenterol and Hepatol, Dec 2004

28 P-28 Insulin Resistance and HCV: Effect on Response to PegIFN/RBV Therapy % SVR in Genotype 1 Homa: Homeostasis model of assessment – HOMA of insulin resistance Romero-Gomez, M et al. Gastroenterology 2005;128:636-641.

29 P-29 Does steatosis affect response to treatment? Geno 2 F0-1 Percent SVR 98% 59% F2,3,4 59% High Viral Load 57% 51% 39% Geno 1,4.5.6 Geno 1,4.5.6 High V Load Geno 1,4.5.6 High V Load F2,3,4 89% 41% 40% 35% 24% 21% Poynard et al. Hepatology 2003. No steatosis Steatosis

30 P-30 Insulin resistance and NAFLD in co-infection Results: In univariate analyses global and semi-quantitative measures of steatosis strongly associated with HOMA-IR (p<0.0001) -see plot ALT (p=0.003) AST (p=0.003) genotype (p=0.049) negative once genotype 3 excluded ethnicity (p=0.024) Significant correlation between HOMA-IR and HAI fibrosis stage (p=0.011) and steatohepatitis stage (p=0.005) BMI correlated with HOMA-IR (p=0.0085) but not histological parameters In logistic regression analyses only IR positively associated (p=0.015 OR=1.08 95%CI 1.01-1.14) with moderate/severe steatosis

31 P-31 Insulin resistance and NAFLD in co-infection Baseline IR 0 10 20 30 40 50 60 NoYes EVR r = -0.282p = 0.031 Baseline Insulin Resistance by EVR

32 P-32 RIBAVIC- ANRS HC02 mitochondrial toxicity event » (MTE) 6 acute pancreatitis (one with hyperlactatemia) 6 acute pancreatitis (one with hyperlactatemia) 7 hyperlactatemia (hospitalization) 7 hyperlactatemia (hospitalization) 4 suspicions of hyperlactatemia 4 suspicions of hyperlactatemia Association with Didanosine treatment* Association with Didanosine treatment* Odds-ratio for ddi = 23 [95% CI : 5-105]

33 P-33 Occurrence of Hepatic Decompensation APRICOT 1.6% 10.5% 0% 0 2 4 6 8 10 12 All PatientsCirrhotic Patients (non-decompensated) (n = 133) Non-cirrhotic Patients (n = 735) Patients (%) (N = 868) n = 14

34 P-34 Risk Factors Total bilirubin  (OR 1.12, P<0.001) Total bilirubin  (OR 1.12, P<0.001) Alkaline phosphatase  (OR 1.02, P<0.001) Alkaline phosphatase  (OR 1.02, P<0.001) Albumin  (OR 0.83, P<0.002) Albumin  (OR 0.83, P<0.002) Platelets  (OR 0.96, P<0.001) Platelets  (OR 0.96, P<0.001) Hemoglobin  (OR 0.53, P=0.001) Hemoglobin  (OR 0.53, P=0.001) Didanosine treatment (OR 4.06, P=0.03) Didanosine treatment (OR 4.06, P=0.03) Lamivudine treatment (OR 0.30, P=0.04) Lamivudine treatment (OR 0.30, P=0.04) PT INR, efavirenz, saquinavir and non- nucleoside inhibitor treatments (P<0.20) PT INR, efavirenz, saquinavir and non- nucleoside inhibitor treatments (P<0.20)

35 P-35 Ribavirin and ddI = “don’t do it” ddI ddI-MP ddA-MP ddA-DP ddA-TP RT  -Pol (-) InositolIMP XMPGTP IMP dehydrogenase Ribavirin-MP Ribavirin (-) Adenosine kinase Ribavirin increases IMP Increases ddATP Increases ddATP Increases inhibition of HIV RT Increases inhibition of HIV RT Increases inhibition of host g-pol Increases inhibition of host g-pol

36 P-36 Summary of Results From Coinfection Trials StudyN Treatment SVR (%) All GT 1 GT non-1 RIBAVIC412 PEG IFN α-2b + RBV 800 27 17* 44 IFN α-2b + RBV 80020 6 43 ACTG133PEG IFN α 2a + RBV 60027 14 73 IFN α -2a + RBV 60012 6 33 APRICOT860PEG IFN α 2a + RBV 80040 29 62 IFN α -2a + RBV 80012 7 20 LAGUNO93PEG IFN α-2b + W/B RBV 44 38 53 IFN α-2b + W/B RBV 21 7 47 50 36 72 G1 48 w 31 72w 52 PRESCO389PEG IFN α-2a + W/B RBV 50 36 72 G1 48 w 31 72w 52 G2 24 w 67 48w 82

37 P-3712% n = 285 20% n = 286 40% n = 289 Apricot Sustained Virologic Response* P = 0.0084 P  0.0001 * Defined as <50 IU/mL HCV RNA at week 72; ITT % Response 0% 10% 20% 30% 40% 50% 60% IFN alfa-2a + RBV PEG-IFN alfa-2a (40 kDa) + Placebo PEG-IFN alfa-2a (40 kDa) + RBV

