Mitochondrial toxicity associated with HAART following liver transplantation in an HIV-infected recipient

✍ Scribed by Charalambos Antoniades; Candice Macdonald; Alexander Knisely; Christopher Taylor; Suzanne Norris

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 136 KB
• Volume: 10
• Category: Article
• ISSN: 1527-6465
• DOI: 10.1002/lt.20109

✦ Synopsis

Antiretroviral therapy is not uncommonly associated with drug toxicities, and hepatotoxicity occurs in approximately 20% of individuals prescribed antiretroviral therapy. Mitochondrial toxicity causing lactic acidosis is a rare but fatal complication that has been described in some HIV-infected patients treated with nucleoside analogue reverse transcriptase inhibitors. In this report, we describe the course of an HIV-infected patient receiving antiretroviral therapy who developed lactic acidosis after liver transplantation for HCV-induced liver disease. (Liver Transpl 2004;10:699-702.)

H ighly active antiretroviral therapy (HAART) has significantly increased the life expectancy of patients infected with human immunodeficiency virus (HIV) 1 in whom HAART also has unmasked hepatitis C virus (HCV) -related comorbidity and mortality. HCV coinfection is now the leading cause of significant illness and death in HIV-infected persons, 2 -5 and HCV-related liver disease has become the most common reason for admission to HIV wards. 4,5 In Western Europe and the United States, 33% of HIV-infected persons are coinfected with HCV. Hepatotoxicity occurs in almost 20% individuals on HAART 6 -13 and frequently in those with HCV-related liver disease. Mitochondrial toxicity can manifest as lactic acidosis, hepatic steatosis, or peripheral neuropathy. We describe the course of an HIV-infected patient receiving HAART who developed severe lactic acidosis after liver transplantation (LT) for HCV-related liver disease.