title: Impact of highly active antiretroviral therapy on the spectrum of liver disease in HCV-HIV coinfection.
abstract: OBJECTIVE
  Hepatitis C virus (HCV) coinfection is common in patients with human immunodeficiency virus (HIV) infection. The mortality associated with HIV has decreased dramatically with the introduction of highly active antiretroviral therapy (HAART). However, the impact of HAART, including protease inhibitors (PIs), nucleoside reverse-transcriptase inhibitors (NRTIs), and non-NRTIs (NNRTIs), on the spectrum of HCV-related liver disease remains unclear. The purpose of this retrospective analysis is to determine the impact of PI and NNRTI use on liver histological characteristics in patients with stable HIV-HCV coinfection (n = 101) compared with HIV-uninfected controls with HCV infection (n = 302).
  
  
  METHODS
  The majority of coinfected patients were men (75%), African American (82%), and had genotype 1 HCV (91%). Mean HIV load was 1.52 log copies/mL, 48% had undetectable HIV RNA and a mean CD4 count of 528 cells/microL, and 11% had a CD4 count < 200 cells/microL. Both mean alanine aminotransferase (ALT) level (83 U/L; 54% had a normal ALT level) and Knodell Histological Activity Index score (7.04; 33% had advanced fibrosis) were similar to those of our control population. Ninety-three percent of patients were administered a mean of 3 antiretroviral medications: NRTIs in 98%, NNRTIs in 45%, and PIs in 54%.
  
  
  RESULTS
  There were no significant differences in biochemical or histological parameters between patients administered or not administered PIs or NNRTIs.
  
  
  CONCLUSIONS
  In this uncontrolled retrospective analysis, we were unable to show a significant impact of either PI or NNRTI use on the spectrum of liver disease.
authors.affiliation: Virginia Commonwealth University, Medical College of Virginia, Richmond, USA. rksterli@hsc.vcu.edu
authors.forename: Richard K
authors.initials: RK
authors.lastname: Sterling
authors.forename: Mary S
authors.initials: MS
authors.lastname: Wilson
authors.forename: Arun J
authors.initials: AJ
authors.lastname: Sanyal
authors.forename: Velimir A
authors.initials: VA
authors.lastname: Luketic
authors.forename: R Todd
authors.initials: RT
authors.lastname: Stravitz
authors.forename: Melissa J
authors.initials: MJ
authors.lastname: Contos
authors.forename: A Scott
authors.initials: AS
authors.lastname: Mills
authors.forename: Mitchell L
authors.initials: ML
authors.lastname: Shiffman
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000453:epidemiology*; D016174:Hepacivirus / Q000235:genetics; D006526:Hepatitis C / Q000097:blood / Q000453:epidemiology* / Q000473:pathology*; D006801:Humans; D008099:Liver / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011480:Protease Inhibitors / Q000627:therapeutic use*; D012367:RNA, Viral / Q000032:analysis; D012189:Retrospective Studies; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use*
chemical_list: D011480:Protease Inhibitors; D012367:RNA, Viral; D018894:Reverse Transcriptase Inhibitors; D000410:Alanine Transaminase