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Co-infection VIH-VHC

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Stanislas Pol, Unité d’Hépatologie, Université Paris Descartes & Inserm U-567, Hôpital Cochin, Paris, France.

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Co-infection VIH-VHC

  1. 1. Co-infection VIH et VHC Stanislas Pol Unité d’Hépatologie, Université Paris Descartes & Inserm U-567 Hôpital Cochin, Paris, France Casablanca, 29.03.2010
  2. 2. Prévalence du VHC et du VHB chez les patients infectés par le VIH ( Etude EUROSIDA) Sud : 623 = 44,9 % Nord : 346 = 24,5 % Centre : 280 = 22,9 24,3 % Est : 412 = 47,7 % Sérologie VHC (+) : 34 % (1 685 / 4 957 pts) Sérologie VHB (+) : 9 % (530 / 5 883 pts) J. Rockstoh et al., CROI 2004 Larsen C et al. BEH 2005; 23: 109-112
  3. 3. Augmentation des hépatites aiguës C chez les homosexuels masculins VIH+ Vogel M et al. J Antimicrobial Chem 2009
  4. 4. Transmission sexuelle VHC chez les homosexuels M. Danta et al. Hepatology 2005; 42:suppl 1: 213A <ul><li>Conclusion : renforcer les messages de prévention ; rapports protégés et risque des drogues partagées (notamment par voie nasale) </li></ul>Transmission VHC chez homosexuels VIH+ MST Pratiques sexuelles à risque Transmission (intranasal) Usage de drogues Comportement sexuel Internet Drogues
  5. 5. Histoire naturelle de la cirrhose hépatite chronique carcinome hépatocellulaire Décompensation Ascite Hémorragie digestive cirrhose décès foie normal
  6. 6. Progression vers la cirrhose et la décompensation de la cirrhose VHC : Impact du VIH Risque relatif 95 % IC ( ) Thomas et al, Hepatology 2002 Cirrhose compensée Benhamou Combined Makris Solo Pol 1 2 10 Cirrhose décompensée 175 Combined Makris Lesens Telfer Eyster 1 6 10
  7. 7. Survie des patients mono- et co-infectés avec cirrhose décompensée Pineda et al, Hepatology 2005
  8. 8. Survie des patients mono- et co-infectés avec CHC Puoti M et al. AIDS 2004
  9. 9. Cytotoxicité directe Cytotoxicité immunomédiée &quot;restauration&quot; Hépatite Chronique Alcool Drogues Médicaments VHC ou VHB VIH MultiTt antiVIH NASH Hépatotoxicité médicamenteuse Pol et al. CID 2003
  10. 10. Stéatose et VIH <ul><li>AIDS era : </li></ul><ul><ul><ul><ul><li>Denutrition </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Opportunistic infections </li></ul></ul></ul></ul><ul><li>HAART era: </li></ul><ul><ul><ul><li>Nucleosides analogues (mitochondrial toxicity) </li></ul></ul></ul><ul><li>Didanosine > stavudine > zidovudine > 3TC/FTC/TFV </li></ul>Bissuel et al. J Intern Med 1995; Chario et al. J Hepatol 1999; Lenzo et al. AIDS 1997 Gaslightwala I et al. J Hepatol 2006
