Progression of liver fibrosis in patients coinfected with hepatitis C virus and human immunodeficiency virus undergoing antiretroviral therapy.

As the immunosuppression caused by human immunodeficiency virus (HIV) accelerates the progression of hepatitis C virus (HCV)-related liver fibrosis, the immune reconstitution associated with highly active antiretroviral therapy (HAART) may have the opposite effect. However, hepatotoxicity related to HAART could enhance the progression of liver fibrosis. Some retrospective studies have shown that therapy with the protease inhibitors may be associated with less severe liver fibrosis, whereas nevirapine use seems to correlate with faster progression. Low-grade liver toxicity associated with nevirapine could account for this effect. However, other studies have not confirmed these findings. Long-term prospective studies are needed to analyse the impact of antiretroviral drugs on the progression of HCV-related liver disease. Meanwhile, no specific recommendations can be made on the use of individual drugs or drug classes in HIV/HCV-coinfected patients. Most importantly however, the inherent benefits of HAART largely outweigh the risk of enhancing fibrosis progression. Additionally, in coinfected patients, other factors that promote fibrogenesis, such as alcohol consumption, should be avoided. Antiviral treatment of chronic hepatitis C could also reduce the risk of liver damage associated with HAART.