Department of Internal Medicine I, University Hospital Cologne, Cologne, Germany.
Department of Medicine I, Bonn University Hospital, Bonn, Germany.
HIV Med. 2019 Mar;20(3):230-236. doi: 10.1111/hiv.12705. Epub 2019 Jan 27.
The aim of the study was to assess the regression of liver stiffness after successful direct-acting antiviral (DAA) treatment in patients with hepatitis C virus (HCV) monoinfection and HCV/-HIV coinfection. In addition, we aimed to identify factors associated with liver stiffness regression.
We studied patients treated with interferon-free DAA regimens with a sustained virological response at week 12 (SVR ) or 24 (SVR ) post-treatment. Liver stiffness was assessed by transient elastography (TE) before the initiation and after the end of treatment (median 12 weeks).
Of 214 enrolled patients, 85 (40%) were HCV monoinfected and 129 (60%) HCV/HIV coinfected. Baseline median TE values were 7.8 kPa [interquartile range (IQR) 5.9-12.0 kPa] in mono-infected patients and 10.7 kPa (IQR 7.8-17.0 kPa) in coinfected patients. Overall, the median TE value decreased from 10.1 to 6.8 kPa (n = 214; P < 0.0001). There was no difference between mono- and coinfected patients (-2.2 versus -3.3 kPa, respectively; P = 0.88), which was verified by an analysis of covariance (ANCOVA) adjusting for baseline TE values. Significant (≥ 30%) regression of liver stiffness was achieved by 45% of patients (54% with baseline TE ≥ 7.1 kPa). In multivariate analysis, a prior HCV treatment was a negative predictor of liver stiffness regression [odds ratio (OR) 0.31; P = 0.001]. A higher baseline TE value was positively associated with achieving a significant regression (OR 1.06; P = 0.02). HIV coinfection status, HCV genotype, age, sex, treatment duration, controlled attenuation parameter value, bilirubin concentration, platelet count and aspartate aminotransferase concentration were not associated with liver stiffness regression.
Regression of liver stiffness after successful DAA treatment did not differ in patients with HCV monoinfection and those with HCV/HIV coinfection. Half of all patients achieved a significant (≥ 30%) regression. Prior treatment for HCV was a negative predictor for this endpoint, while a higher baseline TE value was positively associated with regression.
本研究旨在评估丙型肝炎病毒(HCV)单感染和 HCV/HIV 合并感染患者在成功接受直接作用抗病毒(DAA)治疗后肝硬度的消退情况。此外,我们旨在确定与肝硬度消退相关的因素。
我们研究了接受无干扰素 DAA 方案治疗且在治疗后 12 周(SVR12)或 24 周(SVR24)时病毒学应答持续的患者。在治疗开始前和治疗结束时(中位数为 12 周)通过瞬时弹性成像(TE)评估肝硬度。
在 214 名入组患者中,85 名(40%)为 HCV 单感染,129 名(60%)为 HCV/HIV 合并感染。单感染患者的基线中位数 TE 值为 7.8kPa [四分位距(IQR)5.9-12.0 kPa],合并感染患者为 10.7kPa(IQR 7.8-17.0 kPa)。总体而言,中位 TE 值从 10.1 降至 6.8kPa(n=214;P<0.0001)。单感染和合并感染患者之间没有差异(分别为-2.2 与-3.3kPa;P=0.88),这通过调整基线 TE 值的协方差分析(ANCOVA)得到验证。45%的患者(基线 TE≥7.1kPa 的患者中为 54%)实现了肝硬度有意义(≥30%)的消退。多变量分析显示,既往 HCV 治疗是肝硬度消退的负预测因子[比值比(OR)0.31;P=0.001]。较高的基线 TE 值与实现显著消退呈正相关(OR 1.06;P=0.02)。HIV 合并感染状态、HCV 基因型、年龄、性别、治疗持续时间、衰减参数值、胆红素浓度、血小板计数和天冬氨酸氨基转移酶浓度与肝硬度消退无关。
在 HCV 单感染和 HCV/HIV 合并感染患者中,成功接受 DAA 治疗后肝硬度的消退情况没有差异。所有患者中有一半实现了有意义的(≥30%)消退。既往 HCV 治疗是该终点的负预测因子,而较高的基线 TE 值与消退呈正相关。