  11. 11. <ul><li>AIDS era : </li></ul><ul><ul><ul><ul><li>Denutrition </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Opportunistic infections </li></ul></ul></ul></ul><ul><li>HAART era: </li></ul><ul><ul><ul><li>Nucleosides analogues (mitochondrial toxicity) </li></ul></ul></ul><ul><ul><ul><li>lipodystrophy: IP </li></ul></ul></ul><ul><li>Hyperlipidemia: 74 % </li></ul><ul><li>Insulin resistance: 60 % Metabolic syndrome </li></ul><ul><li>Diabetes: 7 % </li></ul><ul><li>Alcohol </li></ul>Stéatose et VIH
  12. 12. Reporting Rate [ Pts / (TRXs*10,000) ] lamivudine + zidovudine 0 nevirapine efavirenz lamivudine didanosine abacavir zidovudine zalacitabine nelfinavir indinavir ritonavir saquinavir saquinavir mesylate amprenavir delavirdine stavudine 2 4 «Hépatites médicamenteuses» 1996-2000 FDA data base NNRTI’s NRTI’s PI’s
  13. 13. Hépatotoxicité des antirétroviraux Soriano V et al. AIDS 2008 RAL MRV ETV Risque Élevé Risque Faible ddI d4T AZT 3TC FTC ABV TDF EFV NVP SQV ATV LPV APV DRV TPV RTV T20 NRTI NNRTI PI Newer ARVs
  14. 14. Mortalité hépatique et VIH Mortavic 2005 <ul><li>24 000 patients in 2004, 19.4 % co-infectés, 313 décès </li></ul>Rosenthal E et al. AASLD 2007 , A 135 HAART 8 91,6 1,5 6,9 2 84,5 6,6 8,8 1 48,7 36,7 1 47 40,5 48,5 34,8 1,2 Overall Mortality AIDS-related Mortality Liver-related Mortality Other 0 20 40 60 80 100 1995 1997 2001 2003 2005 12,6 16,7 14,3
  15. 15. Histoire naturelle de la cirrhose hépatite chronique carcinome hépatocellulaire Décompensation Ascite Hémorragie digestive cirrhose décès foie normal Traiter
  16. 16. PegIFN + ribavirine et co-infection ACTG5071 APRICOT RIBAVIC Laguno No. with Peg+RBV 66 289 205 52 Type of pegIFN 2a 2a 2b 2b IDUs - 62 % 81 % 75 % Cirrhotics 11 % 15 % 40 % (F3-F4) 19 % Genotypes 1-4 77 % 67 % 69 % 63 % Normal ALT levels - 0 15 % 0 Mean CD4 count - 520 525 512 On HAART - 84 % 82 % 94 % Tx discontinuation - 25 % 41 % 25 % EOT (ITT) 41 % 49 % 36 % 52 % SVR (ITT) 27 % 40 % 27 % 44 %
  17. 17. VPP et VPN des Réponses virologiques rapides (RVR) chez les patients VHC traités F. Poordad # 305 AASLD 2007 *North-C study not included because attainment of RVR was basis of enrollment; Wong data not included because same cohort as Davis et al (both Manns’ cohorts). 1Payan C et al. Gut . 2007;56:1111-1116; 2Pearlman B et al. Hepatology . 2007;44(suppl 1):318A; 3Mangia A et al. N Engl J Med . 2005;352:2609-2617; 4Davis GL et al. Hepatology . 2003;38:645-652; 5Wong JB et al. Hepatology. 2002;36:281A. Abstract 472; 6Segadas-Soares JA et al. Hepatology. 2006;44(4 suppl 1):S334. Abstract 384; 7Dalgard O et al. Hepatology . 2004;40:1260-1265; 8Dalgard O et al. J Hepatol . 2007;46(suppl 1):S57; 9Crespo M et al. J Viral Hepat . 2007;14:228-238; 10 Carrat F et al. JAMA . 2004;292:2839-2848; 11Laguno M et al. AIDS . 2004;18:F27-F36; 12Moreno L et al. AIDS . 2004;18:67-73; 13MuirAJ et al. N Engl J Med . 2004;350:2265-2271; 14Kamal SM et al. Gut . 2005;54:858-866; 15Hasan F et al. Am J Gastroenterol . 2004;99:1733-1737; 16El-Zayadi A-R et al. Am J Gastroenterol . 2005;100:2447-2452.
