Liver fibrosis in HIV: which role does HIV itself, long-term drug toxicities and metabolic changes play?

Abstract

Liver disease is one of the main causes of non-AIDS death in HIV-infected individuals from Europe and North America and has been attributed mainly to coinfection with hepatotropic viruses. However, HIV-induced inflammation as well as long-term antiretroviral drug toxicity may also contribute to clinical relevant liver disease. Therefore, a better understanding of liver disease beyond viral hepatitis coinfection is urgently needed in HIV-infected individuals. Cross-sectional fibroscan studies in HIV-infected patient populations have reported unexpectedly high rates of advance fibrosis in HIV-infected patients even without underlying viral hepatitis or alcohol abuse suggesting that HIV itself may contribute independently to liver disease. Finally, HIV therapy itself either through direct hepatotoxicity or long-term metabolic changes, such as dyslipidemia and/or insulin resistance, may additionally cause liver damage in life long treatment. Therefore, aging of the liver in HIV may play a much more pivotal role in the future considering age-related effects, coinfection with hepatotropic viruses and the toxicity of long-term antiviral treatment. Thus, adequate monitoring of liver disease and development of management algorithms are clearly needed to optimize outcome and care of the aging liver in an HIV-infected individual.