Transcript Document

Management of HIV-HCV
coinfected patients
3rd. Paris Hepatitis Conference,
Paris, 19. January 2009
Stanislas Pol, MD, PhD
Unité d’Hépatologie &
Inserm U-567
Hôpital Cochin, Paris, France
Jürgen Rockstroh
Medizinische Klinik I
Universitätsklinikum Bonn
Prevalence of Hepatitis C
(1960/5957 patients = 33%)
North: 359 = 23,2 %
Regions:
south
central
East: 613 = 46,9 % north
Central: 293 = 19,6 %
east
Rockstroh J et al.,
South: 695 = 41,4 %
J Inf Dis 2005
Prevalence of Hepatitis Coinfection in
Germany
 Patients from the German Competence
Network HIV/AIDS with complete hepatitis
serology, HAART treatment information and
still under observation and accesible in the
cohort after the 1.01.2007 were included
 Overall 2692 patients were evaluated
• a chronic hepatitis B infection (persistent HBsAg+) was present in 157 patients (5.8%)
• a chronic hepatitis C infection was determined
in 351 Patienten (13.0%)
Rockstroh J et al. DÖAK 2007;C19
Acute Hepatitis C cases reported
in Germany





Berlin 110
Hamburg 25
NRW 12
Hessen 6
Bayern / BW 3
Risk factors in the transmission of
acute HCV in HIV+
Schmidt et al. IAS 2007 MOPEB037
Question
If an HIV patient gets infected with
hepatitis C how high is his probability
of spontaneously clearing HCV?
1. > 50% (yellow)
2. 40% (green)
3. < 25% (red)
Hepatitis coinfection in EuroSIDA
• HCV genotype distribution and percentage of naturally cleared HCV infection
within EuroSIDA
• Studied relationship between HCV genotype and/or HCV RNA level and risk for
developing liver disease related death, or all cause mortality
Results
• Of 2263 HCVAb+ patients, 1677 (74.1%) were serum HCV RNA+ (95% CI: 71–
78%)
Distribution of HCV by genotype (1–4) in European regions
60%
40%
20%
0%
1
2
3
4
Southern Europe
1
2
3
4
Northern Europe
1
2
3
4
Central Europe
Soriano V, et al. 11th EACS, Madrid 2007; PS8/1, Soriano V et al. Clin Infect Dis 2008
1
2
3
4
Eastern Europe
Clusters of sexual transmission
4
2
Phylogénie NS5b : 10/12 patients
avec génotype 4d au CHU Necker
5
6
1b
999
4aY11604
4aFrSSD25
1000
4d FRSSD50
4d FRSSD171
1000
4d FRSSD65
3
4d MRS95
4d P9 RCP
1a
4d FRSSD58
1 (other)
4d FRSSD37
900
Genotypes VHC, France, 2003
PAT 9- 2003
PAT 5- 2001
La comparaison des
PAT 10-2002
PAT 12- 2004
séquences NS5b confirme
PAT 4- 2002
l’homogéneité des souches
PAT 8- 2002
(variabilité moyenne : 0,01 %)
PAT 2- 2002
PAT 7- 2003
PAT 11- 2003
J Serpaggi, AIDS 2006
PAT 1- 2002
Treatment of acute hepatitis C
Acute hepatitisC
No
Jaundice
Yes
Yes
HIV +
PEG-IFN and ribavirin
24 weeks
HCV RNA at W12
+
No treatment
Natural history of acute HCV in HIVinfected patients
150 patients
Week
S 1212
23 23
HCV
PCR
PCR-
S 12 12
Week
127
127HCV
PCRPCR
+ +
14 remained
14 not treated
untreated
2525
declined
refusedtreatment
treatment
Week
S 4848
6 PCR –
8 PCR +
Week
S 4848
5 PCR –
20 PCR +
Spontaneous HCV Clearance at W48
=11/150 overall (7%)
Azwa et al, EACS Madrid 2007
=11/39 untreated (28%)
PegIFN + ribavirin combination in acute hepatitis
Collaborative european study: 44 treated patients
with SVR in 25/44 (57%)
Male
All patients
n=44
SVR
no SVR
43 (98%)
n=25
n=19
Characteristic acute HCV
• patient age (years)
• symptomatic hepatitis
• Max ALT elevation (IU/ml)
•HCV-RNA (IU/ml, log10)
38 (33 – 45)
4/25 (16%)
362 (141–592)
6.33 (5.24-6.89)
39 (34 – 43)
1/19 (5%)
250 (157–555)
6.26(5.36-6.86)
0.741
0.370
0.655
0.790
Characteristic HIV
• Use of HAART
• HIV-RNA < LOD
• HIV-RNA (cop/ml, log10)
• CD4 cell-count (/µl)
14/25 (56%)
14/24 (58%)
1.70(1.70 – 4.75)
389 (335–612)
12/19 (63%)
8/14 (57%)
2.29(1.70-4.53)
452 (362–618)
0.760
