title: Hepatic steatosis in HIV-HCV coinfected patients receiving antiretroviral therapy is associated with HCV-related factors but not antiretrovirals.
abstract: 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.
authors.affiliation: Service de Mdecine Interne et Immunologie Clinique, Assistance Publique-Hpitaux de Paris, INSERM UMR_S 996, Universit Paris Sud, Hpital Antoine Bclre, 157 Rue de la Porte de Trivaux, 92141 Clamart, France. valerie.martinez@abc.aphp.fr
authors.forename: Valrie
authors.initials: V
authors.lastname: Martinez
authors.forename: Thi Dieu Ngan
authors.initials: TD
authors.lastname: Ta
authors.forename: Zahra
authors.initials: Z
authors.lastname: Mokhtari
authors.forename: Marguerite
authors.initials: M
authors.lastname: Guiguet
authors.forename: Patrick
authors.initials: P
authors.lastname: Miailhes
authors.forename: Marc-Antoine
authors.initials: MA
authors.lastname: Valantin
authors.forename: Frderic
authors.initials: F
authors.lastname: Charlotte
authors.forename: Philippe
authors.initials: P
authors.lastname: Bertheau
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Molina
authors.forename: Christine
authors.initials: C
authors.lastname: Katlama
authors.forename: Eric
authors.initials: E
authors.lastname: Caumes
mesh_terms: D000328:Adult; D044966:Anti-Retroviral Agents / Q000627:therapeutic use; D060085:Coinfection / Q000150:complications* / Q000188:drug therapy / Q000821:virology; D005234:Fatty Liver / Q000150:complications*; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy / Q000821:virology; D016174:Hepacivirus / Q000235:genetics / Q000502:physiology; D006526:Hepatitis C / Q000150:complications* / Q000188:drug therapy / Q000821:virology; D054884:Host-Pathogen Interactions; D006801:Humans; D008099:Liver / Q000473:pathology / Q000821:virology; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012189:Retrospective Studies; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use; D018570:Risk Assessment / Q000379:methods; D012307:Risk Factors; D012720:Severity of Illness Index; D019562:Viral Load
chemical_list: D044966:Anti-Retroviral Agents; D018894:Reverse Transcriptase Inhibitors