Human immunodeficiency virus, hepatitis C, and inflammatory biomarkers in individuals with alcohol problems: a cross-sectional study
1 Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA, USA
2 Data Coordinating Center, Boston University School of Public Health, Boston, MA, USA
3 Clinical Addiction Research and Education (CARE) Unit, Section of General Internal Medicine, Boston Medical Center and Boston University School of Medicine, Boston, MA, USA
4 Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA
5 Departments of Pathology and Biochemistry, College of Medicine, University of Vermont, Burlington, VT, USA
6 Department of Medicine, University of Minnesota, Hennepin County Medical Center, Minnesota, MN, USA
7 Department of Community Health Sciences, Boston University School of Public Health, Boston, MA, USA
8 Division of General Internal Medicine, Center for Research on Health Care, University of Pittsburgh Medical Center, 230 McKee Pl, Suite 600, Pittsburgh, PA 15213, USA
BMC Infectious Diseases 2013, 13:399 doi:10.1186/1471-2334-13-399Published: 29 August 2013
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.
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.
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).
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.