Liver Unit, Hospital Clínic, IDIBAPS, University of Barcelona, Barcelona, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, Spain.
Liver Unit, Hospital Clínic, IDIBAPS, University of Barcelona, Barcelona, Spain; Centro de Investigación Biomédica Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, Spain; Barcelona Hepatic Hemodynamic Laboratory, Health Care Provider of the European Reference Network on Rare Liver Disorders (ERN-Liver), Barcelona, Spain.
Clin Gastroenterol Hepatol. 2022 Oct;20(10):2276-2286.e6. doi: 10.1016/j.cgh.2021.10.023. Epub 2021 Oct 21.
BACKGROUND & AIMS: Portal hypertension is the strongest predictor of hepatic decompensation and death in patients with cirrhosis. However, its discriminatory accuracy in patients with nonalcoholic fatty liver disease (NAFLD) has been challenged because hepatic vein catheterization may not reflect the real portal vein pressure as accurately as in patients with other etiologies. We aimed to evaluate the relationship between hepatic venous pressure gradient (HVPG) and presence of portal hypertension-related decompensation in patients with advanced NAFLD (aNAFLD).
Multicenter cross-sectional study included 548 patients with aNAFLD and 444 with advanced RNA-positive hepatitis C (aHCV) who had detailed portal hypertension evaluation (HVPG measurement, gastroscopy, and abdominal imaging). We examined the relationship between etiology, HVPG, and decompensation by logistic regression models. We also compared the proportions of compensated/decompensated patients at different HVPG levels.
Both cohorts, aNAFLD and aHVC, had similar baseline age, gender, Child-Pugh score, and Model for End-Stage Liver Disease score. Median HVPG was lower in the aNAFLD cohort (13 vs 15 mmHg) despite similar liver function and higher rates of decompensation in aNAFLD group (32% vs 25%; P = .019) than in the aHCV group. For any of the HVPG cutoff analyzed (<10, 10-12, or 12 mmHg) the prevalence of decompensation was higher in the aNAFLD group than in the aHCV group.
Patients with aNAFLD have higher prevalence of portal hypertension-related decompensation at any value of HVPG as compared with aHCV patients. Longitudinal studies aiming to identify HVPG thresholds able to predict decompensation and long-term outcomes in aNAFLD population are strongly needed.
门静脉高压症是肝硬化患者肝失代偿和死亡的最强预测因素。然而，其在非酒精性脂肪性肝病（NAFLD）患者中的区分准确性受到了挑战，因为肝静脉导管插入术可能无法像其他病因患者那样准确地反映真实的门静脉压力。我们旨在评估晚期 NAFLD（aNAFLD）患者的肝静脉压力梯度（HVPG）与存在门静脉高压相关失代偿之间的关系。
多中心横断面研究纳入了 548 例 aNAFLD 患者和 444 例晚期 RNA 阳性丙型肝炎（aHCV）患者，这些患者均进行了详细的门静脉高压评估（HVPG 测量、胃镜检查和腹部影像学检查）。我们通过逻辑回归模型检查了病因、HVPG 和失代偿之间的关系。我们还比较了不同 HVPG 水平下代偿/失代偿患者的比例。
aNAFLD 和 aHVC 两组患者的基线年龄、性别、Child-Pugh 评分和终末期肝病模型评分均相似。尽管 aNAFLD 组的肝功能相似，但 HVPG 中位数较低（13 与 15mmHg），且失代偿发生率较高（32%与 25%；P=.019）。对于分析的任何 HVPG 临界值（<10、10-12 或 12mmHg），aNAFLD 组的失代偿发生率均高于 aHCV 组。
与 aHCV 患者相比，任何 HVPG 值的 aNAFLD 患者门静脉高压相关失代偿的发生率更高。需要进行前瞻性研究以确定 HVPG 阈值，从而能够预测 aNAFLD 患者的失代偿和长期结局。
