Portal pressure and liver stiffness measurements in the prediction of fibrosis regression after sustained virological response in recurrent hepatitis C
Portal pressure and liver stiffness measurements in the prediction of fibrosis regression after sustained virological response in recurrent hepatitis C
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DOI：
10.1002/hep.29557
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发表时间：
2018-05-01
期刊：
影响因子：
13.5
通讯作者：
Navasa, Miquel
中科院分区：
文献类型：
--
作者：
Mauro, Ezequiel;Crespo, Gonzalo;Navasa, Miquel
持续病毒学应答（SVR）可提高肝移植（LT）后复发丙型肝炎患者的生存率。然而，SVR对纤维化消退的影响尚未明确。此外，评价SVR术后肝纤维化及门脉高压症（PH）的非侵入性方法的性能几乎没有得到评价。我们的目的是研究SVR后纤维化消退的程度（减少1 METAVIR分期）及其相关因素在复发性丙型肝炎，以及非侵入性方法在评估肝纤维化和PH病毒清除后的诊断能力。我们评估了2001年至2015年期间达到SVR的112名丙型肝炎病毒感染的LT接受者。在治疗前和SVR后12个月进行肝活检。同时测定肝静脉压差（HVPG）、肝硬度测量（LSM）和增强型肝纤维化（ELF）评分。67%的队列呈现纤维化消退：肝硬化受者中为43%，其余阶段为72%-85%（P = 0.002）。SVR后HVPG、LSM和ELF显着降低。肝功能显著改善，实现纤维化消退的患者生存率显著提高。基线HVPG和LSM以及治疗前的失代偿是纤维化消退的独立预测因素。SVR后1年，LSM具有较高的诊断准确性，可排除晚期纤维化（AF）和临床显著PH（AUROC，0.902和0.888）。结论：总之，移植后SVR可诱导大多数患者的纤维化消退，从而产生显著的临床获益。治疗前HVPG和LSM是纤维化消退可能性的重要决定因素。最后，LSM准确预测SVR后1年AF和PH的存在，因此可用于确定监测策略。（Hepatology 2018;67：1683-1694）。
Sustained virological response (SVR) improves survival in post-liver transplant (LT) recurrent hepatitis C. However, the impact of SVR on fibrosis regression is not well defined. In addition, the performance of noninvasive methods to evaluate the presence of fibrosis and portal hypertension (PH) post-SVR has been scarcely evaluated. We aimed to investigate the degree of fibrosis regression (decrease 1 METAVIR stage) after-SVR and its associated factors in recurrent hepatitis C, as well as the diagnostic capacity of noninvasive methods in the assessment of liver fibrosis and PH after viral clearance. We evaluated 112 hepatitis C virus-infected LT recipients who achieved SVR between 2001 and 2015. A liver biopsy was performed before treatment and 12 months post-SVR. Hepatic venous pressure gradient (HVPG), liver stiffness measurement (LSM), and Enhanced Liver Fibrosis (ELF) score were also determined at the same time points. Sixty-seven percent of the cohort presented fibrosis regression: 43% in recipients with cirrhosis and 72%-85% in the remaining stages (P = 0.002). HVPG, LSM, and ELF significantly decreased post-SVR. Liver function significantly improved, and survival was significantly better in patients achieving fibrosis regression. Baseline HVPG and LSM as well as decompensations before therapy were independent predictors of fibrosis regression. One year post-SVR, LSM had a high diagnostic accuracy to discard the presence of advanced fibrosis (AF) and clinically significant PH (AUROC, 0.902 and 0.888). Conclusion: In conclusion, SVR post-LT induces fibrosis regression in most patients, leading to significant clinical benefits. Pretreatment HVPG and LSM are significant determinants of the likelihood of fibrosis regression. Finally, LSM accurately predicts the presence of AF and PH 1 year after SVR and thus can be used to determine monitoring strategies. (Hepatology 2018;67:1683-1694).