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HBeAg, hepatitis B e antigen; HCC, hepatocellular carcinoma.
 
This slide highlights the risk of cancer. A patient can progress to cancer from any of the 4 highlighted states.
These data are consistent with a recent observation in the French GERMIVIC cohort. In this cohort in 2003 proportion of liver related death shows a slight decrease and there is a stabilization from 2001 to 2003 after some years of progressive increase. In the same period the proportion of liver related death occurring in HBsAg positive subjects  showed a sharp decrease. These data indirectly support the hypothesis that HBV related mortality is decreasing with the availability of anti-retrovirals with anti HBV activity and that this decrease is one of the causes in the stabilization of liver related mortality observed in HIV infected patients in some very recent reports.
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Audsley J, et al. (#63)
Background
Entecavir (ETV) is a guanosine analogue approved for the treatment of HBV and possesses in vitro anti-HBV and anti-HIV activity.
Entecavir has been previously described to induce a key mutation (M184V) associated with resistance to NRTIs approved for the treatment of HIV.
Methods
The objective was to further characterize entecavir’s anti-HIV activity and to determine risk factors associated with development of the M184V mutation.
HIV RNA viral load, HBV DNA viral loads, HIV polymerase sequencing and other clinical data was abstracted from the medical records from July 2004 and while receiving entecavir monotherapy (until July 2007).
Results
A median 1 log10 reduction in HIV RNA viral load (range 0.5 – 2) after a median of 113 days (17 – 291) of entecavir monotherapy occurred in ART-naïve patients.
A median 1.1 log10 reduction in HIV RNA viral load (range 0.1 – 2.3) after a median of 96 days (range 75 – 215) of entecavir monotherapy occurred in ART-naïve patients.
12 of 17 HBV/HIV patients who received ETV monotherapy demonstrated a 0.5 log10 reduction in HIV RNA VL or greater, including 7 of the 10 ART naïve patients and 5 of the 7 ART-experienced patients.
4 patients had a rebound of HIV RNA VL of 0.5 log10 or greater after achieving a nadir HIV RNA VL.
The graphic on the bottom left of the slide depicts the rates of M184V development. 
Conclusions
ETV monotherapy resulted in clinically significant reduction in HIV RNA in the majority of patients and can select for the M184V mutation.
ETV should not be used as monotherapy in HIV/HBV co-infected patients.
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Soriano V, et al. PS8/1
Background
It is unknown which determine the rate of spontaneous clearance of HCV in HIV + patients
Goal: To characterize anti-HCV Ab+ HIV-infected patients within the EuroSIDA cohort with regard to level of serum HCV-RNA and genotype distribution
Methods
All anti-HCV Ab+, interferon-naive patients were examined for serum HCV-RNA (lower limit of detection: 615 IU/ml) and HCV genotype.
Logistic regression was used to identify which variables were associated with HCV-genotype 1 (HCV-1) infection and spontaneous HCV clearance, after adjustment for demographic, clinical and therapeutic factors.
Results
Injecting drug users were less likely to have cleared spontaneously HCV infection compared to men-having-sex-with-men (22% vs 34%, adjusted odds ratio(aOD)=0.43(95%CI:0.32-0.58), whereas persons infected with HBV (HBsAg+) were more likely to have cleared HCV infection (46% in HBsAg+ vs 25% in HBsAg-, aOD=2.48 (95%CI:1.82- 3.38).
Being female (aOD=0.72(0.56-0.92) and older age [aOD=0.78/10 years older, (0.67-0.92)] were also independently associated with a lower odds of being infected with HCV-1, whereas having a higher HCV-RNA level was associated with increased odds of HCV-1 [1.29/log10 HCV-RNA (1.14-1.47)].
Conclusions
3/4 of HIV patients with detectable anti-HCV Ab in EuroSIDA show active HCV replication.
Viremia was more likely in injecting drug-users and in persons not chronically infected with HBV.
Of patients with active HCV replication, 53% were infected by HCV-1. HCV-1 infection was associated with higher HCV-RNA-load and male gender, and less prevalent in Eastern Europe.
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Slide Ribavirin in HIV/HCV Co-infection
Ribavirin causes anemia particularly in patients receiving AZT aNR other pyrimidine nucleoside analogs. The hemolytic anemia appears to be dose depeNRent aNR respoNRs to dose reduction or treatment with erythropoietin.
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Cette étude rétrospective a inclus 426 patients entre 2002 et 2005 dans 3 hôpitaux espagnols.
Elle retrouve l’impact négatif de l’Abacavir sur la réponse au traitement par PEG-IFN + RBV confirmant les données récentes issues de l’étude RIBAVIC.
La disparition de cet effet négatif, ou son caractère moins marqué, chez les malades ayant des taux sériques élevés de RIBAVIC suggère aux auteurs l’existence d’une inhibition compétitive entre les deux molécules lors des étapes de la phosphorylation intra-cellulaire. Le caractère rétrospectif de l’étude et le nombre relativement faible de malades ayant bénéficié de dosage de Ribavirine invite néanmoins à la prudence quant à ces conclusions.
Ces résultats et ceux de l’étude RIBAVIC conduisent bien sur à s’interroger sur le maintien d’un traitement par abacavir après celui de la ddI, de la d4T et de l’AZT lors d’un traitement anti-VHC. S’ils sont confirmés, ils réduisent de façon très importante la possibilité d’utiliser les analogues de nucléosides dans cette situation.
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