icon-    folder.gif   Conference Reports for NATAP  
 
  20th Conference on Retroviruses and
Opportunistic Infections
Atlanta, GA March 3 - 6, 2013
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Does persistent hepatitis C viremia lead to advanced liver fibrosis progression early after acute hepatitis C infection in HIV coinfection?
 
 
  Reported by Jules Levin
CROI 2013
 
from Jules: this study goes to the point ,that has been controversial, does an HIV+ person who contracts acute HCV have a increased risk for developing more advanced/accelerated fibrosis, advanced liver disease, in a short time span. In this case 12% of MSM in Europe who contracted acute HCV developed advanced liver fibrosis. The poster is not clear but presumably these men already had HIV before getting acute HCV, and that is part of the premise, that the immune system is damaged due to having HIV already so then contracting acute HCV may have a more accelerated track to advanced liver disease, there has been controversy with some researchers not believing this and others do, I think it has merit, that these individuals are at increased risk, in this study 12% developed advanced liver disease, median follow-up time was 130 weeks (IQR 60-228). The next point was raised by Daniel Fierer at CROI , was a study he presented, and he has been at the forefront in reporting the data of accelerated fibrosis risk for these men who contract acute HCV after having had HIV, the study Fierer presented at CROI was to treat acutely HCV infected HIV+ MSM with triple telaprevir+P/R therapy during acute or early infection. Here is link to his study, which received some criticism because 65% of the study participants were CC genotype, easier to treat, and although the overall SVR/response rate was good, about 80-85%, the of the 7 harder-to-treat non-CC patients 3 failed, so although it does make sense to treat acute HCV as prior studies have shown better response rates, this study had some gaps. However in the future when we have IFN-free oral HCV regimens with very high, 95-100% cure rates with 12 weeks therapy, there will be studies treating acute HCV and I expect this will be a paradigm: to identify acutely HCV-infected either mono or coinfected & treat right away.
 
CROI: Treatment of Acute HCV in HIV-infected MSM Incorporating Telaprevir - (03/13/13)
 
Christoph Boesecke1, Thomas Reiberger2, Stefan Mauss3, Hans-Jurgen Stellbrink4, Mattias Mandorfer2, Mark Nelson5, Sanjay Bhagani6, Marc-Antoine Valantin7, Patrick Ingiliz8, Jurgen K. Rockstroh1, and the NEAT study group Bonn University Hospital, Bonn, Germany; 2) Medical University of Vienna, Vienna, Austria; 3) Center for HIV and Hepatogastroenterology, Dusseldorf, Germany; 4) ICH Study Center, Hamburg, Germany; 5) Chelsea and Westminster Hospital, London, UK; 6) Royal Free Hospital, London, UK; 7) AP-HP, Hopital La Pitie Salpetriere, Paris, France; 8) MiB, Berlin, Germany
 
CONCLUSIONS
 
Advanced liver fibrosis within the first years after acute hepatitis C infection in HIV-positive patients occurs in up to 12% of patients, mostly in patients with persistent hepatitis C viremia. This highlights the need for early identification of new cases of AHC and timely initiation of antiviral treatment to benefit from higher chances of treatment induced clearance in the acute phase of HCV infection.
 
ABSTRACT
 
Background: The epidemic of sexually transmitted acute hepatitis C (AHC) infection among HIV-seropositive MSM is still ongoing. The rate of liver fibrosis progression after AHC is of particular interest as more advanced fibrosis progression has been claimed in retrospective case series from HIV infected subjects following acute HCV. Here we prospectively evaluate the impact of persistent hepatitis C viremia on liver fibrosis progression after AHC in HIV coinfection.
 
Methods: 122 HIV-infected patients from 3 European countries with diagnosed acute HCV infection were followed prospectively and evaluated for liver fibrosis by means of transient elastography. A value >9.0kPa was considered as advanced fibrosis. Fisher's exact, chi-square and Mann-Whitney U test were used for statistical analysis.
 
Results: All patients were male, median age was 42 years. Main routes of transmission were MSM (93.4%) and IVDU (5.7%). In 73% of patients clinical symptoms of acute hepatic infection were missing. 80% of patients were infected with HCV GT 1, 4.2% with GT 3 and 15.8% with GT 4. Median baseline HCV RNA was 1.700.000IU/ml and median CD4 T cell count 546 cells/ul. 84.3% of all patients received cART, 75.7% had baseline HIV RNA <200cop/ml. Median ALT was 352 U/l. Median follow-up time was 130 weeks (IQR 60-228). 61.5% of all patients cleared AHC (10.7% spontaneously and 50.8% by successful HCV therapy), 38.5% had persistent viremia (13.9% chronic course or 24.6% with unsuccessful treatment). By univariate analysis, there were no statistical differences at baseline for HCV or HIV characteristics between viremic and aviremic patients.
 
Overall 11.5% (14/122) of all patients developed advanced liver fibrosis during follow-up. Advanced fibrosis developed significantly more often in viremic patients (9/46) than in patients with AHC clearance (5/76) (19.6% vs. 6.6% respectively; p=0.04). There was no significant correlation between advanced fibrosis and follow-up time, BMI, alcohol or drug abuse, diabetes, lipodystrophie, cART duration, or exposure to d-drugs.
 
Conclusions: Advanced liver fibrosis within the first years after acute hepatitis C infection in HIV-positive patients occurs in up to 12% of patients, mostly in patients with persistent hepatitis C viremia. This highlights the need for early identification of new cases of AHC and timely initiation of antiviral treatment to benefit from higher chances of treatment induced clearance in the acute phase of HCV infection.
 
BACKGROUND
 
The epidemic of sexually transmitted acute hepatitis C (AHC) infection among HIV-seropositive MSM is still ongoing. The rate of liver fibrosis progression after AHC is of particular interest as more advanced fibrosis progression has been claimed in retrospective case series from HIV infected subjects following acute HCV. Here we prospectively evaluate the impact of persistent hepatitis C viremia on liver fibrosis progression after AHC in HIV coinfection.
 
Methods
 
122 HIV-infected patients from 3 European countries with diagnosed acute HCV infection were followed prospectively and evaluated for liver fibrosis by means of transient elastography. A value >9.0kPa was considered as advanced fibrosis. Fisher's exact, chi-square and Mann-Whitney U test were used for statistical analysis.
 
RESULTS
 
All patients were male, median age was 42 years. Main routes of transmission were MSM (93.4%) and IVDU (5.7%). In 73% of patients clinical symptoms of acute hepatic infection were missing. 80% of patients were infected with HCV GT 1, 4.2% with GT 3 and 15.8% with GT 4. Median baseline HCV RNA was 1.700.000IU/ml and median CD4 T cell count 546 cells/μl. 84.3% of all patients received cART, 75.7% had baseline HIV RNA <200cop/ml. Median ALT was 352 U/l. Median follow-up time was 130 weeks (IQR 60-228) (see table 1).

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