1.000
0.808
0.636
19 (7 – 26)
11/25 (44%)
20/25 (80%)
18/20 (90%)
27 (23 – 47)
8 (3 – 18)
13/19 (68%)
18/19 (95%)
7/24 (29%)
24 (14 – 33)
0.081
0.135
0.213
<0.001
0.237
Mean age (Years)
38.5 (33.5 – 43.5)
Transmission-risk
• IVDU
• IVDU and UPSI
• UPSI
• unknown
1 (2%)
2 (5%)
34 (77%)
7 (16%)
Reason for HCV-Testing
• abnormal LFT
• Symptoms hepatitis
• History of transmission risk (IVDU, positive partner)
• routine screen
30 (68%)
4 (9%)
8 (18%)
2 (5%)
Other STD at diagnosis of HCV
6 (14%)
Use of HAART
26 (59%)
HCV-RNA (IU/ml, log10)
6.3 (5.4 – 6.9)
ALT (IU/ml)
326 (154 – 565)
CD4 cell-count (/µl)
400 (350 – 614)
HIV-RNA (copies/ml, log10)
pvalue
1.7 (1.7 – 4.5)
Time between diagnosis and treatment (weeks)
11 (4 – 25)
Duration of treatment (weeks)
24 (20 – 43)
HCV-Treatment
• delay treatment (weeks)
• start within 12 weeks
• start within 6 months
• HCV-RNA neg. week 4
• duration treatment (weeks)
Vogel et al, EACS Madrid 2007
Liver-related mortality in HIV:
Mortavic 2005
24 000 patients in 2004, 19.4 % HCV co-infected, 313 deaths
HAART
100
91,6
84,5
80
60
48,7
20
40,5
36,7
40
8
0
6,9
1,5
1995
Overall
Mortality
6,6
8,8
2
14,3
1
1997
AIDS-related
Mortality
48,5
47
16,7
12,6
1
2001
34,8
1,2
2003
Liver-related
Mortality
2005
Other
AASLD 2007 – Rosenthal E, France, Abstract 135
Optimization of HCV treatment
• To diagnose
• To evaluate liver disease
• Adaptation of ARV
• HCV antiviral treatement
• To improve efficacy
HIV/HCV co-infection
Evaluation of liver fibrosis
FIB-4/Shasta/Fibrometre/Hepascore …
LB
UI / L
AST
FIB-4 = AGE x
Plaquette x
Années
109 / L
ALT
UI / L
Liver stiffness
Fibrotes
t
H. Fontaine et al (HAS). GCB 2007
Dynamics of liver fibrosis
Unfair evaluation in F1+-F3Graphe
en boîtes
Aire
de fibrose
(%)
Eclaté par : Colonne 1
30
25
F0
Unités
20
F1
F2
15
F3
10
F4
5
0
F0
F1
Colonne 2
F2
F3
F4
Evaluation
Biopsy and/or non invasive markers (NIM)
A2-A3
F2-F4
Antiviral
treatment
A0-A1
F0-F1
Biopsy /3 y
NIM/y
Progression to cirrhosis
1.00
4682 patients
Hazard function
0.83
0.67
180 HIV-HCV
701 Alcohol
0.50
812 HBV
382 Hemochromatosis
0.33
2313 HCV
0.17
93 Steatosis BMI>25
200 PBC
0.00
0
20
40
Age in years
60
80
Poynard et al J Hepatol 2003;38: 257-65
Main reasons to treat chronic
HCV in HIV-infected patients
 HIV patients live longer
 Faster progression to liver cirrhosis
 Increased mortality due to ESLD (end
stage liver disease)
 Higher risk of hepatotoxicity
following treatment with ART drugs
SVR to IFN-RBV reduces liver-related
complications in HIV/HCV coinfection
Kaplan-Meier estimate of liver-related
events stratified according to response
to IFN-RBV
100
80
Percentage
GESIDA 3603 study cohort
• Determine effect of achieving
SVR on mortality, liver-related
morbidity, HIV progression
• 711 HIV/HCV+ pts from Spain,
started IFN-RBV between Jan
2000 and Dec 2005
• SVR defined as undetectable
serum HCV-RNA level 24 wks
after discontinuation of therapy
(achieved by 31% of pts)
60
SVR
No SVR
40
p<0.001 by
log-rank test
20
• Analyses were adjusted for
baseline liver fibrosis and benefit
was highest in that group
Berenguer J, et al. 15th CROI, Boston 2008, #60
0
0
6 12 18 24 30 36 42 48
Follow-up (months)
19
Case # 1
 49-y-old patient with HIV/HCV coinfection
• IVDU transmission risk factor for HIV and HCV, no
drug abuse more for >15 years
• HAART since 2002 (lopinavir/r/[AZT/3TC])
• HIV-RNA < 50 copies/ml for > 3 years
• CD4-count 535 /µl, 26%
• ALT 2-3 x ULN
• HCV-RNA 4.600.000 IU, HCV GT 1a
• Liver Fibroscan 60 KPa (F4-Fibrosis)
• No clinical signs of advanced liver disease, but
decreased platelets of 70.000/µl
Question
1.
