University Clinic for Visceral Surgery and Medicine, Inselspital, Bern University Hospital, Department of Biomedical Research, University of Bern, Switzerland.
Division of Gastroenterology and Hepatology, McGill University Health Centre, Royal Victoria Hospital, Montreal, Canada.
Clin Gastroenterol Hepatol. 2020 Dec;18(13):3017-3025.e6. doi: 10.1016/j.cgh.2020.04.018. Epub 2020 Apr 11.
BACKGROUND & AIMS: Some patients with compensated advanced chronic liver disease (cACLD) require use of an extralarge probe for liver stiffness measurement (LSM), owing to overweight or obesity. However, the ability of noninvasive markers of portal hypertension and the controlled attenuation parameter (CAP) to determine which of these patients are at risk for decompensation has not been fully assessed.
We collected data from 272 patients with cACLD (LSM ≥10 kPa by XL probe; 57% with nonalcoholic steatohepatitis; mean body mass index, 33.8 ± 6.5 kg/m; median Child-Pugh score, 5; median LSM, 16.8 kPa; mean CAP, 318 ± 66 dB/m) evaluated at 2 academic centers from 2015 through 2018. We collected clinical data on decompensation (ascites, portal hypertension bleeding, jaundice, hepatic encephalopathy) and severe bacterial infections; patients were followed up for a median of 17 months (interquartile range, 11-24 mo). We evaluated associations between these events and LSM, CAP, LSM∗spleen size/platelet count (LSPS), and portal hypertension risk scores.
Decompensation occurred in 12 patients and severe bacterial infections developed in 5 patients. LSM, LSPS, and the portal hypertension risk score identified patients with decompensation with area under the receiver operating characteristic curve values of 0.848 (95% CI, 0.720-0.976; P < .0001), 0.881 (95% CI, 0.798-0.954; P < .0001), and 0.890 (95% CI, 0.814-0.966; P < .0001), respectively. In multivariate Cox regression analysis, in patients with nonalcoholic steatohepatitis, LSM and CAP were associated independently with decompensation and severe bacterial infection; CAP ≥ 220 dB/m was associated with a reduced risk of decompensation (hazard ratio, 0.043, 95% CI, 0.004-0.476; P = .01).
LSM, LSPS, and the portal hypertension risk score identify obese or overweight patients with cACLD who are at increased risk of decompensation and severe bacterial infection.
一些代偿期晚期慢性肝病（cACLD）患者因超重或肥胖需要使用特大探头进行肝脏硬度测量（LSM）。然而，尚未充分评估门静脉高压的非侵入性标志物和受控衰减参数（CAP）确定这些患者发生失代偿风险的能力。
我们收集了 2015 年至 2018 年期间在 2 个学术中心评估的 272 例 cACLD 患者的数据（XL 探头的 LSM≥10kPa；57%患有非酒精性脂肪性肝炎；平均体重指数为 33.8±6.5kg/m；中位 Child-Pugh 评分为 5；中位 LSM 为 16.8kPa；平均 CAP 为 318±66dB/m）。我们收集了失代偿（腹水、门静脉高压出血、黄疸、肝性脑病）和严重细菌感染的临床数据；中位随访时间为 17 个月（四分位距，11-24mo）。我们评估了这些事件与 LSM、CAP、LSM*脾大小/血小板计数（LSPS）和门静脉高压风险评分之间的关联。
12 例患者发生失代偿，5 例患者发生严重细菌感染。LSM、LSPS 和门静脉高压风险评分识别失代偿患者的受试者工作特征曲线下面积分别为 0.848（95%CI，0.720-0.976；P<.0001）、0.881（95%CI，0.798-0.954；P<.0001）和 0.890（95%CI，0.814-0.966；P<.0001）。多变量 Cox 回归分析显示，在非酒精性脂肪性肝炎患者中，LSM 和 CAP 与失代偿和严重细菌感染独立相关；CAP≥220dB/m 与失代偿风险降低相关（风险比，0.043，95%CI，0.004-0.476；P=0.01）。
LSM、LSPS 和门静脉高压风险评分可识别肥胖或超重的 cACLD 患者，这些患者发生失代偿和严重细菌感染的风险增加。
