晚期纤维化或肝硬化患者丙型肝炎治愈后肝细胞癌发病率的

StephenW

晚期纤维化或肝硬化患者丙型肝炎治愈后肝细胞癌发病率的荟萃分析
肝病学 2022 年 1 月 14 日 - Ian Lockart1,2, Malcolm G. H. Yeo1, Behzad Hajarizadeh3, Gregory J. Dore2,3, Mark Danta1,2

随着时间的推移，HCC 风险的下降对肝硬化患者具有重要意义，目前建议他们在 HCV 治愈后进行无限期监测。我们的研究结果表明，在 HCV 治愈后的某个时间点，可能有一部分肝硬化患者可以降级到不太密集的监测计划。潜在地，这些患者将可以使用正在开发的预测模型来识别，以便在 SVR 之后使用。15、44、58、59 随着 HCC 风险随着时间的推移而降低，这些模型将需要是动态的，并且随着时间的推移纳入风险因素的变化，以便提供精确的风险估计和个性化的监测建议。 HCC 风险随时间下降的原因可能与肝纤维化的消退有关，这是根除 HCV 后的缓慢过程。 60-63 尽管我们的结果似乎合乎逻辑，但应该注意的是来自美国退伍军人事务部 (VA) 医疗保健系统的数据尚未证明所有患者（基于 IFN 和 DAA 治疗）在 HCV 治愈后 HCC 风险随时间下降。9、29 我们承认，我们发现发病率随时间下降可能是由于选择偏倚有利于随访时间较长的研究向上。我们的结果应该鼓励进一步的研究来评估 HCC 风险随着时间的推移，使用来自大型多中心队列的个体水平数据和更长的随访时间。

抽象的
背景与目标

丙型肝炎病毒 (HCV) 治愈可降低但不能消除肝细胞癌 (HCC) 的风险。建议对每年发病率超过 1.5% 的人群进行 HCC 监测。在肝硬化中，应在 HCV 治愈后继续监测 HCC，尽管不确定这是否应该是无限期的。对于晚期纤维化 (F3) 患者，指南中的建议不一致。我们评估了 F3 纤维化或肝硬化患者 HCV 治愈后 HCC 的发生率。
方法与结果

这项系统回顾和荟萃分析确定了 44 项研究（107,548 人年随访）评估 F3 纤维化或肝硬化患者 HCV 治愈后 HCC 的发生率。肝硬化患者的 HCC 发病率为 2 1/100 人年 (95% CI 1 9-2 4)，而 F3 纤维化患者的 HCC 发病率为 0 5/100 人年 (95% CI 0 3-0 7) .在肝硬化患者的荟萃回归分析中，年龄较大（平均/中位年龄每增加 10 年的调整率比 [aRR]：1 32；95% CI 1 00-1 73）和既往失代偿（aRR 每 10%先前失代偿的患者比例增加：1 06；95% CI 1 01-1 12）与 HCC 发病率增加有关。 HCV 治愈后更长的随访与 HCC 发病率的降低相关（aRR 平均/中位随访每年增加：0 87；95% CI 0 79-0 96）。
结论

在肝硬化患者中，HCC 的发生率在 HCV 治愈后随时间降低，并且在年龄较小的代偿期肝硬化患者中最低。 F3 纤维化的发生率显着降低，低于成本效益筛查的推荐阈值。结果应鼓励开发经过验证的预测模型，以更好地识别高危个体，特别是在 F3 纤维化患者中。

StephenW

Hepatocellular carcinoma incidence after hepatitis C cure among patients with advanced fibrosis or cirrhosis: a meta-analysis
Hepatology Jan 14 2022 - Ian Lockart1,2, Malcolm G. H. Yeo1, Behzad Hajarizadeh3, Gregory J. Dore2,3, Mark Danta1,2

The declining HCC risk over time has significant implications for patients with cirrhosis, who are currently recommended to have indefinite surveillance after HCV cure. Our findings suggest there may be a sub-group of patients with cirrhosis who could step-down to a less intensive surveillance program, at some point after HCV cure. Potentially, these patients will be identifiable using predictive models being developed for use after SVR.15, 44, 58, 59 As HCC risk decreases over time, these models will need to be dynamic and incorporate changes in risk factors over time in order to provide precise risk estimates and individualised surveillance recommendations. The reason why HCC risk declines over time probably relates to regression of liver fibrosis, which is a slow process after HCV eradication.60-63 Although our results seem logical, it should be noted that data from the US Veterans Affairs (VA) healthcare system has not demonstrated declining HCC risk over time among all patients (IFN-based and DAA-therapy) after HCV cure.9, 29 We acknowledged that our finding of a declining incidence over time could be due to a selection bias favouring studies with longer follow up. Our results should encourage further studies to evaluate HCC risk over time, using individual-level data from large multicentre cohorts with longer follow-up.

Abstract
Background & Aims

Hepatitis C virus (HCV) cure reduces but does not eliminate the risk of hepatocellular carcinoma (HCC). HCC surveillance is recommended in populations where the incidence exceeds 1.5% per year. In cirrhosis, HCC surveillance should continue after HCV cure, although it’s uncertain if this should be indefinite. For patients with advanced fibrosis (F3), guidelines are inconsistent in their recommendations. We evaluated the incidence of HCC after HCV cure among patients with F3 fibrosis or cirrhosis.
Approach & Results

This systematic review and meta-analysis identified 44 studies (107,548 person-years follow-up) assessing the incidence of HCC after HCV cure among patients with F3 fibrosis or cirrhosis. The incidence of HCC was 2 1 per 100 person-years (95% CI 1 9-2 4) among patients with cirrhosis, and 0 5 per 100 person-years (95% CI 0 3-0 7) among patients with F3 fibrosis. In meta-regression analysis among patients with cirrhosis, older age (adjusted rate ratio [aRR] per 10-year increase in mean/median age: 1 32; 95% CI 1 00-1 73) and prior decompensation (aRR per 10% increase in the proportion of patients with prior decompensation: 1 06; 95% CI 1 01-1 12) were associated with an increased incidence of HCC. Longer follow-up after HCV cure was associated with a decreased incidence of HCC (aRR per year increase in mean/median follow-up: 0 87; 95% CI 0 79-0 96).
Conclusions

Among patients with cirrhosis, the incidence of HCC decreases over time after HCV cure and is lowest in patients with younger age and compensated cirrhosis. The substantially lower incidence in F3 fibrosis is below the recommended threshold for cost-effective screening. The results should encourage the development of validated predictive models that better identify at-risk individuals, especially among patients with F3 fibrosis.