Rosen, Ann K. Daly, Lucy Golden-Mason “
“The purpose of this study was to evaluate the usefulness of liver stiffness measurement (LSM) for assessing the risk of hepatocellular carcinoma (HCC) in chronic hepatitis C (CHC) patients receiving interferon (IFN) therapy. One hundred fifty-one CHC patients who underwent LSM and received IFN therapy were included in the estimation

cohort, and 56 were included in the validation study. The cumulative HCC incidences were evaluated using Venetoclax supplier Kaplan–Meier plot analysis and the log-rank test. Multivariate Cox proportional hazard analyses were used to estimate the hazard ratios (HRs) of variables for HCC. In the estimation cohort, 9 of 151 patients developed HCC during the median follow-up time of 722 days. Multivariate

analysis identified three independent risk factors for HCC: LSM (≥ 14.0 kPa, HR 5.58, P = 0.020), platelet count (< 14.1 × 104/μL, HR 5.59, P = 0.034), and non-sustained virological response (HR 8.28, P = 0.049). The cumulative incidence of HCC development at 3 years was 59.6%, 8.2%, and 0.0% in patients with all three risk factors, one to two risk factors, and none of these risk factors, respectively. The click here incidence of HCC was significantly different between these groups (P < 0.001). In the validation cohort, HCC incidence was also significantly different with respect to these risk factors (P = 0.037). LSM, platelet count, and IFN-therapeutic effect could be used to successfully stratify the risk of HCC in patients receiving IFN therapy and demonstrate the usefulness of LSM before IFN therapy for the management of CHC patients. Persistent hepatitis C virus

(HCV) infection is one of the major causes of chronic liver disease leading to the development of HCC, the fifth most common cancer, and the third most common cause of cancer-related death worldwide.[1] HCV is responsible for 27–75% of the HCC cases in Europe and the United States and > 80% of the HCC cases in Japan.[2, 3] In fact, HCV-positive Etofibrate patients have a 20-fold higher risk of developing HCC than HCV-negative patients,[4] indicating a significant carcinogenic role for persistent HCV infection. Because of this connection, many chronic hepatitis C (CHC) patients are treated with interferon (IFN)-based antiviral therapy because it not only eradicates HCV but also reduces the rate of HCC development. IFN therapy is most effective at decreasing the risk of developing HCC in patients that achieve a sustained virological response (SVR);[5-7] however, the risk of HCC development persists after IFN therapy even in patients who do achieve SVR.[8] HCC might develop immediately after IFN therapy in some cases, or during long-term IFN therapy in others.[9, 10] Because assessing the risk of developing HCC is clinically important in the management of CHC patients, it is necessary to establish predictors for HCC development in patients who receive IFN therapy.