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Hepatocellular Carcinoma After Sustained Virologic Response: Leave No One Behind.

76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 114 115 116 117 Thepatitis is increasing. In 2013, viral hepatitis was the seventh leading cause of death worldwide, owing to cirrhosis and hepatocellular carcinoma (HCC). HCC is the fastest increasing cause of cancer-related death in many countries, including the United States and Australia. The prognosis for HCC remains poor despite advances in diagnosis and treatment. Surveillance programs for HCC lead to earlier detection and increase the likelihood that curative treatment will be possible. Surveillance for HCC is recommended to be cost effective if the risk exceeds 1.5% per year in people with hepatitis C. The risk of HCC in people with chronic hepatitis C is greatest among those who have established cirrhosis, where annual incidence is 2%–8%. Guidelines, therefore, recommend that all people with hepatitis C virus (HCV)-related cirrhosis be enrolled in HCC surveillance programs, involving liver ultrasound monitoring every 6 months. Eradication of HCV, or sustained virologic response (SVR), was shown to reduce the risk of HCC in the interferon (IFN) era. However, the risk of HCC persists after SVR. Given the uncertainty about if, and when, annual risk falls below 1.5% per year, guidelines continue to recommend surveillance in all people with cirrhosis after HCV eradication. In an era of escalating health care costs and an increased focus on fiscal responsibility, there is a need for biomarkers that stratify the risk of HCC after SVR, such that high-risk individuals can be prioritised to continue long-term surveillance, and low-risk individuals can discontinue surveillance. Risk factors that predict an increased likelihood of HCC in this population include older age, lower platelet count, high a-fetoprotein (AFP) levels, persistence (vs regression) of liver fibrosis or liver stiffness, current or past HBV infection, smoking, and comorbid nonalcoholic steatohepatitis. However, to date no clinical algorithm has had sufficient predictive accuracy to be routinely recommended in practice. Host genomic predictors may improve personalisation of risk calculations. In this issue of Gastroenterology, Matsuura et al present the first genome-wide association study (GWAS) looking for genetic variants associated with the development of HCC after HCV eradication by IFN-based therapy. The study identified SNP rs17047200, located