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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Von Willebrand factor as new noninvasive predictor of portal hypertension, decompensation and mortality in patients with liver cirrhosis
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Von Willebrand factor as new noninvasive predictor of portal hypertension, decompensation and mortality in patients with liver cirrhosis

机译:Von Willebrand因子可作为肝硬化患者门脉高压,代偿失调和死亡率的新的非侵入性预测因子

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von Willebrand factor antigen (vWF-Ag) is elevated in patients with liver cirrhosis, but the clinical significance is unclear. We hypothesized that vWF-Ag levels may correlate with portal pressure, measured by hepatic venous pressure gradient (HVPG), and predict clinically significant portal hypertension (CSPH; HVPG ≥10 mmHg), decompensation and mortality. Portal hemodynamics were assessed by HVPG measurement, whereas vWF-Ag levels were measured by enzyme-linked immunosorbent assay. During follow-up, complications of liver cirrhosis, death or transplantation were recorded. Two hundred and eighty-six patients (205 male and 81 female; mean age, 56 years) with liver cirrhosis were included. vWF-Ag correlated with HVPG (r = 0.69; P < 0.0001) and predicted CSPH independently of Child Pugh score. Higher vWF-Ag levels were associated with varices (odds ratio [OR] = 3.27; P < 0.001), ascites (OR = 3.93; P < 0.001) and mortality (hazard ratio: 4.41; P < 0.001). Using a vWF-Ag cut-off value of ≥241%, the AUC for detection of CSPH in compensated patients was 0.85, with a positive predictive value and negative predictive value of 87% and 80%, respectively. Compensated patients had 25% mortality after 53 months if the vWF-Ag was <315% compared to 15 months in patients with vWF-Ag >315% (P < 0.001). Decompensated patients had a mortality of 25% after 37 and 7 months if their vWF-Ag was <315% and >315%, respectively (P = 0.002). In compensated patients with a vWF-Ag >315% median time to decompensation or death was 32 months compared with 59 months in patients with vWF-Ag <315%. vWF-Ag equals Model for End-Stage Liver Disease (MELD) in mortality prediction (area under the curve [AUC] = 0.71 for vWF-Ag versus AUC = 0.65 for MELD; P = 0.2). Conclusion: vWF-Ag is a new, simple and noninvasive predictor of CSPH. A vWF-Ag cut-off value at 315% can clearly stratify patients with compensated and decompensated liver cirrhosis in two groups with completely different survival. vWF-Ag may become a valuable marker for the prediction of mortality in patients with liver cirrhosis in clinical practice.
机译:肝硬化患者中von Willebrand因子抗原(vWF-Ag)升高,但临床意义尚不清楚。我们假设vWF-Ag水平可能与门静脉压力相关,通过肝静脉压力梯度(HVPG)进行测量,并预测临床上显着的门静脉高压症(CSPH; HVPG≥10mmHg),代偿失调和死亡率。门静脉血流动力学通过HVPG测量进行评估,而vWF-Ag水平通过酶联免疫吸附测定进行测量。在随访期间,记录了肝硬化,死亡或移植的并发症。包括286例肝硬化患者(男205例,女81例;平均年龄56岁)。 vWF-Ag与HVPG相关(r = 0.69; P <0.0001),并且独立于Child Pugh评分预测CSPH。较高的vWF-Ag水平与静脉曲张(优势比[OR] = 3.27; P <0.001),腹水(OR = 3.93; P <0.001)和死亡率(危险比:4.41; P <0.001)相关。使用vWF-Ag截止值≥241%,用于补偿患者的CSPH检测的AUC为0.85,阳性预测值和阴性预测值分别为87%和80%。如果vWF-Ag <315%,则代偿患者在53个月后死亡率为25%,而vWF-Ag> 315%(P <0.001)则为15个月。如果失代偿患者的vWF-Ag分别<315%和> 315%,则其在37和7个月后的死亡率为25%(P = 0.002)。在vWF-Ag> 315%的补偿患者中,失代偿或死亡的中位时间为32个月,而vWF-Ag <315%的患者为59个月。在死亡率预测中,vWF-Ag等于终末期肝病模型(MELD)(vWF-Ag曲线下面积[AUC] = 0.71,而MELD的AUC = 0.65; P = 0.2)。结论:vWF-Ag是CSPH的一种新型,简单且无创的预测因子。 vWF-Ag截止值为315%可以清楚地将两组肝硬化代偿和代偿失调的患者分为两组,其生存率完全不同。在临床实践中,vWF-Ag可能成为预测肝硬化患者死亡率的重要标志。

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