With HGM-3 <0.135 for F<3, 57 patients were correctly identified and two patients were misclassified. We found the presence of F<3 with 96.6% certainty. The negative likelihood ratio (LR) was <0.1 and the diagnostic odds ratio (DOR) was >40. With HGM-3 >0.570 in the EG for F≥3, 31 patients were correctly identified, and five patients were misclassified. We found the presence of F≥3 with 86.1% certainty. The positive LR was >12 and the DOR was >40. For the VG, the diagnostic accuracy values were similar to the values for the EG. HGM-3 appears to be an accurate noninvasive method for the diagnosis

of bridging fibrosis and cirrhosis in HIV/HCV-coinfected patients. HIV infection adversely impacts the natural pathology of hepatitis C virus (HCV) infection, causing a more rapid progression to fibrosis and the development of cirrhosis, TGF-beta family hepatic decompensation, hepatocellular

carcinoma and death [1–5]. For this reason, all HIV-infected individuals should be screened for HCV infection, Gemcitabine and all individuals with positive results for HCV RNA should be candidates for anti-HCV treatment, provided that HIV infection is well controlled and there are no contraindications to therapy with interferon or ribavirin. Grading and staging of liver inflammation and fibrosis are considered essential components of the management of patients with chronic hepatitis C. Patients with bridging fibrosis are at a high risk of developing cirrhosis in the ensuing decade [6], so there is little doubt that these patients as well as patients with established liver cirrhosis have a real need to initiate HCV antiviral therapy. The latter group of patients also need more careful monitoring and additional diagnostic tests including periodic oesophagogastroduodenoscopy to detect oesophageal varices as well as imaging and other techniques to screen for hepatocellular carcinoma. selleck The survival rate of HIV/HCV-coinfected patients with cirrhosis after the first episode of hepatic decompensation is extremely poor [7,8]. Liver biopsy

is still considered the ‘reference standard’ for the assessment of liver fibrosis [9]. However, this procedure has several limitations, including its invasive nature, which can lead to complications, inadequate biopsy size, intra- and inter-observer variability, tissue fragmentation, cost, and low acceptance by most patients [10–12]. In recent years, these limitations have led to the development of alternative noninvasive procedures to measure the degree of liver fibrosis. These methods are currently divided into two main categories: imaging methods, such as transient elastography [13], and assays based on serum biomarkers [14]. The potential advantages of these methods are that they are noninvasive, are easier to perform for patients and clinicians, and can be repeated periodically.