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Focus on the Liver: Alcohol Use, Highly Active Antiretroviral Therapy, and Liver Disease In HIV-Infected Patients

Since the introduction of highly active antiretroviral therapy (HAART) in the 1990s, liver disease is emerging as a major cause of morbidity and mortality among HIV-infected patients. This is attributed to a variety of factors, including HAART hepatotoxicity, coinfection with hepatitis B and C virus...

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Detalles Bibliográficos
Autores principales: Barve, Shirish, Kapoor, Rama, Moghe, Akshata, Ramirez, Julio A., Eaton, John W., Gobejishvili, Leila, Joshi-Barve, Swati, McClain, Craig J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: National Institute on Alcohol Abuse and Alcoholism 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860514/
https://www.ncbi.nlm.nih.gov/pubmed/23584064
Descripción
Sumario:Since the introduction of highly active antiretroviral therapy (HAART) in the 1990s, liver disease is emerging as a major cause of morbidity and mortality among HIV-infected patients. This is attributed to a variety of factors, including HAART hepatotoxicity, coinfection with hepatitis B and C virus (HBV and HCV, respectively), and alcohol abuse. Several studies have examined the effects of HAART and HCV/HBV coinfection on liver toxicity. However, the impact of alcohol consumption as a cofactor for hepatotoxicity in HIV patients is only beginning to be understood. Similar to the general population, alcohol use is common in the HIV population but is often overlooked by health care providers. Approximately 25 percent of recently diagnosed HIV patients are alcohol dependent; moreover, alcohol dependence has been associated with HIV treatment failure. Alcohol/HAART interactions appear crucial for the development of liver disease in HIV patients. Recent research has shown that alcohol abuse is associated with severe hepatotoxicity in patients on HAART. Importantly, alcoholic- and HAART-induced liver disease share many potential mechanisms of injury, including altered metabolism of certain signaling molecules (i.e., cytokines) and dysfunction of some cell components (i.e., proteasomes and mitochondria).