Asrani Sumeet K, Talwalkar Jayant A, Kamath Patrick S, Shah Vijay H, Saracino Giovanna, Jennings Linda, Gross John B, Venkatesh Sudhakar, Ehman Richard L
Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN, United States; Baylor University Medical Center, Dallas, TX, United States.
Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN, United States.
J Hepatol. 2014 May;60(5):934-9. doi: 10.1016/j.jhep.2013.12.016. Epub 2013 Dec 19.
BACKGROUND & AIMS: Non-invasive predictors identifying subjects with compensated liver disease at highest risk for transitioning to a decompensated state are lacking. We hypothesized that liver shear stiffness as measured by magnetic resonance elastography is an important non-invasive predictor of hepatic decompensation.
Among patients with advanced fibrosis undergoing magnetic resonance elastography (2007-2011), a baseline cohort and follow up cohort (compensated liver disease) were established. Cause specific cox proportional hazards analysis adjusting for competing risks was utilized to determine the association between elevated liver shear stiffness and development of decompensation (hepatic encephalopathy, ascites, variceal bleeding).
In the baseline cohort (n=430), subjects with decompensated liver disease had a significantly higher mean liver shear stiffness (6.8kPa, IQR 4.9-8.5) as compared to subjects with compensated liver disease (5.2kPa, IQR 4.1-6.8). After adjustment for Model for End Stage Liver Disease score, hepatitis C, age, gender, albumin, and platelet count, the mean liver shear stiffness (OR=1.13, 95% CI 1.03-1.27) was independently associated with decompensated cirrhosis at baseline. Over a median follow up of 27months (n=167), 7.2% of subjects with compensated disease experienced hepatic decompensation. In the follow up cohort, the hazard of hepatic decompensation was 1.42 (95% CI 1.16-1.75) per unit increase in liver shear stiffness over time. The hazard of hepatic decompensation was 4.96 (95% CI 1.4-17.0, p=0.019) for a subject with compensated disease and mean LSS value ⩾5.8kPa as compared to an individual with compensated disease and lower mean LSS values.
Baseline liver shear stiffness assessed by magnetic resonance elastography is independently associated with decompensated liver disease.
目前缺乏能够识别代偿期肝病患者向失代偿期转变风险最高的非侵入性预测指标。我们推测，通过磁共振弹性成像测量的肝脏剪切波弹性值是肝失代偿的一项重要非侵入性预测指标。
在接受磁共振弹性成像检查的晚期纤维化患者（2007 - 2011年）中，建立了一个基线队列和一个随访队列（代偿期肝病患者）。采用针对竞争风险进行调整的病因特异性Cox比例风险分析，以确定肝脏剪切波弹性值升高与失代偿（肝性脑病、腹水、静脉曲张出血）发生之间的关联。
在基线队列（n = 430）中，与代偿期肝病患者（5.2kPa，四分位间距4.1 - 6.8）相比，失代偿期肝病患者的平均肝脏剪切波弹性值显著更高（6.8kPa，四分位间距4.9 - 8.5）。在对终末期肝病模型评分、丙型肝炎、年龄、性别、白蛋白和血小板计数进行调整后，平均肝脏剪切波弹性值（OR = 1.13，95%可信区间1.03 - 1.27）在基线时与失代偿期肝硬化独立相关。在中位随访27个月（n = 167）期间，7.2%的代偿期疾病患者发生了肝失代偿。在随访队列中，随着时间推移，肝脏剪切波弹性值每增加一个单位，肝失代偿的风险为1.42（95%可信区间1.16 - 1.75）。与平均肝脏剪切波弹性值较低的代偿期疾病患者相比，平均肝脏剪切波弹性值⩾5.8kPa的代偿期疾病患者肝失代偿的风险为4.96（95%可信区间1.4 - 17.0，p = 0.019）。
通过磁共振弹性成像评估的基线肝脏剪切波弹性值与失代偿期肝病独立相关。