  18. 18. Génotypes 1 et 4 Génotypes 2 et 3 35.9 % 27.3 % 21.0 % 17.8 % 0 20 40 48 w. 72 w. 24 w. 48 w. Genotypes 1 & 4 (n = 237) Genotypes 2 & 3 (n = 152) * ** 30.1 % 53.3 % 66.7 % 82.1 % 0 40 80 48 w. 72 w. 24 w. 48 w. 59/192 24/45 64/96 46/56 <ul><li>p = 0.004 </li></ul><ul><li>** p = 0.04 versus short treatment </li></ul>% SVR % relapse % % Co-infection VIH-VHC “ Renforcement thérapeutique” Vispo et al. Antivir Ther 2008, 13: 511-7 PRESCO trial (SVR)
  19. 19. Retraitement par PEG-IFN + RBV des non répondeurs <ul><li>Retreatment by PEG-IFN α-2a (180 μg/w) + RBV (weight-adapted), 48 w, in 51 co-infected non responders (NR : 64%) or relapsers (R : 36%) to PEG-IFN + RBV 800 mg, IFN + RBV or IFN </li></ul>0 20 40 60 Réponse virologique soutenue (%) 80 100 p = ns p = 0.02 Labarga P et al., AASLD 200 , A 345 All NR R G 1 G 2-3 p = 0.02 > 9.5 kPa ≤ 9.5 kPa Liver stiffness 39 % 30 % 58 % 27 % 70 % 18 % 60 % % SVR
  20. 20. Impact du traitement antiviral C <ul><li>Prospective follow-up of 383 HIV/HCV </li></ul><ul><li>co-infected RIBAVIC patients </li></ul><ul><li>Median follow-up of 60 months </li></ul><ul><li>Analysis of « liver » events : </li></ul><ul><ul><li>Cirrhosis « decompensation » </li></ul></ul><ul><ul><li>Hepatocellular carcinoma </li></ul></ul><ul><ul><li>Liver transplantation </li></ul></ul><ul><ul><li>Liver-related deaths </li></ul></ul><ul><li>Event in 21 (5 %) patients : </li></ul><ul><ul><li>All non responders </li></ul></ul><ul><ul><li>20/21 with fibrosis ≥ F3 </li></ul></ul>Factors associated with survival without event in Multivariate analysis Bani-Sadr et al. EASL 2007, A 259 Responders p = 0.02 Fibrosis < F3 p < 0.001 CD4>350/ml p = 0.001 1 0,90 0,85 0,95 1 0,90 0,85 0,95 1 0,90 0,85 0,95 12 24 36 48 60 72 Non responders CD4 ≤ 350 /ml Fibrosis ≥ F3
  21. 21. Bénéfices : inactivation et réversion de la fibrose voire de la cirrhose Mallet V et al. Antiviral Therapy 2007 A B
  22. 22. Histoire naturelle de la cirrhose carcinome hépatocellulaire Décompensation Ascite Hémorragie digestive cirrhose décès foie normal Surveiller hépatite chronique
  23. 23. Dépistage échographique du CHC Le rapprochement du délai des échographies augmente l’incidence de détection des nodules mais pas celle de la détection des petits CHC Trinchet JC et al. EASL 2007 , A 126 1 200 cirrhotiques (87,5 % Child A, 12,5 % Child B) 2,0 % 2,9 % 0 10 20 30 40 50 60 70 Mois 0 0,02 0,04 0,06 0,08 0,1 p = 0,72 CHC < 3 cm Echo tous les 6 mois Echo tous les 3 mois 2 ans
  24. 24. Radiodestruction d’un nodule de CHC
  25. 25. VO grade 2
  26. 26. Surveillance de la cirrhose <ul><li>Echographie: au moins trimestrielle [Rapport Yeni 2008] </li></ul><ul><li>Alpha féto-protéine: au moins semestrielle </li></ul><ul><li>Fibroscopie oeso-gastro-duodénale: </li></ul><ul><ul><li>pas de VO: tous les 2 ans </li></ul></ul><ul><ul><li>VO grade I: tous les ans </li></ul></ul><ul><ul><li>VO grade II: prophylaxie primaire par  - </li></ul></ul><ul><ul><li>VO grade III: LVO? </li></ul></ul>
  27. 27. Histoire naturelle de la cirrhose carcinome hépatocellulaire Décompensation Ascite Hémorragie digestive cirrhose décès foie normal Traiter et surveiller TH TH hépatite chronique
  28. 28. Histoire naturelle de la cirrhose carcinome hépatocellulaire Décompensation Ascite Hémorragie digestive cirrhose décès foie normal Anticipation du traitement antiviral: Plus d’efficacité Moins d’effets secondaires TH TH hépatite chronique
  29. 29. Traitement antifibrosant du co-infecté non répondeur ou intolérant?
