Abstract：
OBJECTIVE: While several predictive models for the development of hepatocellular carcinoma (HCC) have been proposed, including those for patients with chronic hepatitis C virus (HCV) infection who have achieved sustained virologic response (SVR), the best model may differ between regions. We compared the ability of six reported models to stratify the risk of post-SVR HCC in Japan, where rigorous surveillance and early detection of HCC is common.
METHODS: A total of 6048 patients with no history of HCC who achieved SVR by oral direct-acting antiviral drugs were enrolled in this nationwide study. Patients continued HCC surveillance every 6 months after SVR. The incidence of post-SVR HCC was compared between risk groups using the aMAP score, FIB-4 index, Tahata model, GAF4 criteria, GES score, and ADRES score.
RESULTS: During the observation period with a median duration of 4.0 years after SVR, post-SVR HCC developed in 332 patients (5.5%). All six models performed significantly at stratifying the incidence of HCC. However, Harrell\'s C-index was below 0.8 for all models (range, 0.660-0.748), indicating insufficient stratification ability.
CONCLUSIONS: Although all six proposed models demonstrated a good ability to predict the development of post-SVR HCC, their ability to stratify the risk of post-SVRHCC was unsatisfactory. Further studies are necessary to identify the best model for assessing the risk of post-SVR HCC in regions where early detection of HCC is common.
METHODS: A total of 6048 patients with no history of HCC who achieved SVR by oral direct-acting antiviral drugs were enrolled in this nationwide study. Patients continued HCC surveillance every 6 months after SVR. The incidence of post-SVR HCC was compared between risk groups using the aMAP score, FIB-4 index, Tahata model, GAF4 criteria, GES score, and ADRES score.
RESULTS: During the observation period with a median duration of 4.0 years after SVR, post-SVR HCC developed in 332 patients (5.5%). All six models performed significantly at stratifying the incidence of HCC. However, Harrell\'s C-index was below 0.8 for all models (range, 0.660-0.748), indicating insufficient stratification ability.
CONCLUSIONS: Although all six proposed models demonstrated a good ability to predict the development of post-SVR HCC, their ability to stratify the risk of post-SVRHCC was unsatisfactory. Further studies are necessary to identify the best model for assessing the risk of post-SVR HCC in regions where early detection of HCC is common.
摘要：
目的：虽然已经提出了几种肝细胞癌（HCC）发展的预测模型，包括那些已实现持续病毒学应答（SVR）的慢性丙型肝炎病毒（HCV）感染患者，最佳模型可能因地区而异。我们比较了六个报告模型对日本SVR后HCC风险进行分层的能力，在那里，严格的监测和早期发现肝癌是常见的。
方法：这项全国性研究共纳入6048例没有肝癌病史的患者通过口服直接作用抗病毒药物获得SVR。患者在SVR后每6个月继续进行HCC监测。使用aMAP评分在风险组之间比较SVR后HCC的发生率，FIB-4指数，Tahata模型,GAF4标准，GES得分,和ADRES得分。
结果：在SVR后中位持续时间为4.0年的观察期内，后SVR肝癌发展332例（5.5％）。所有六个模型在对HCC的发病率进行分层时都有显着表现。然而,所有型号的哈雷尔C指数均低于0.8(范围，0.660-0.748),表明分层能力不足。
结论：尽管所有六个提出的模型都显示出预测SVR后HCC发展的良好能力，他们对SVRHCC后风险进行分层的能力并不令人满意.进一步的研究是必要的，以确定最好的模型来评估后SVRHCC的风险在早期检测HCC是常见的地区。
方法：这项全国性研究共纳入6048例没有肝癌病史的患者通过口服直接作用抗病毒药物获得SVR。患者在SVR后每6个月继续进行HCC监测。使用aMAP评分在风险组之间比较SVR后HCC的发生率，FIB-4指数，Tahata模型,GAF4标准，GES得分,和ADRES得分。
结果：在SVR后中位持续时间为4.0年的观察期内，后SVR肝癌发展332例（5.5％）。所有六个模型在对HCC的发病率进行分层时都有显着表现。然而,所有型号的哈雷尔C指数均低于0.8(范围，0.660-0.748),表明分层能力不足。
结论：尽管所有六个提出的模型都显示出预测SVR后HCC发展的良好能力，他们对SVRHCC后风险进行分层的能力并不令人满意.进一步的研究是必要的，以确定最好的模型来评估后SVRHCC的风险在早期检测HCC是常见的地区。
