CID：HCV相关肝硬化患者实现SVR后仍长期处于肝细胞癌风险中

在世界范围内，HCV（丙型肝炎病毒）感染是导致肝硬化和肝细胞癌（HCC）的主要原因。罹患肝硬化的患者更容易发展为HCC。因此，肝硬化患者被建议每个6个月进行一次关于HCC的超声监测。目前尚未完全清楚抗病毒疗法所引起的持续病毒学应答（SVR）对HCV感染合并肝硬化患者发展为HCC、肝脏并发症、肝相关死亡和全因死亡风险的长期影响。基于上述情况，来自瑞典卡罗林斯卡大学医院胃肠病学和肝脏病学部门的Soo Aleman等人展开一项研究，研究结果在线发表于2013年4月24日的《临床感染疾病》（Clinical Infectious Diseases）杂志上。作者发现，在实现SVR后，HCV相关肝硬化患者的HCC、肝脏并发症以及死亡风险明显降低，但在随后长达8年的时间里，患者仍然长期存在发展成为HCC的风险。

研究人员通过对351例HCV相关肝硬化患者的长期随访对上述风险进行了评估。这项起始于2001年的多中心前瞻性队列研究纳入了110例获得SVR的患者，193例未获得SVR的患者，以及48例未经治疗的患者，平均随访时间为5.3 ± SD 2.8年。他们通过利用来自国家注册中心的补充随访资料，从而尽量减少随访期间患者信息的损失。

研究结果如下：有6例获得SVR的患者在实现SVR后的0.04、0.64、2.4、7.4、7.4和7.6年时发展为HCC。SVR组每100人年的HCC、任何肝脏并发症、肝相关死亡和全因死亡的发生率（1.0, 0.9, 0.7, 1.9）均显著低于无SVR组（2.3, 3.2, 3.0, 4.1）和未经治疗组（4.0, 4.9, 4.5, 5.1）。与前3年的随访相比，3年之后的长期后果并未显著降低。

研究发现，在实现SVR后，HCV相关肝硬化患者的HCC、肝脏并发症以及死亡风险明显降低，但在随后长达8年的时间里，患者仍然存在发展成为HCC的长期风险。因此，应当对那些实现SVR的慢性丙型肝炎患者进行长期HCC监测。未来需要进一步的研究以更好地鉴别出长期存在HCC风险的患者。
与肝硬化相关的拓展阅读：

• AJG：肝硬化门静脉血栓形成预测因素
• Hepatology：丙肝肝硬化大多因酗酒导致
• J Hepatol：肝硬化患者骨折风险增高
• GUT：急性肾损害或将影响肝硬化腹水患者的预后
• GUT：轻度急性肾损害会影响肝硬化腹水患者的预后
• Lancet：长期替诺福韦酯治疗可逆转慢乙肝肝硬化
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A risk for hepatocellular carcinoma still persists long-term after sustained virological response in patients with hepatitis C associated liver cirrhosis.
Background
The long-term effect of sustained virological response (SVR) to antiviral therapy on the risk to develop hepatocellular cancer (HCC), liver complications, liver-related deaths and overall death in hepatitis C (HCV) infected patients with liver cirrhosis is not fully known.
Methods
These risks were evaluated during long-term follow-up in in 351 patients with HCV related cirrhosis. 110 with SVR, 193 with non-SVR and 48 untreated patients were included in a multi-center cohort which was initiated 2001 and prospectively followed-up for a mean 5.3 ±SD 2.8 years. Complementary follow-up data from national registries were used to minimize the loss of patients during follow-up.
Results
Six patients with SVR developed HCC at 0.04, 0.64, 2.4, 7.4, 7.4 and 7.6 years after achieving SVR. The incidence of HCC, any liver complication, liver-related and overall death per 100 person-years was significantly lower in SVR time with 1.0, 0.9, 0.7, 1.9, compared to 2.3, 3.2, 3.0, 4.1 and 4.0, 4.9, 4.5, 5.1 in non-SVR and untreated time, respectively. The long-term consequences did not decline significantly after more than 3-year versus during the first 3-year of follow-up.
Conclusions
The risk for HCC, liver decompensation, and death in patients with liver cirrhosis related to HCV was markedly reduced after SVR, but a long-term risk to develop HCC remains for up to 8 years. Cirrhotic patients with HCV who achieve SVR should therefore maintain long-term surveillance for HCC. Future studies aimed to better identify those with remaining long-term risk for HCC are needed.