2.
3.
4.
How would you manage hepatitis C in this
patient?
Cirrhosis and low platelets are
contraindications for interferon therapy;
therefore no HCV therapy (yellow)
Start with PEG-IFN/RBV (green)
First optimize HAART and switch [AZT/3TC]
to different NUC-backbone (blue)
Prepare patient for liver transplantation
(red)
Zidovudine: impact on HCV
treatment
RBV dose reduction
by week 4
3,14
HB loss (g/dl)
3
1,96
2
1
0
ZDV
No ZDV
Patients with RBV decrease
HB decrease by week 4
60%
52%
40%
20%
20%
0%
ZDV
No ZDV
Alvarez D et al. 12th Conference on Retroviruses and Opportunistic Infections
(Abstract #: P-192). Boston, MA USA, February 22–25, 2005
n=398
0
PEGASYS® 180 µg plus
COPEGUS®
1000–1200 mg
PRESCO trial: design
12
G1,4
Follow-up
n=192
G1,4
Follow-up
n=45
G2,3
n=96
Follow-up
G2,3
24
n=56
Follow-up
36
48
60
72
84
Wochen
Patients achieving an EVR (>2 log10 decrease in HCV RNA at week 12) continue their
treatment
96
HCV RNA Abfall (% Patienten)
Ribavirin-Dosis in Genotype 1 - EVR:
APRICOT (800 mg) vs PRESCO (1000 –1200 mg)
90
84%83%
80
APRICOT (n=176)
78%
PRESCO (n=94)
70
63%
60%
60
50
40
34%
30
20
10
0
>1 log
On-treatment Analysis
>2 log
Negative (<50 IU/mL)
Week 12
Ramos B, et al. J Viral Hepatitis 2007
EOT and SVR Rate in PRESCO
100
90
80
70
60
50
40
30
20
10
0
90 %
72 %
67 %
50 %
55 %
41 %
36 %
33 %
Total
GT 1
GT 2/3
GT 4
262 193
n=389
106 68
n=191
137 110
n=152
19 15
n=46
EOT
SVR
Nunez M et al., AIDS Res Hum Retroviruses 2007
Case # 1
 Patient is switched from [AZT/3TC] +
lopinavir/r to tenofovir/FTC + lopinavir/r;
after 3 months of therapy and continued
successful therapy with HIV-RNA < 50
copies/ml,
HCV-therapy is initiated with PEG-IFN and
ribavirin 1200mg weight adapted
 After 12 weeks of HCV-therapy HCV viral
load has dropped to 2000 IU; In parallel
CD4-count has decreased to 160/µl (27%)
Question
How would you continue to
manage this patient?
