• Potential conflict of interest: Nothing to report.


We appreciate the comments of Brady et al. related to our recent study in which we analyzed the survival of hepatitis C virus (HCV)-infected patients with decompensated cirrhosis.1 They raise two very interesting issues.

First, they suggest that highly active antiretroviral therapy (HAART) could be associated with an increased risk of death in HIV/HCV-coinfected patients with advanced liver disease. They support such a hypothesis based on the fact that antiretroviral therapy–induced hepatotoxicity may lead to an enhancement of liver damage. However, an acceleration of liver fibrosis progression in HIV/HCV-coinfected patients has been associated with immunosupression.2 Consequently, immune restoration is expected to influence positively the evolution of liver disease after starting HAART. In our study, 34 (34%) of the 100 HIV-infected deceased patients took HAART, whereas 43 (54%) of 80 coinfected survivors were under HAART (P = .008). This seemingly protective factor is in agreement with other studies in which an association between HAART and a lower liver-related mortality has been observed.3, 4

Second, Brady et al. state that HIV-related central nervous system damage might have been misinterpreted as hepatic encephalopathy (HE) because of the diagnosis criteria we used. However, we think this is very unlikely. In fact, in our hospitals, cerebral computed tomography, brain magnetic resonance imaging, and, in most cases, studies of cerebrospinal fluid are included in routine diagnostic examinations of HIV-infected patients with neurological symptoms. Moreover, measurement of plasma ammonia levels and electroencephalography help us to support the diagnosis of HE. Finally, although there are no specific clinical manifestations of this disorder, symptoms and signs included in a commonly used grading system of HE are required to establish such a diagnosis.5 Thus it is unlikely that a false diagnosis of HE in this population would have occurred.

We agree with Brady and colleagues that prospective studies on the interplay of HIV/HCV infection on liver disease are needed. We are pleased that our study stimulates such questions.

Juan A. Pineda Ph.D.*, José A. García-García M.D.*, * Unidad de Enfermedades Infecciosas, Servicio de Medicina Interna, Hospital Universitario de Valme, Seville, Spain.