Road to identifying endpoint biomarkers in the treatment of nonalcoholic steatohepatitis: are we there yet?
In the United States (US), the landscape of chronic liver disease has been in flux in recent years as chronic hepatitis C virus (HCV) infection is no longer the leading indication for liver transplantation and now ranks behind alcoholic liver disease (ALD) and nonalcoholic steatohepatitis (NASH) as the third leading indication for liver transplantation (1). The approval of second-generation direct-acting antiviral (DAA) agents in late 2013 heralded a revolutionary era in the treatment of HCV infection. In a recent population-based study, there was a marked increase in age-standardized mortality for HCV infection with annual percent change (APC) of 2.2% in the pre-DAA era [2007-2014], but a marked decline in age-standardized mortality rates for HCV in the DAA-era [2014-2017] with -6.5% of APC (2). While HCV-related mortality declined along with the introduction of DAA therapies, nonalcoholic fatty liver disease (NAFLD)-related death was on the rise at an accelerated pace in the US adults (3). Notably, age-standardized mortality for NASH-related cirrhosis increased significantly between 2007 and 2016 (APC: 15.4%; 95% CI: 14.1 to 16.7) (4). NAFLD-related advanced fibrosis remains a topic of interest because of its association with end-stage liver disease and hepatocellular carcinoma. During the last 10 years from 2005 to 2016, NAFLD-related advanced fibrosis increased from 3% among subjects with NAFLD in 2005-2008 to 6% in 2013-2016 in the US adults (5). The prevalence of NAFLD-related advanced fibrosis is now estimated to be four million US adults (5). Longitudinal cohort studies looking into patients with NAFLD suggest that the fibrosis stage, and not the presence of NASH, predicted both the risk of overall and cause-specific mortality (6,7). Therefore, NASH with presence of fibrosis has been
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2020-04-03（万方平台首次上网日期，不代表论文的发表时间）
共3页
244-246
