한빛사논문
Donghee Kim1,∗, Peter Konyn1, George Cholankeril1, Robert J. Wong2, Zobair M. Younossi3,4, Aijaz Ahmed1
1Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA, United States
2Division of Gastroenterology and Hepatology, Highland Hospital, Oakland, CA, United States
3Betty and Guy Beatty Center for Integrated Research, Inova Health System, Falls Church, VA, Unites States
4Department of Medicine, Center for Liver Diseases, Inova Fairfax Hospital, Falls Church, VA, United States
*Corresponding author
Abstract
Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related deaths in the world, accounting for 810,000 fatalities in 2015.1 With the introduction of direct-acting antiviral (DAA) agents in late 2013, the overall sustained virological response (SVR) for HCV infection increased significantly and it allowed treatment of patients over a wide spectrum of clinical disease severity including those with end-stage liver disease who were in the past deemed poor candidates for antiviral therapy. Therefore, it is plausible to hypothesize that a highly potent DAA-based antiviral regimen may reduce the risk of HCC by eradicating the HCV infection followed by regression in hepatic fibrosis and an improvement in survival partly due to reduction in the incidence of HCC.2 Furthermore, smaller studies have proposed an association between the use of DAA agents and HCC.3 In patients with history of successful response HCC treatment in the setting of HCV-related cirrhosis, hepatic decompensation may have a higher contribution to mortality than HCC recurrence.4 We studied the temporal trends in etiologybased HCC- and cirrhosis-related mortality in the United States (US) from 2009 to 2018.
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