This was a multicenter prospective cohort study conducted in seven hospitals in Andalusia, southern Spain. In February 2006, a prospective cohort of HIV/HCV-coinfected with compensated liver cirrhosis, diagnosed on the basis

of LS, was created. From this date, all consecutive HIV-infected patients attending the participant hospitals were enrolled in this cohort if they met the following criteria: (1) HCV coinfection with detectable plasma HCV RNA at inclusion; (2) new diagnosis of liver cirrhosis based on the presence of LS > 14 kPa as measured BAY 73-4506 by TE; (3) no evidence of metabolic or autoimmune liver disease according to clinical history, appropriate laboratory tests, and, when available, histological examination; and (4) No decompensation of liver disease before entering the cohort. Subjects who presented with a liver decompensation or hepatocellular carcinoma (HCC) at the time of cirrhosis diagnosis were excluded. HCC and decompensations of cirrhosis, which included portal hypertensive gastrointestinal Selleck BGJ398 bleeding (PHGB), ascites, hepatorrenal syndrome (HRS), spontaneous bacterial peritonitis (SBP), and hepatic encephalopathy (HE), were diagnosed according to criteria stated elsewhere.3, 4, 25 As stated above, cirrhosis was

diagnosed by TE when LS ≥ 14 kPa was present. This threshold has been demonstrated to accurately predict the presence of cirrhosis in HIV/HCV-coinfected patients, with a reported area under the receiver operating characteristic curve (AUROC) and a positive predictive

value (PPV) for the diagnosis of cirrhosis Endonuclease of 0.95% and 86%, respectively.14 TE examinations were performed by a single experienced operator in each center using the M-probe. In 12 (5%) patients who were overweight and an invalid LS measurement with the M-probe, the XL-probe was used. During follow-up, all individuals enrolled in the cohort were managed according to a specific protocol of care created by the investigator team. Thus, patients were evaluated at least every 6 months. In each visit, an assessment of symptoms and signs of HIV disease or hepatic decompensation was performed and routine hematological, immunological, virological, and biochemical examinations were done. Plasma HIV viral load was measured using a quantitative polymerase chain reaction (PCR) assay (Cobas AmpliPrep-Cobas TaqMan HIV-1 Test, v. 2.0; Roche Diagnostic Systems, Branchburg, NJ). Plasma HCV-RNA load measurements were performed using a quantitative PCR assay according to the available technique at each institution (Cobas AmpliPrep-Cobas TaqMan; Roche Diagnostic Systems, Meylan, France: detection limit of 50 IU/mL; Cobas TaqMan; Roche Diagnostic Systems, Pleasanton, CA: detection limit of 10 IU/mL). Antiretroviral therapy (ART) was prescribed along the follow-up according to the recommendations of international guidelines.