Unreliable Estimation of Fibrosis Regression During Treatment by Liver Stiffness Measurement in Patients With Chronic Hepatitis B.
Unreliable Estimation of Fibrosis Regression During Treatment by Liver Stiffness Measurement in Patients With Chronic Hepatitis B.
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DOI：
10.14309/ajg.0000000000001239
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发表时间：
2021-08-01
期刊：
影响因子：
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通讯作者：
Yang Y
中科院分区：
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作者：
Ji D;Chen Y;Shang Q;Liu H;Tan L;Wang J;Chen Y;Li Q;Long Q;Song L;Jiang L;Xiao G;Yu Z;Chen L;Hu X;Wang X;Chen D;Li Z;Dong Z;Chen G;Yang Y
关于肝脏硬度测量（LSM）对于监测治疗期间肝纤维化变化的有用性，几乎没有可靠的证据报道。我们的目的是评估慢性乙型肝炎患者 LSM 变化与组织学结果之间的关联。在这项前瞻性多中心研究中，分析了 727 名接受恩替卡韦为基础治疗的初治患者，他们在治疗基线和第 72 周接受了配对活检。 LSM 的变化定义为减少 ≥30%、微小变化和增加 ≥30%。使用多变量逻辑回归来估计 LSM 变化对临床结果的优势比 (OR)，并考虑到均值回归。根据受试者工作曲线建立了新的治疗中 LSM 阈值。纤维化总体消退、炎症改善、显着组织学反应、病毒学反应、丙氨酸转氨酶正常化和乙型肝炎e抗原血清转换分别为51.2%、74.4%、22.0%、86.0%、83.5%和13.3%。 LSM 的变化与炎症改善之间的关联是非线性的 (P = 0.012)。 LSM降低≥30%与纤维化消退（OR 1.501，95%置信区间[CI] 1.073–2.099，P = 0.018）、显着的组织学反应（OR 1.726，95% CI 1.124–2.652，P = 0.013）和丙氨酸转氨酶正常化（OR 2.149， 95%置信区间 1.229–3.757，P = 0.007）。调整回归平均值后，LSM 增加≥30% 与上述 3 个结果呈负相关。建立了新的治疗中 LSM 截止值 5.4 kPa，用于指示显着的组织学反应。 LSM 的变化对于估计治疗期间纤维化的消退是不可靠的；治疗中 LSM 的既定临界值可以优化慢性乙型肝炎患者组织学结果的监测策略。
Little reliable evidence has been reported regarding usefulness of liver stiffness measurement (LSM) for monitoring the hepatic fibrosis changes during treatment. We aimed to assess the association between changes in LSM and histological outcomes in patients with chronic hepatitis B. In this prospective multicenter study, 727 treatment-naive patients receiving entecavir-based therapy, who underwent paired biopsies at treatment baseline and week 72, were analyzed. Changes in LSM were defined as ≥30% decrease, minor change, and ≥30% increase. Multivariate logistic regression was used to estimate odds ratios (ORs) of changes in LSM on clinical outcomes accounting for regression to the mean. A new on-treatment LSM threshold was established by receiver operating curve. Overall regression of fibrosis, improvement of inflammation, significant histological response, virologic response, alanine aminotransferase normalization, and hepatitis B e antigen seroconversion were 51.2%, 74.4%, 22.0%, 86.0%, 83.5%, and 13.3%, respectively. The association between changes in LSM and improvement of inflammation was nonlinear (P = 0.012). LSM decrease ≥30% was associated with regression of fibrosis (OR 1.501, 95% confidence interval [CI] 1.073–2.099, P = 0.018), significant histological response (OR 1.726, 95% CI 1.124–2.652, P = 0.013), and alanine aminotransferase normalization (OR 2.149, 95% CI 1.229–3.757, P = 0.007). After adjusting for regression to the mean, LSM increase ≥30% became negatively associated with the above 3 outcomes. A new on-treatment LSM cutoff value of 5.4 kPa was established for indicating the significant histological response. Changes in LSM are unreliable to estimate regression of fibrosis during treatment; the established cutoff value of on-treatment LSM can optimize monitoring strategy for histological outcomes in patients with chronic hepatitis B.