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Curr Opin HIV AIDS. 2014 Jul;9(4):365-70. doi: 10.1097/COH.0000000000000064.

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

Author information

1
aDepartment of Medicine I, University Hospital Bonn bGerman Centre for Infection Research (DZIF), partner site Bonn-Cologne, Bonn cDepartment of Medicine, University Hospital Hannover dGerman Centre for Infection Research (DZIF), partner site Hannover, Hannover, Germany.

Abstract

PURPOSE OF REVIEW:

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.

RECENT FINDINGS:

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.

SUMMARY:

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.

PMID:
24840057
DOI:
10.1097/COH.0000000000000064
[Indexed for MEDLINE]

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