Division of Gastroenterology, University of California San Diego, La Jolla, California; Division of Biomedical Informatics, University of California San Diego, La Jolla, California.
Gastroenterology Unit, Department of Medical Sciences, University of Foggia, Foggia, Italy.
Clin Gastroenterol Hepatol. 2018 Jan;16(1):27-38.e4. doi: 10.1016/j.cgh.2017.04.038. Epub 2017 May 4.
BACKGROUND & AIMS: We performed a systematic review and meta-analysis to estimate the decrease in liver stiffness, measured by vibration-controlled transient elastrography (VCTE), in patients with hepatitis C virus infection who achieved a sustained virologic response (SVR).
We searched the literature through October 2016 for observational studies or randomized controlled trials of adults with hepatitis C virus infection who received antiviral therapy (either direct-acting antiviral agents or interferon-based therapies), underwent liver stiffness measurement using VCTE before starting therapy, and had at least 1 follow-up VCTE after completion of therapy; studies also provided data on mean or median liver stiffness measurements for patients who did and did not achieve an SVR. We identified 24 studies, and estimated weighted mean difference (and 95% confidence interval) in liver stiffness in patients with versus without SVR using random-effects meta-analysis.
In patients who achieved SVR, liver stiffness decreased by 2.4 kPa at the end of therapy (95% CI, -1.7 to -3.0), by 3.1 kPa 1-6 months after therapy (95% CI, -1.6 to -4.7), by 3.2 kPa 6-12 months after therapy (90% CI, -2.6 to -3.9), and 4.1 kPa 12 months or more after therapy (95% CI, -3.3 to -4.9) (median decrease, 28.2%; interquartile range, 21.8-34.8). In contrast, there was no significant change in liver stiffness in patients who did not achieve an SVR (at 6-12 months after therapy, decrease of 0.6 kPa; 95% CI, -1.7 to 0.5). Decreases in liver stiffness were significantly greater in patients treated with direct-acting antiviral agents than with interferon-based therapy (decrease of 4.5 kPa vs decrease of 2.6 kPa; P = .03), cirrhosis at baseline (decrease of 5.1 kPa vs decrease of 2.8 kPa in patients with no cirrhosis; P = .02), or high pretreatment levels of alanine aminotransferase (P < .01). Among patients with baseline liver stiffness >9.5 kPa, 47% (95% CI, 27%-68%) achieved posttreatment liver stiffness of <9.5 kPa.
In a systematic review and meta-analysis, we associated eradication of hepatitis C virus infection (SVR) with significant decreases in liver stiffness, particularly in patients with high baseline level of inflammation or patients who received direct-acting antiviral agents. Almost half the patients considered to have advanced fibrosis, based on VCTE, before therapy achieved posttreatment liver stiffness levels <9.5 kPa. Clinical Trial Registration no: CRD42016051034.
我们进行了一项系统评价和荟萃分析，以评估丙型肝炎病毒（HCV）感染患者在获得持续病毒学应答（SVR）后，通过振动控制瞬态弹性成像（VCTE）测量的肝硬度下降情况。
我们检索了截至 2016 年 10 月的文献，纳入了接受抗病毒治疗（直接作用抗病毒药物或基于干扰素的治疗）的 HCV 感染成年患者的观察性研究或随机对照试验。这些患者在开始治疗前接受了 VCTE 检查，并在治疗完成后至少进行了一次随访 VCTE。研究还提供了 SVR 患者和非 SVR 患者的平均或中位数肝硬度测量数据。我们使用随机效应荟萃分析，比较了 SVR 患者和非 SVR 患者的肝硬度加权平均差异（及其 95%置信区间）。
在获得 SVR 的患者中，治疗结束时肝硬度下降 2.4 kPa（95%CI，-1.7 至-3.0），治疗后 1-6 个月时下降 3.1 kPa（95%CI，-1.6 至-4.7），治疗后 6-12 个月时下降 3.2 kPa（90%CI，-2.6 至-3.9），治疗后 12 个月或更长时间时下降 4.1 kPa（95%CI，-3.3 至-4.9）（中位数下降 28.2%；四分位距，21.8-34.8）。相比之下，未获得 SVR 的患者的肝硬度没有明显变化（治疗后 6-12 个月时下降 0.6 kPa；95%CI，-1.7 至 0.5）。与基于干扰素的治疗相比，直接作用抗病毒药物治疗的患者肝硬度下降更显著（下降 4.5 kPa 与下降 2.6 kPa；P =.03），基线时存在肝硬化（下降 5.1 kPa 与无肝硬化患者下降 2.8 kPa；P =.02）或高预处理丙氨酸氨基转移酶水平（P<.01）。在基线肝硬度>9.5 kPa 的患者中，47%（95%CI，27%-68%）在治疗后达到<9.5 kPa 的肝硬度。
在一项系统评价和荟萃分析中，我们发现丙型肝炎病毒感染的消除（SVR）与肝硬度的显著下降相关，特别是在基线炎症水平较高或接受直接作用抗病毒药物治疗的患者中。在治疗前，几乎一半的患者（基于 VCTE）被认为存在晚期纤维化，但在治疗后达到了<9.5 kPa 的肝硬度水平。
CRD42016051034。