38 P-38 Results: treatment factors predictive of an SVR The relationship between various treatment factors and SVR rates were examined The relationship between various treatment factors and SVR rates were examined Cumulative peginterferon- alfa-2a (40KD) dose was strongly correlated with cumulative ribavirin dose (r=0.87) Cumulative peginterferon- alfa-2a (40KD) dose was strongly correlated with cumulative ribavirin dose (r=0.87) Ribavirin dose also correlated with ribavirin treatment duration (r=0.98) Ribavirin dose also correlated with ribavirin treatment duration (r=0.98) 0 20 40 60 100 80 020406080 100 Cumulative ribavirin dose Cumulative peginterferon- alfa-2a (40KD) dose SVR No SVR

39 P-39 MLR analysis: impact on SVR rates Receipt of ≥80/80/80 (vs <80/80/80) Body mass index (per 1 unit increase) Baseline HCV RNA (per 1-log increase) 0.11.0 10.0 0.85 (0.75–0.95) (p=0.0062) 0.32 (0.19–0.54) (p<0.0001) 6.55 (2.43–17.7) (p=0.0002) Odds ratio (95% CI) Less likely to have an SVRMore likely to have an SVR Only factors with a significant (p<0.05) effect are shown

40 P-40 74% 22% 4% 62% 30% 8% 69% 26% 5% 0% 10% 20% 30% 40% 50% 60% 70% 80% Histological Response in Patients with an SVR % of Patients No Change = Change of +1, -1 or 0 in HAI score; Worsening = ≥2-point increase in HAI score n = 19n = 1n = 3n = 4n = 11n = 6n = 51n = 23n = 20 Improved No change Worsened PEG-IFN alfa-2a (40KD) + Placebo IFN alfa-2a + RBV PEG-IFN alfa-2a (40KD) + Placebo PEG-IFN alfa-2a (40KD) + RBV

41 P-41 32% 43% 25% 30% 36% 34% 43% 34% 23% Histological Response in Patients without an SVR n = 21n = 26n = 33n = 14n = 35n = 45n = 26n = 29n = 34 0% 10% 20% 30% 40% 50% 60% 70% 80% % of Patients Improved No change Worsened IFN alfa-2a + RBV PEG-IFN alfa-2a (40KD) + Placebo PEG-IFN alfa-2a (40KD) + RBV No Change = Change of +1, -1 or 0 in HAI score; Worsening = ≥2-point increase in HAI score

42 P-42 Zidovudine: impact on HCV treatment Alvarez D et al. 12th Conference on Retroviruses and Opportunistic Infections (Abstract #: P-192). Boston, MA USA, February 22–25, 2005

43 P-43 Dieterich D, et al. CROI 2004 Hematologic Response Mean Hb (g/dL) 10 1Baseline Epoetin alfa (n=30) SOC (n=22) 23481216 11 12 13 14 Hematologic Response Time (Weeks) *P<.001 vs. BL †P<.001 for epoetin alfa vs. SOC. ‡P=.503 vs. BL * ‡ 13.7 ± 0.4 11.7 ± 0.3 †

44 P-44 Hematologic Response: AZT vs. no AZT Dieterich D, et al. CROI 2004 Mean Hb (g/dL) 10 1Baseline23481216 11 12 13 14 Hematologic Response: AZT vs. no AZT Time (Weeks) ‡ 13.8 ± 0.5 13.6 ± 0.7 12.3 ± 0.5 11.0 ± 0.4 * *P<.090 for epoelin alfa-treated patients receiving AZT vs. not receiving AZT. †P<.001 for epoetin alfa-treated patients receiving AZT vs. SOC patients reciving AZT. ‡P=.001 for epoetin alfa-treated patients not receiving AZT vs. SOC patients not receiving AZT.

45 P-45 PRESCO trial: design Study weeks 0 96 72 48 24 60 84 PEGASYS ® 180 µg plus COPEGUS ® 1000–1200 mg 12 36 Follow-up G2,3 G1,4 G2,3 Follow-up Patients who achieved EVR (>2 log 10 drop in HCV RNA at week 12) continued treatment n=398

46 P-46 Presco Results

47 P-47 Follow-up US study in HIV–HCV co-infected NR to IFN ± RBV (Dieterich, Sulkowski) Study weeks 24 120 048 NR to IFN or IFN/RBV, n=100 7296 HCV RNA pos HCV RNA neg Follow-up Peg-IFNα-2a 90 µg Follow-up Peg-IFNα-2a 180 µg plus RBV 800–1200 mg Peg-IFNα-2a 180 µg plus RBV 1200 mg No treatment Randomisation

48 P-48 Untreated Follow-up SLAM-C trial in HIV–HCV co-infected non-responders (Sherman) Peg-IFNα-2a 180 µg plus RBV 800–1200 mg HCV RNA  2 log drop NR and naïve n=200 HCV RNA <2 log drop 12 weeks Peg-IFNα-2a 180 µg plus RBV 800–1200 mg Peg-IFNα-2a 180 µg Stop treatment, observation period 60 weeks 72 weeks 24 weeks Randomisation