1. Stop HCV therapy (yellow)
2. Continue therapy (red)
3. Consider PEG-IFN dose
reduction (blue)
Median Change from Baseline
in CD4+ Counts*
Median Change from Baseline
in CD4+ Count (cells/L)
IFN alfa-2a 3 MIU + RBV 800 mg (n = 174)
PEG-IFN alfa-2a (40 kDa) 180 ug + Placebo (n = 196)
PEG-IFN alfa-2a (40 kDa) 180 ug + RBV 800 mg (n = 217)
60
40
20
0
-20
-40
-60
-80
-100
-120
-140
-160
BL
0 4
4/25/2020
8 12 16 20 24 28 32 36 40 44 48 52 56 60 64 68 72 76
* Patients receiving 48 weeks of treatment
Time (Weeks)
Torriani F et al., N Eng J Med 2004
Mean Change from Baseline in HIV
RNA: Patients with Detectable HIV
RNA at Baseline*
IFN alfa-2a 3 MIU + RBV 800 mg (n = 64)
PEG-IFN alfa-2a (40 kDa) 180 ug + Placebo (n = 78)
PEG-IFN alfa-2a (40 kDa) 180 ug + RBV 800 mg (n = 89)
Change in Log10 HIV RNA
2,0
1,5
1,0
0,5
0,0
-0,5
-1,0
-1,5
-2,0
BL
4
8
* Patients receiving 48 weeks of treatment
12
24
36
48
52
60
72
Time (Weeks)
Torriani F et al., N Eng J Med 2004
SVR-Raten in the PRESCO-trial
82%
90
80
67%
% SVR
70
53%
60
50
40
31%
30
20
59/192
24/45
64/96
46/56
48 weeks
72 weeks
24 weeks
48 weeks
10
0
HCV GT 1/4 (n=237)
Discontinuations due to
Patient wish:
15
(8%)
36 (80%)
HCV GT 2/3 (n=152)
4 (4%)
9 (16%)
Nunez M et al., ICAAC 2006
APRICOT Study: SVR Rates in relation
to virological response
Genotype 1
Genotype 2/3
SVR = 82 %
SVR = 6 %
no EVR
17 %
RVR 13 %
SVR = 1 %
no EVR
40 %
SVR = 63 %
complete
EVR 22 %
partial
EVR 26 %
SVR = 17 %
SVR = 18 %
partial
EVR 12 %
RVR 37 %
SVR = 94 %
complete
EVR 35 %
SVR = 70 %
Rodriguez-Torres M et al., CROI (2008), Poster 1073
HIV Medicine 2008
Proposed optimal duration of HCV therapy in
HCV/HIV-coinfected patients.
W4
HCV-RNA
neg
W12
W24
G2/3
24 weeks
therapy *
W48
G1/4
> 2 log drop
in HCV-RNA
HCV-RNA
pos
HCV-RNA
neg
HCV-RNA
pos
< 2 log drop
in HCV-RNA
G2/3
G1/4
W72
48 weeks
therapy
72 weeks
therapy
Stop
Stop
* In patients with baseline low viral load and minimal liver fibrosis.
HIV Medicine 2008
Case 2
 42-y-old hemophiliac with HIV/HCV
coinfection
– HIV first diagnosed 01/95, CDC C3
– CMV-Retinitis 2003
– 08/07 HAART for 4 years with
Abacavir/3TC/lopinavir/r
– HIV-RNA <50 copies/ml
– CD4 430/µl (27%)
 Patient is referred to our HIV-Hepatitis
Clinic for further workup
 HCV-RNA 1.093.527 IU/ml; GT 3 infection
 Fibroscan 10.2 KPa F2-F3 Fibrosis
Question

How would you manage this patient?
Start PEG-IFN/RBV therapy for 48 weeks
(yellow)
2. Switch Abacavir/3TC to Tenofovir/FTC and
then start HCV-therapy (green)
3. Start PEG-IFN/RBV therapy for 24 weeks
(blue)
4. Would not treat this patient for HCV at all
(red)
1.
