Patients were enrolled in the study during the period October 2007 to January 2010 at two large university hospitals in Asturias (northwestern Spain). HIV-1-infected patients older than 18 years who were also coinfected with HCV and had active HCV infection, as determined this website by plasma RNA measurements, were considered for inclusion. At the time of inclusion, the patients underwent a complete clinical and laboratory evaluation, including measurement of HIV-1 and HCV viral loads, CD4 cell counts and liver stiffness, among other parameters. Diverse historical data mainly related
to toxic habits, nadir CD4 cell counts, clinical Centers for Disease Control and BMS-777607 purchase Prevention (CDC) classification and current and past antiretroviral regimens were also recorded. Among these, the date of onset of IDU habit was recorded and used to calculate the estimated date of HCV infection, as the date of the first positive serological analysis was clearly not representative of the true date
of infection. Thus, considering that the vast majority of patients were IDUs, that there is a high prevalence of infection among IDUs in Spain and that it was common practice to share needles several years ago, when most patients became infected, the estimated date of infection was established at 1 year after the onset of the IDU habit. Pregnant patients and those who had an acute episode of cytolysis or cholestasis,
which could influence the transient elastometry (TE) measurements, were excluded. A total of 1066 patients were considered for inclusion, but 61 of them were excluded because TE measurements were technically difficult to obtain or not reliable or because of a lack of HIV-1 RNA measurements. Also, 200 additional HCV-infected patients, as determined by positive serology, were excluded because of a lack of detection of plasma HCV RNA, although their data were also recorded. Therefore, the study group was composed of 805 patients who had active HCV infection, treated or not treated with ART, but who were not receiving anti-HCV therapy at the time of inclusion. Serological diagnosis of HIV-1 and HCV infection was performed on the basis of the presence of specific antibodies by enzyme Beta adrenergic receptor kinase immunoassay (EIA) (MEIA AxSYM; Abbott Diagnostics, Abbott Park, IL, USA). HIV-1 RNA and HCV RNA were measured by quantitative polymerase chain reaction (PCR) (Cobas TaqMan; Roche, Mannheim, Germany). The detection limits were 50 copies/mL for HIV-1 and 40 IU/mL for HCV. HCV genotypes were analysed by line-probe assay (Versant HCV; Siemens, Camberley, UK). Routine biochemical parameters were measured by standardized laboratory methods. The evaluation of liver stiffness was carried out by TE using FibroScan (EchoSens, Paris, France).