title: Human immunodeficiency virus, hepatitis C, and inflammatory biomarkers in individuals with alcohol problems: a cross-sectional study.
abstract: BACKGROUND
  Assessing whether hepatitis C (HCV) co-infection with human immunodeficiency virus (HIV) is associated with increased inflammation is complex. The liver, integral to inflammatory biomarker synthesis, is compromised by HCV and alcohol abuse. Using single liver-synthesized biomarkers (e.g. C-reactive protein) to represent inflammation may not be appropriate in HIV/HCV co-infection. We hypothesized that 1) detectable HIV/HCV RNA was independently associated with increased inflammation; 2) a composite inflammation measure describes inflammation differently from single inflammatory biomarkers.
  
  
  METHODS
  We compared inflammation by HIV/HCV group in a cohort of 361 HIV infected participants from the HIV-Longitudinal Interrelationships of Viruses and Ethanol study. Inflammatory biomarkers >75th percentile were considered elevated. Associations between HIV/HCV group and elevated biomarkers were analyzed as a composite measure (inflammatory burden) or individually. We defined inflammatory burden as number of concurrently elevated biomarkers. Biomarkers included interleukin-6 (IL-6), C-reactive protein (CRP), cystatin C, serum amyloid-A (SAA), tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10). Covariates: alcohol, liver fibrosis, comorbidities, CD4 count, antiretroviral therapy, substance use.
  
  
  RESULTS
  Detectable HIV and HCV RNA (OR = 2.49; 95% CI = 1.05-5.89) and detectable HCV RNA alone (2.95; 1.08-8.01) were independently associated with increased odds of having a greater inflammatory burden compared to undetectable viremia. Elevated IL-10 (7.79; 1.90-31.97) and TNF-α (7.70; 1.42-41.83) were independently associated with detectable HIV and HCV RNA. Elevated IL-10 was also associated with detectable HCV RNA alone (5.51; 1.17, 25.84).
  
  
  CONCLUSIONS
  Detectable HIV and HCV replication versus undetectable replication was associated with inflammatory burden and certain inflammatory biomarkers independently of alcohol consumption, liver fibrosis and other comorbidities.
authors.affiliation: Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA, USA. freibergms@upmc.edu.
authors.forename: Kaku A
authors.initials: KA
authors.lastname: Armah
authors.forename: Emily K
authors.initials: EK
authors.lastname: Quinn
authors.forename: Debbie M
authors.initials: DM
authors.lastname: Cheng
authors.forename: Russell P
authors.initials: RP
authors.lastname: Tracy
authors.forename: Jason V
authors.initials: JV
authors.lastname: Baker
authors.forename: Jeffrey H
authors.initials: JH
authors.lastname: Samet
authors.forename: Matthew S
authors.initials: MS
authors.lastname: Freiberg
mesh_terms: D000328:Adult; D000428:Alcohol Drinking / Q000097:blood / Q000276:immunology*; D015415:Biomarkers / Q000097:blood; D015331:Cohort Studies; D060085:Coinfection / Q000097:blood / Q000276:immunology / Q000821:virology; D003430:Cross-Sectional Studies; D005260:Female; D015658:HIV Infections / Q000097:blood / Q000276:immunology* / Q000821:virology; D006526:Hepatitis C / Q000097:blood / Q000276:immunology* / Q000821:virology; D006801:Humans; D008297:Male; D008875:Middle Aged
chemical_list: D015415:Biomarkers