BACKGROUND: In HIV and hepatitis C virus (HCV) coinfected patients, the role of antiretroviral therapy (ART) on hepatic steatosis (HS) remains controversial. METHODS: HIV/HCV coinfected patients receiving ART and previously untreated for HCV who underwent a liver biopsy were included. Cumulative duration of exposure to each antiretroviral was recorded up to liver biopsy date. Logistic regression analyses evaluated factors associated with steatosis and its severity. RESULTS: 184 patients were included: median age 41 years, 84% male, 89% Caucasian, 61% with a past history of intravenous drug use. HCV genotypes were 1 (55%), 2 (6%), 3 (26%), and 4 (13%). Median HCV-RNA was 6.18 log10 IU/ml. HIV-RNA was undetectable (<400 copies/ml) in 67% of patients. Median CD4 count was 321/mm3. All patients had been exposed to nucleoside reverse transcriptase inhibitors (median cumulative exposure 56 months); 126 received protease inhibitors (23 months), and 79 non-nucleoside reverse transcriptase inhibitors (16 months). HS was observed in 102 patients (55%): 41% grade 1; 5% grade 2, and 9% grade 3. In multivariate analysis, HCV genotype 3 and HCV viral load were moderately associated with mild steatosis but strongly with grade 2-3 steatosis. After adjustment for the period of biopsy, no association was detected between HS and exposure to any antiretroviral class or drug, or duration of ART globally or comparing genotype 3 to others. CONCLUSIONS: Among our ART-treated HIV-HCV cohort predominantly infected with genotype 1, 55% of patients had HS which was associated with HCV-related factors, but not ART class or duration of exposure.
BACKGROUND: In HIV and hepatitis C virus (HCV) coinfected patients, the role of antiretroviral therapy (ART) on hepatic steatosis (HS) remains controversial. METHODS:HIV/HCV coinfectedpatients receiving ART and previously untreated for HCV who underwent a liver biopsy were included. Cumulative duration of exposure to each antiretroviral was recorded up to liver biopsy date. Logistic regression analyses evaluated factors associated with steatosis and its severity. RESULTS: 184 patients were included: median age 41 years, 84% male, 89% Caucasian, 61% with a past history of intravenous drug use. HCV genotypes were 1 (55%), 2 (6%), 3 (26%), and 4 (13%). Median HCV-RNA was 6.18 log10 IU/ml. HIV-RNA was undetectable (<400 copies/ml) in 67% of patients. Median CD4 count was 321/mm3. All patients had been exposed to nucleoside reverse transcriptase inhibitors (median cumulative exposure 56 months); 126 received protease inhibitors (23 months), and 79 non-nucleoside reverse transcriptase inhibitors (16 months). HS was observed in 102 patients (55%): 41% grade 1; 5% grade 2, and 9% grade 3. In multivariate analysis, HCV genotype 3 and HCV viral load were moderately associated with mild steatosis but strongly with grade 2-3 steatosis. After adjustment for the period of biopsy, no association was detected between HS and exposure to any antiretroviral class or drug, or duration of ART globally or comparing genotype 3 to others. CONCLUSIONS: Among our ART-treated HIV-HCV cohort predominantly infected with genotype 1, 55% of patients had HS which was associated with HCV-related factors, but not ART class or duration of exposure.
Authors: Arun J Sanyal; Melissa J Contos; Richard K Sterling; Velimir A Luketic; Mitchell L Shiffman; R Todd Stravitz; A Scott Mills Journal: Am J Gastroenterol Date: 2003-09 Impact factor: 10.864
Authors: Luz Martín-Carbonero; Yves Benhamou; Massimo Puoti; Juan Berenguer; José Mallolas; Carmen Quereda; Ana Arizcorreta; Antonio Gonzalez; Jurgen Rockstroh; Victor Asensi; Pilar Miralles; Montse Laguno; Leonor Moreno; José Antonio Girón; Martin Vogel; Javier García-Samaniego; Marina Nuñez; Miriam Romero; Santiago Moreno; Juan José de la Cruz; Vincent Soriano Journal: Clin Infect Dis Date: 2003-12-08 Impact factor: 9.079
Authors: Ke-Qin Hu; Namgyal L Kyulo; Eric Esrailian; Kevin Thompson; Resa Chase; Donald J Hillebrand; Bruce A Runyon Journal: J Hepatol Date: 2004-01 Impact factor: 25.083
Authors: A H Mohsen; P J Easterbrook; C Taylor; B Portmann; R Kulasegaram; S Murad; M Wiselka; S Norris Journal: Gut Date: 2003-07 Impact factor: 23.059