Ribavirin in HIV/HCV Co-infection
 Dose-dependent hemolytic anemia:  mean 2.5 - 3 g/dL Hb
< 4 wks
 Drug-drug interactions
• Anti-HIV antagonism with pyrimidine nucleoside analogs - AZT,
D4T, DDC (in vitro)1
• Inhibits intracellular phosphorylation
• Increased intracellular levels of DDI metabolites (in vitro); increased
risk for lactic acidosis
• Recent data suggests decreased SVR under abacavir treatment;
caveat abacavir treated patients had more fibrosis upon baseline
and were more HAART experienced2,3,4
1) Vogt MW. Science 1987;235:1376, Baba AAC 1987;31:1613
2) Margt NA and Miller MD, 2nd IAS Conference on HIV Pathogenesis and Treatment, Paris
2003; P980
3) RIBAVIC Subanalyses CROI 2007; 4) CROI 2008
Effect of ABC on SVR rates in HCV patients
treated with RBV
• Proposed intracellular competition
between ABC and RBC (guanosine
analogs)
• Retrospective study of 256 HIV/HCV
pts on HAART starting peg-IFN + RBV1
p=0.01
60
50
SVR (%)
– Differences between NRTI combinations
mainly observed in subjects receiving
lower RBV doses and in those needing
higher RBV doses (GT 1 pts)
– Use of TDF/3TC was associated with
improved SVR
Response by NRTI group1
52
p=0.02
45
40
30
33
29
20
10
• No difference in SVR with regard to
NRTI choice (TDF vs ABC)2
0
ITT analysis
n = 70 186
Per-protocol
analysis
n = 57 160
ABC+ 3TC
TDF+ 3TC or FTC
1 Mira J, et al. 15th CROI, Boston 2008, #1074; 2 Moreno A, et al. ibid, #1075
37
Negative impact of abacavir on SVR (2)
Negative impact of abacavir at W4, W12, W48 & W72 is significant only when
ribavirine levels are < 2.2 μg/ml, suggesting a putative interaction between ribavirin
and abacavir
Relapse rate according to abacavir and ribavirin levels
p = 0.44
p = 0.08
100
Relapsers (%)
•
80
with ABC
60
without ABC
40
20
0
Number of patients
RBV > 2.2 μg/ml
RBV < 2.2 μg/ml
55
27
AASLD 2007 – Barreiro P et al.Abstract 342
38
Ribavirin monitoring (1)
• 22 HIV/HCV co-infected patients treated by PEG-IFN
a2a 180 ug/sem + ribavirin 800-1 200 mg/d
– Genotype 1 : n = 10 ; 3 : n = 8
– 50 % with F > 2
– HCV RNA = 6 log10 copies/ml
• Measure of plasmatic (Cp) and erythrocyte (Ce)
ribavirin levels (= 12 h after) at W4 and W12 :
– Significant correlation between Cp and Ce
– Correlation between Cp, Ce and hemoglobin decline
CROI 2007, Dominguez S et al. abst 893
Ribavirin monitoring (2)
Correlation between Cp, Ce at W4 and
EVR
– Cut off Cp = 1,6 mg/l
(génotypes 1,4)
RBV-P Cmin (mg.l-1)
– Cut off Ce = 140 mg/l
RBV-E Cmin (mg.l-1)
2,4
220
2,2
2
180
1,8
140
1,6
100
1,4
1,2
60
1
20
Non responders
Responders
Non responders
Responders
CROI 2007, Dominguez S et al. abst 893
Case 3
• 35-y-old female patient with HIV/HCV coinfection
–
–
–
–
HIV first diagnosed 01/08, CDC B2
HIV-RNA 11.763 copies/ml
CD4 311/µl (23%)
No HAART
• Patient is referred to our HIV-Hepatitis Clinic for further
•
•
•
workup
Liver enzymes are slightly elevated (Grade 1)
HCV-RNA 943.527 IU/ml; GT 3 infection
Fibroscan 8.2 KPa F2 Fibrosis
41
Question
•
1.
2.
3.
4.
How would you manage this patient?
Start PEG-IFN/RBV therapy for 48 weeks (yellow)
Start HAART first and then treat HCV-infection (green)
Would not treat this patient for HCV at all (blue)
Something different (red)
42
Rate of SVR increases with higher CD4 %:
APRICOT
73
Min – Q1
CD4%
69
Q1 – Med
Med – Q3
62
SVR rates
Q3 – Max
47
47
41
36
34
33
29
27
16
All patients
(n=242)
HCV genotype 1
(n=150)
HCV genotypes 2-3
(n=78)
Opravil et al. J AIDS 2008
Use of ARV in co-infected patients
treated for HCV (1)
• Use of ARV :
– Cautious use of nevirapine (AII)
– Same recommendations for initiation of ARV in coinfected patients than in HIV mono-infected (BII)
– If CD4 count at the limit of the recommended level
 ARV are prioritary (BIII)
– Avoid severe immune status (CD4 < 200/mm3) in coinfected patients (BII)
Alberti et al. ECC. J Hepatol 2006
Use of ARV in co-infected patients
treated for HCV (2)
• ddI
– Contra-indicated if cirrhosis (EI)
