在晚期慢性肝脏疾病和门静脉高压症患者中，控制衰减参数的性能。
Performance of Controlled Attenuation Parameter in Patients with Advanced Chronic Liver Disease and Portal Hypertension.
机构信息
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria.
出版信息
Dig Dis Sci. 2019 Dec;64(12):3642-3651. doi: 10.1007/s10620-019-05702-7. Epub 2019 Jun 17.
BACKGROUND
Liver stiffness (LS) measured by vibration-controlled transient elastography (VCTE) is influenced by liver fibrosis and hepatic perfusion pressure. VCTE-based controlled attenuation parameter (CAP) is a noninvasive marker for hepatic steatosis (HS).
AIMS
To investigate the diagnostic performance of CAP in patients with advanced chronic liver disease (ACLD)/portal hypertension (PHT: hepatic venous pressure gradient (HVPG) ≥ 6 mmHg).
METHODS
Eighty-eight patients with LS ≥ 10 kPa and/or HVPG ≥ 6 mmHg who underwent simultaneous liver biopsy, CAP, and HVPG measurement were included. HS was histologically graded according to the modified Brunt classification.
RESULTS
Patient characteristics: Mean MELD:11 (standard derivation [SD] ± 4), median HVPG:16 (interquartile range [IQR]10-19) mmHg, median LS:27.4 (IQR 16.2-48.9) kPa, and mean CAP:221 (SD ± 75) dB/m. According to histology, 47 (53.4%) patients had no HS (S0), 28 (31.8%) had S1, 11 (12.5%) had S2, and 2 (2.3%) had S3. The area under the receiver operating characteristic curve (AUROC) of CAP for diagnosing any HS (S0 vs. ≥ S1) was 0.692 (95% confidence interval [95% CI] 0.582-0.802) in the overall cohort, 0.830 (95% CI 0.637-1.0) in patients with HVPG < 10 mmHg, and 0.629 (95% CI 0.497-0.761) in patients with clinically significant portal hypertension (CSPH; HVPG ≥ 10 mmHg; n = 69). Using the established cutoff for any HS (248 dB/m), the sensitivity/specificity of CAP was only 48.8%/76.6%, respectively. In contrast, the AUROC and sensitivity/specificity (cutoff 268 dB/m) for diagnosing HS ≥ S2 were 0.842 (95% CI 0.747-0.936) and 84.6%/81.3%, respectively. CAP correlated with the percentage of steatotic hepatocytes (Spearman's ρ = 0.402; p ≤ 0.001) and showed a weak correlation with liver stiffness (ρ = 0.225; p = 0.035).
CONCLUSIONS
The diagnostic performance of CAP for any HS seems to be limited in patients with ACLD, if CSPH is present.
背景
通过振动控制瞬时弹性成像（VCTE）测量的肝硬度（LS）受肝纤维化和肝灌注压的影响。基于 VCTE 的受控衰减参数（CAP）是肝脂肪变性（HS）的非侵入性标志物。
目的
探讨 CAP 在伴有晚期慢性肝病（ACLD）/门静脉高压（PHT：肝静脉压力梯度（HVPG）≥6mmHg）患者中的诊断性能。
方法
纳入 88 例 LS≥10kPa 和/或 HVPG≥6mmHg 且同时进行肝活检、CAP 和 HVPG 测量的患者。根据改良 Brunt 分级对 HS 进行组织学分级。
结果
患者特征：平均 MELD：11（标准差[SD]±4），中位 HVPG：16（四分位距[IQR]10-19）mmHg，中位 LS：27.4（IQR 16.2-48.9）kPa，平均 CAP：221（SD±75）dB/m。根据组织学，47 例（53.4%）患者无 HS（S0），28 例（31.8%）为 S1，11 例（12.5%）为 S2，2 例（2.3%）为 S3。在整个队列中，CAP 诊断任何 HS（S0 与≥S1）的受试者工作特征曲线（AUROC）面积为 0.692（95%置信区间[95%CI]0.582-0.802），HVPG<10mmHg 的患者为 0.830（95%CI 0.637-1.0），临床显著门静脉高压（CSPH；HVPG≥10mmHg；n=69）的患者为 0.629（95%CI 0.497-0.761）。使用任何 HS 的既定截断值（248dB/m），CAP 的敏感性/特异性分别仅为 48.8%/76.6%。相比之下，用于诊断 HS≥S2 的 CAP 的 AUROC 和敏感性/特异性（截断值 268dB/m）分别为 0.842（95%CI 0.747-0.936）和 84.6%/81.3%。CAP 与脂肪变性肝细胞的百分比呈正相关（Spearman ρ=0.402；p≤0.001），与肝硬度呈弱相关（ρ=0.225；p=0.035）。
结论
如果存在 CSPH，CAP 诊断 ACLD 患者任何 HS 的性能似乎受到限制。
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