In the overall cohort, 9.3% of patients showed clinical signs of liver cirrhosis at 35 years after infection. Liver disease progression largely depended on HCV infection status. The highest proportion of patients with clinical signs of end-stage liver disease was observed in the non-SVR group (15.3%), whereas decreased cirrhosis rates were detected click here in the SVR group (6%) and in patients with self-limited HCV infection (1.1%; P = 6.2 × 10−6). Overall survival was significantly enhanced after SVR, compared to treatment-naïve patients or non-SVR (P = 0.027). Conclusion: The present study provides further evidence for a mild, but significant, disease progression at 35 years

after infection in the German HCV (1b)-contaminated

anti-D cohort. Patients with self-limited HCV infection or SVR after antiviral treatment Angiogenesis inhibitor were protected from progressive liver disease and showed the best clinical long-term outcome. (Hepatology 2014;58:49–57) Hepatitis C virus (HCV) infection is the leading cause of end-stage liver disease (ESLD) in the world and represents a major burden for national health systems.[1] The World Health Organisation (WHO) and international consensus conferences refer to the high chronification rate of HCV infection, the risk of subsequent HCV-related complications, including end-stage liver cirrhosis and hepatocellular carcinoma (HCC) and the high costs for antiviral therapy, respectively, liver transplantation (LT).[2, 3] It is estimated that HCV-related morbidity and mortality

will increase in the next decade.[4-6] The predicted cumulative probability of cirrhosis approximates 20% at 20 years after HCV infection and increases to 45% at 30 years after infection.[7] However, recent estimates on the natural fibrosis progression rates of hepatitis C largely depend on study design, study setting, and the selected study population. In theory, prospective multicenter, community-based long-term follow-up studies in large representative patient cohorts with a defined onset of HCV infection from a single identified source constitute the optimal setting for the evaluation of the natural course of chronic HCV infection.[8] Therefore the well-documented iatrogenic MycoClean Mycoplasma Removal Kit single-source HCV outbreaks in recipients of HCV-contaminated anti-D immunoglobulin (Ig) in Ireland (1977-1978) and Germany (1978-1979) provided valuable insight into the acute and chronic course of HCV infection in the past.[9-12] We have previously reported on the outcome of the German HCV (1b)-contaminated anti-D cohort at 20 and 25 years after infection and demonstrated a very low cirrhosis rate of only 0.5% in the overall cohort at 25 years after infection.[11, 12] The aim of the present 35-year follow-up study was to reevaluate the liver disease progression in this unique cohort after another decade of data accrual in our prospective, community-based, multicenter study.