49 P-49 Approach to non-responders METAVIR 0–1 Wait for new treatment options (Helicase, protease inhibitors, polymerase inhibitors) Wait for new treatment options (Helicase, protease inhibitors, polymerase inhibitors) METAVIR 2–3 Retreat with Peg-IFN + RBV Retreat with Peg-IFN + RBV Consider Peg 360 and wt based RBV Consider Peg 360 and wt based RBV Treat with insulin sensitizer Treat with insulin sensitizer METAVIR 3–4 Retreat with Peg-IFN + RBV Retreat with Peg-IFN + RBV Antifibrotic treatment strategy Antifibrotic treatment strategy Consider Peg 360 and wt based RBV Consider Peg 360 and wt based RBV Treat with insulin sensitzer Treat with insulin sensitzer Liver biopsy

50 P-50 Orthotopic Liver Transplantation 23 HIV + compared to UNOS (11,453 HIV -) 23 HIV + compared to UNOS (11,453 HIV -) HCV, 14 and HBV, 9 HCV, 14 and HBV, 9 CD4, 200 (range 76 – 506) CD4, 200 (range 76 – 506) MELD 16 MELD 16 HCV worse than HBV HCV worse than HBV Drug-drug interaction (tacrolimus) Drug-drug interaction (tacrolimus) Outcome not associated with HIV RNA or CD4 Outcome not associated with HIV RNA or CD4 Ragni M. Survival in HIV-infected Liver Transplant Recipients. 10 th CROI #155

51 P-51 Nelfinavir: interaction with tacrolimus Mean 38-fold tacrolimus dose reduction for patients taking nelfinavir compared to placebo Mean 38-fold tacrolimus dose reduction for patients taking nelfinavir compared to placebo Mean dose for patients (n = 5) on nelfinavir: 0.26mg/d Mean dose for patients (n = 5) on nelfinavir: 0.26mg/d Frequent drug level monitoring and great caution are necessary when introducing or withdrawing HAART in HIV-positive organ transplant recipients Frequent drug level monitoring and great caution are necessary when introducing or withdrawing HAART in HIV-positive organ transplant recipients Jain et al. Liver Transpl. 2002;8:841-845

52 P-52 Patient Survival compared with OPTN One Year Patient Survival Three Year Patient Survival All OPTN87.6 (87.0, 88.2) 95.6 (95.4, 95.8) 79.9 (79.3, 80.5) 90.8 (90.5, 91.1) 65 years+ OPTN80.5 (77.9, 83.0) 90.4 (89.4, 91.3) 69.6 (66.9, 72.2) 78.0 (76.6, 79.4) HIV-infected study subjects 90.9 (73.9, 100) 93.8 (81.9, 100) 80.8 (56.8, 100) 93.8 (81.9, 100) LiverKidney LiverKidney Based on OPTN data as of February 4, 2005. One year survival is based on 1999 - 2001 transplants, and 3 year survival is based on 1996 - 1999 transplants.

53 P-53 Participating Centers (visit the study website for updated list of centers and contact information) Atlanta Emory University (K) Baltimore University of Maryland (K) Boston Beth Israel Deaconess Medical Center (K, L) Charlottesville University of Virginia (K, L) Chicago University of Chicago (K, L, Peds K, Peds L) Cincinnati University of Cincinnati (K, L) Cleveland Cleveland Clinic (K, L) Los Angeles Cedars-Sinai (L) Miami University of Miami (K) New Orleans Tulane (K, L) New York Mount Sinai School of Medicine (K, L, Peds K) New York Columbia University (L, Peds L) Philadelphia Drexel University (K) Philadelphia University of Pennsylvania (K, L) Pittsburgh University of Pittsburgh (K, L) San Francisco University of California (K, L, Peds K, Peds L) Washington, D.C. Washington Hospital Center (K) Washington, D.C. Georgetown Medical Center (K, L) Chicago Rush University (K, L)

54 P-54 Conclusions HCV is a major, if not the major cause of morbidity and mortality in HIV+ patients today HCV is a major, if not the major cause of morbidity and mortality in HIV+ patients today Successful treatment of HCV (cure) in HIV+ patients is possible and even likely with pegylated interferon and ribavirin Successful treatment of HCV (cure) in HIV+ patients is possible and even likely with pegylated interferon and ribavirin Side effects can be effectively managed to ensure treatment success Side effects can be effectively managed to ensure treatment success Liver (and kidney) transplant is possible and is being investigated in HIV+ patients Liver (and kidney) transplant is possible and is being investigated in HIV+ patients

55 P-55 For more information, please visit www.virology-education.com Acute Hepatitis C- epidemiology and treatment Chronic Hepatitis C- kinetics, current treatment and new therapies Hepatitis B - Treatment strategies Liver Transplantation- selection and management Steatosis in HIV and HCV Non invasive measures of fibrosis End stage of liver disease managment Tayloring ART therapy in Hepatitis Update on new drugs for HCV and HBV Clinical cases Topics Registration: Early reg.Feb. 15 -March 15, 2007 Regular reg.March 16-April 30, 2007 Late reg.May 1-May 31, 2007 Abstract submission: DeadlineApril 30, 2007 More information Timelines


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