The association of HIV viral load with indirect markers of liver injury
- PMID: 22239520
- PMCID: PMC3261587
- DOI: 10.1111/j.1365-2893.2011.01529.x
The association of HIV viral load with indirect markers of liver injury
Abstract
This study assessed the association of HIV RNA with indirect markers of liver injury including FIB-4 index, liver enzymes and platelet counts in a high-risk Hispanic population. The data were derived from a prospective study that included 138 HIV/hepatitis C (HCV)-coinfected and 68 HIV-infected participants without hepatitis C or B co-infection (mono-infected). In unadjusted analyses, detectable HIV viral load (vs undetectable, <400 copies/mL) was associated with a 40% greater odds (OR 1.4, 95% CI: 1.1-1.9, P = 0.016) of FIB-4 > 1.45 in the HIV/HCV-coinfected group and 70% greater odds of FIB-4 > 1.45 (OR 1.7, 95% CI: 1.0-2.8; P = 0.046) in the HIV-mono-infected group. In multivariable analyses, a 1 log(10) increase in HIV RNA was associated with a median increase in FIB-4 of 12% in the HIV/HCV-coinfected group and 11% in the HIV-mono-infected group (P < 0.0001). Among the HIV/HCV-coinfected group, the elevating effect of HIV RNA on FIB-4 was strongest at low CD4 counts (P = 0.0037). Among the HIV-mono-infected group, the association between HIV RNA and FIB-4 was independent of CD4 cell counts. HIV RNA was associated with alterations in both liver enzymes and platelet counts. HIV antiretroviral therapy was not associated with any measure of liver injury examined. This study suggests that HIV may have direct, injurious effects on the liver and that HIV viral load should be considered when these indirect markers are used to assess liver function.
© 2011 Blackwell Publishing Ltd.
Conflict of interest statement
Dr. Forrester does not report any conflicts of interest. Dr. Rhee is an Associate Director in Clinical Research at Gilead Sciences, and reports owning stock and stock options in Gilead Sciences. Dr. McGovern reports serving as a member of scientific advisory boards for Vertex Pharmaceuticals and Merck; and serving on the speaker’s bureau for Roche pharmaceuticals. Dr. Sterling reports serving as a member of scientific advisory boards for Roche, Schering-Plough, Wako Diagnostics, and Vertex Pharmaceuticals; receiving research support from Roche and Bristol-Myers Squibb; and serving on speaker’s bureau for Roche, Schering-Plough, and GlaxoSmithKline. Dr. Knox does not report any conflicts of interest. Dr. Terrin does not report any conflicts of interest.
References
-
- Bica I, McGovern B, Dhar R, et al. Increasing mortality due to end-stage liver disease in patients with human immunodeficiency virus infection. Clin Infect Dis. 2001;32:492–7. - PubMed
-
- Konopnicki D, Mocroft A, de Wit S, et al. Hepatitis B and HIV: prevalence, AIDS progression, response to highly active antiretroviral therapy and increased mortality in the EuroSIDA cohort. AIDS. 2005;19:593–601. - PubMed
-
- Tatsunami S, Taki M, Shirahata A, Mimaya J, Yamada K. Increasing incidence of critical liver disease among causes of death in Japanese hemophiliacs with HIV-1. Acta Haematol. 2004;111:181–4. - PubMed
-
- Selik RM, Byers RH, Dworkin MS. Trends in diseases reported on US death certificates that mention HIV infection, 1987–1999. J Acquir Immune Def Syndr. 2002;29:378–87. - PubMed
-
- Weber R, Sabin CA, Friis-Moller N, et al. Liver-related deaths in persons infected with the human immunodeficiency virus: the D:A:D study. Arch Intern Med. 2006;166:1632–41. - PubMed
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical
Research Materials