– To avoid in patients with less severe liver disease (EII)
Alberti et al. ECC. J Hepatol 2006
Kaplan Meier Analysis of Overall
and Liver-related Mortality
A) Overall-Mortality
A) Liver-related-Mortality
P<0.0001
Cumulative survival
Cumulative survival
1,1
Patients with HAART
,9
,7
,5
Patients with ART
P<0.018
1,1
Patients with HAART
,9
Patients with ART
untreated Patients
,7
,5
untreated Patients
,3
0
,3
1000 2000 3000 4000 5000 6000
0
Observation time[days]
Patients under observation:
HAART-group:93 79
33
ART-group: 55
46
30
Untreated-group: 137
94
15
49
9
37
1000 2000 3000 4000 5000 6000
Observation time[days]
1
32 27
Patients under observation:
HAART-group:93 79
33
ART-group: 55
46
30
Untreated-group: 137
94
15
49
9
37
1
32 27
Qurishi N et al., Lancet 2003:362:1708-1713
Probability of remaining free of developing a
hepatic decompensation
Pineda JA et al., Hepatology 2007;46:622-630
Interventions for HCV/HIV-coinfected nonresponders/relapsers to prior interferon-based therapies
Category
Recommended intervention
Suboptimal prior treatment schedules:
Re-treatment using combination
therapy with peginterferon plus
weight-based ribavirin doses
• Interferon (monotherapy or with ribavirin)
• Low ribavirin doses
• Short length of therapy
Limiting toxicities & poor adherence
Optimal support (psychiatric,
pharmacists, use of hematopoietic
growth factors)
Virological failure
• Wait until new antivirals come to
the market in the rest
Soriano V, Puoti M, Sulkowski M, Cargnel, Benhamou Y, Peters M, Mauss S, Brau N, Hatzakis A, Pol S, Rockstroh J. AIDS 2007
Study design: ACTG 5178
peg-IFN
maintenance
peg-IFN +
Wt-based
RBV
12 wks
NR
*
6 wks
Untreated
controls
72 wks
Liver
biopsy
Liver
biopsy
*NR, non-response
Liver
biopsy
Absolute change in Metavir Fibrosis Score
Sustained long-term antiviral maintenance with
peg-IFN in HCV/HIV coinfected patients (SLAM-C)
6
5
4
3
2
1
0
-1
-2
-3
-4
-5
-6
Fibrosis change: Paired sample
analysis
n=24
n=21
peg-IFN
Observation
Treatment arm
• Lack of fibrotic progression in
observation arm precludes ability to find
efficacy in maintenance therapy
Sherman K, et al. 15th CROI, Boston 2008, #59
49
Liver transplantation
•
Suivi de 99 patients VIH-VHC et VIH-VHB après leur première consultation dans un centre
de transplantation entre décembre 1999 et septembre 2006
– VIH-VHC (n = 75), VIH-VHB (n = 8), VIH-VHB-VHC (n = 8),
hépatite fulminante (n = 3), HNR (n = 3), autre cirrhose (n = 2)
Survie après la première consultation
(n = 72)
100
100
73 %
61 %
79 %
80
61 %
60
34 %
40
Survie (%)
Survie (%)
80
87 %
79 %
60
44 %
40
20
20
0
0
Transplantation hépatique
(n = 56)
25 %
Décès avant TH (n = 16)
0
1
2
3
4
5
Années
6
7
8
9
10
0
1
2
3
4
5
6
7
8
9
10
Années
Duclos-Vallée J.C , EASL 2007, A 154
Survival of co-infected after liver
transplantation
• 51 patients co-infectés VIH-VHC suivis dans
14 centres et transplantés en 2002-2005 (75 %
d’hommes, 14 % AgHBs+, 16 % avec HCC)
Survie greffons
VIH+
VIH-
• Comparés à 1 177 patients mono-infectés VHC
greffés dans la même période
1 an
82 %
78 %
2 ans
72 %
71 %
• Critères sélection pour transplantation :
3 ans
61 %
65 %
– Pas d’antécédent d’affection classante SIDA
– CD4 >100/mm3
– ARN VIH indétectable ou possibilité
d’indétectabilité
• Résultats/commentaires
– Survie à 3 ans comparable entre patients VIH+
et VIH- (mais suivi médian 1,4 an)
– Résultats meilleurs que dans les autres séries
européennes (France, Royaume Uni)
Survie patients
VIH+
VIH-
1 an
88 %
81%
2 ans
75 %
74 %
3 ans
64 %
69 %
Miro JM et al., ICAAC 2007, A H1732
Summary
 Chronic hepatitis C can be found in 30% of all
HIV-patients
 HCV/HIV coinfected patients show a faster
progression to cirrhosis and increased liverrelated mortality
 With availability of pegylated interferon Hepatitis
C specific treatment options should be considered
before onset of immunodeficiency in HIVcoinfected patients
 HAART should not be withheld in coinfected
patients