  30. 30. Traitement antifibrosant du co-infecté non répondeur ou intolérant? - Espoir des années 2005 - Déception des années 2007-2008
  31. 31. COPILOT Résultats finaux (1) <ul><li>600 patients VHC non-repondeurs, fibrose avancée (F ≥3) ou cirrhise CP <7 </li></ul><ul><li>Etude randomisée controlée évaluant le PEG-INF α -2b (0,5µg/kg/sem) versus colchicine 0,6mg x2/j. evaluation à 4 ans </li></ul>Afdhal et al. EASL 2008 abstract 3 Critères de jugement primaires, en ITT Suivie sans évènements, ITT
  32. 32. <ul><li>PEG-INF n’est pas supérieur à la cochicine en ITT, notamment pour la prévention du CHC mais réduit les évènements chez les cirrhotiques avec HTP </li></ul>COPILOT Résultats finaux (2) Afdhal et al. EASL 2008 abstract 3
  33. 33. Incidence du CHC dans l’étude HALT-C <ul><li>Etude contrôlée, randomisée, multicentrique, ouverte </li></ul><ul><li>1005 sur les 1050 malades VHC+, non-répondeurs PEG-INF + RBV, fibrose sévère ont été analysés dans cette sous -étude </li></ul>Lok et al. EASL 2008-Abstract 101
  34. 34. Sherman et al. CROI 2008, A 59 Évolution fibrose Analyse sur échantillons appariés (n = 45) Traitement d’entretien chez le co-infecté ACTG 5178-SLAM C PEG-IFN (n = 44) Pas de TRT (n = 42) Analyse intermédiaire n = 45 patients (n = 24) (n = 21) Progression Patients VIH-VHC non répondeurs à S12 d’une bi-TRT PEG-IFN RBV (n = 96) Observation PEG-IFN n = 24 n = 21 -6 -5 -4 -3 -2 -1 0 1 2 3 4 5 6 Changement en valeur absolue du score de fibrose (METAVIR)
  35. 35. La transplantation hépatique <ul><li>Suivi de 99 patients VIH-VHC et VIH-VHB après leur première consultation dans un centre de transplantation entre décembre 1999 et septembre 2006 </li></ul><ul><ul><li>VIH-VHC (n = 75), VIH-VHB (n = 8), VIH-VHB-VHC (n = 8), hépatite fulminante (n = 3), HNR (n = 3), autre cirrhose (n = 2) </li></ul></ul>Duclos-Vallée J.C , EASL 2007, A 154 Survie après la première consultation (n = 72) 0 0 20 40 60 80 100 1 2 3 4 5 6 7 8 9 10 Années Survie (%) 73 % 61 % 61 % 34 % 0 0 20 40 60 80 100 1 2 3 4 5 6 7 8 9 10 Années Survie (%) 87 % 79 % 79 % 44 % 25 % Transplantation hépatique (n = 56) Décès avant TH (n = 16)
  36. 36. Transplantation hépatique pour CHC chez le co-infecté VIH/VHB ou VHC (2) Récidive tumorale : 4/15 VIH+ (26 %) versus 7/53 VIH- (13 %) ; p = NS Survie globale après transplantation Duclos-Vallée JC et al. AASLD 2008 , Abstract 70 Survie (%) Mois 100 80 60 40 20 0 0 10 20 30 40 50 60 Suivi VIH- : 25 + 16 mois Log-rank ; p = 0,01 24 mois VIH+ VIH- 94 % 98 % 72 % 72 % Suivi VIH+ : 20 + 15 mois
  37. 37. Conclusions <ul><li>Dépister la co-infection </li></ul><ul><li>Evaluer son impact hépatique </li></ul><ul><li>Lutter contre les co-morbidités: alcool, syndrome métabolique, déficit immunitaire </li></ul><ul><li>Traiter plus tôt que la mono-infection VHC </li></ul><ul><li>Optimiser l’efficacité du premier traitement antiviral et des suivants </li></ul><ul><li>Surveillance accrue des cirrhotiques </li></ul>

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