Abstract
After the introduction of antiretroviral treatment (ART) back in 1996, the lifespan of people living with HIV (PLWH) has been substantially increased, while the major causes of morbidity and mortality have switched from opportunistic infections and AIDS-related neoplasms to cardiovascular and liver diseases. HIV itself may lead to liver damage and subsequent liver fibrosis (LF) through multiple pathways. Apart from HIV, viral hepatitis, alcoholic and especially non-alcoholic liver diseases have been implicated in liver involvement among PLWH. Another well known cause of hepatotoxicity is ART, raising clinically significant concerns about LF in long-term treatment. In this review we present the existing data and analyze the association of LF with all ART drug classes. Published data derived from many studies are to some extent controversial and therefore remain inconclusive. Among all the antiretroviral drugs, nucleoside reverse transcriptase inhibitors, especially didanosine and zidovudine, seem to carry the greatest risk for LF, with integrase strand transfer inhibitors and entry inhibitors having minimal risk. Surprisingly, even though protease inhibitors often lead to insulin resistance, they do not seem to be associated with a significant risk of LF. In conclusion, most ART drugs are safe in long-term treatment and seldom lead to severe LF when no liver-related co-morbidities exist.
Highlights
The human immunodeficiency virus (HIV) infection constitutes a major global public health issue, affecting 37 million people worldwide, of whom 34 million are adults [1]
After the introduction of antiretroviral treatment (ART) back in 1996, the leading causes of morbidity and mortality among people living with HIV (PLWH) in industrialized countries have switched to non-acquired immune deficiency syndrome (AIDS) related events, especially cardiovascular and liver disorders [2,3,4,5]
In a study of 201 HIV/HCV co-infected patients whose liver fibrosis (LF) was assessed by a liver biopsy, Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) and especially NVR were found to be associated with a low probability of significant LF, a finding not observed in patients treated with Protease Inhibitors (PIs) [108]
Summary
The human immunodeficiency virus (HIV) infection constitutes a major global public health issue, affecting 37 million people worldwide, of whom 34 million are adults [1]. After the introduction of antiretroviral treatment (ART) back in 1996, the leading causes of morbidity and mortality among people living with HIV (PLWH) in industrialized countries have switched to non-AIDS related events, especially cardiovascular and liver disorders [2,3,4,5]. NAFLD especially affects a growing number of PLWH [17,18,19,20,21] since eating habits, drugs used in ART and HIV infection per se promote liver steatosis, steatohepatitis and subsequent liver fibrosis (LF), cirrhosis and hepatocellular carcinoma [19,20,21,22,23,24]. The potential pathophysiological pathways leading to liver damage and the existing data regarding the real risk of LF for each antiretroviral drug will be discussed
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