Slower fibrosis progression in HIV/HCV-coinfected patients with successful HIV suppression using antiretroviral therapy

Bräu, Norbert; Salvatore, Mirella; Ríos-Bedoya, Carlos F.; Fernández-Carbia, Alberto; Paronetto, Fiorenzo; Rodríguez-Orengo, José F.; Rodríguez-Torres, Maribel; for the Puerto Rico-New York Hepatitis Study Group,

doi:10.1016/j.jhep.2005.07.006

« Previous Next »Journal of Hepatology
Volume 44, Issue 1 , Pages 47-55, January 2006

Slower fibrosis progression in HIV/HCV-coinfected patients with successful HIV suppression using antiretroviral therapy☆

Norbert Bräu
- Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine, New York, NY, USA
- Corresponding author. Address: Bronx VA Medical Center, Infectious Diseases Section (111F), 130 West Kingsbridge Road, Bronx NY 10468. Tel.: +1 718 584 9000x6672; fax: +1 718 367 4850.
Mirella Salvatore
- Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine, New York, NY, USA
Carlos F. Ríos-Bedoya
- Ponce School of Medicine, Ponce, PR, USA
Alberto Fernández-Carbia
- University Pathologists, San Juan, PR, USA
Fiorenzo Paronetto
- Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine, New York, NY, USA
José F. Rodríguez-Orengo
- University of Puerto Rico School of Medicine, San Juan, PR, USA
Maribel Rodríguez-Torres
- Ponce School of Medicine, Ponce, PR, USA
- Fundación de Investigación de Diego, San Juan, PR, USA
for the Puerto Rico-New York Hepatitis Study Group

Received 2 March 2005; received in revised form 27 June 2005; accepted 1 July 2005. published online 28 July 2005.

Background/Aims

HIV/HCV-coinfected patients reportedly have a faster fibrosis progression rate (FPR) than HCV-monoinfected patients. This study examined whether HIV suppression through highly active antiretroviral therapy (HAART) attenuates this accelerated fibrosis progression.

Methods

In two hepatitis C centers, a retrospective analysis identified 656 consecutive treatment-naïve HCV-infected patients who had undergone a liver biopsy, had a presumed date of HCV infection, and had been tested for HIV, 274 of them HIV-positive (95.2% on HAART) and 382 HIV-negative. The primary outcome measure was the FPR, defined as Ishak fibrosis score [0–6] over estimated duration of HCV infection.

Results

Among HIV/HCV-coinfected patients, 51.2% had undetectable HIV RNA (<400copies/mL). There was no difference in FPR between HIV/HCV-coinfected and HCV-monoinfected patients (0.136 vs. 0.128 Ishak fibrosis units/year, P=0.29). However, HIV/HCV-coinfected patients with any detectable HIV viral load >400copies/mL had a faster FPR (0.151) than HCV-monoinfected patients (0.128, P=0.015) and than HIV/HCV-coinfected patients with undetectable plasma HIV RNA (0.122, P=0.013) who in turn had the same FPR as HCV-monoinfected subjects (0.128, P=0.52). An accelerated FPR in HIV viremic patients was seen with CD4+ cells <500/mm³ (0.162 vs. 0.123, undetectable HIV RNA, P=0.005) but not with CD4+ cells >500/mm³ (0.118 vs. 0.121, P=0.89). In multivariable linear regression analysis of HIV/HCV-coinfected patients, log₁₀ HIV RNA level, necroinflammation, and age at HCV infection were independently correlated to FPR, but not alcohol use or CD4+ cell count (r²=0.45 for model).

Conclusions

HIV/HCV-coinfected patients with undetectable HIV RNA through HAART have a slower FPR than those with any HIV RNA level and an FPR similar to HCV-monoinfected individuals.

Keywords: Hepatitis C, HIV, Viral load, Fibrosis progression, Highly-active antiretroviral therapy

Abbreviations: HCV, hepatitis C virus, HIV, human immunodeficiency virus, HAART, highly active antiretroviral therapy, IDU, injection drug use, ALT, alanine aminotransferase, FPR, fibrosis progression rate, IshFU/yr, Ishak fibrosis units per year