PDF(Pubmed)
Abstract：
UNASSIGNED: Portal hypertension is a major complication of liver cirrhosis. Hepatic venous pressure gradient (HVPG) appears to be one of the best surrogates of clinical outcomes. However, the utility of elevated HVPG in predicting subsequent clinical decompensation is unclear.
UNASSIGNED: We analyzed 410 patients who underwent HVPG assessment between 2014 and 2018. Of these, we identified and analyzed 20 patients with HVPG >12 mmHg without evidence of clinical decompensation (defined as ascites, non-bleeding esophageal varices or bleeding esophageal varices, hepatic encephalopathy, hepato-pulmonary syndrome, or hepatic hydrothorax). Additionally, we compared this group to 40 randomly selected cirrhotic patients with HVPG >12 mmHg with signs of clinical decompensation. Clinical events were subsequently assessed (mean = 33 months) after HVPG measurement.
UNASSIGNED: Patients with high HVPG without evidence of clinical decompensation had significantly lower model for end stage liver disease (MELD) scores (8 ± 4) compared to decompensated patients (13 ± 8, P = 0.05). HVPG measurements were similar in compensated (17 ± 6 mmHg) and decompensated (18 ± 4 mmHg) patients. Over follow-up for 33 months, 8/20 compensated patients had a decompensating event and neither MELD (8 and 8, respectively) nor HVPG (17 mmHg and 18 mmHg, respectively) differentiated patients who remained compensated vs. those that decompensated. Serum albumin at the time of HVPG measurement was significantly higher in patients who remained compensated than those with a decompensating event (3.5 g/dL vs. 2.6 g/dL, respectively, P = 0.05).
UNASSIGNED: A small, unique, population of cirrhotic patients with substantially elevated HVPG appear to remain free of complications over long term follow-up.
UNASSIGNED: We analyzed 410 patients who underwent HVPG assessment between 2014 and 2018. Of these, we identified and analyzed 20 patients with HVPG >12 mmHg without evidence of clinical decompensation (defined as ascites, non-bleeding esophageal varices or bleeding esophageal varices, hepatic encephalopathy, hepato-pulmonary syndrome, or hepatic hydrothorax). Additionally, we compared this group to 40 randomly selected cirrhotic patients with HVPG >12 mmHg with signs of clinical decompensation. Clinical events were subsequently assessed (mean = 33 months) after HVPG measurement.
UNASSIGNED: Patients with high HVPG without evidence of clinical decompensation had significantly lower model for end stage liver disease (MELD) scores (8 ± 4) compared to decompensated patients (13 ± 8, P = 0.05). HVPG measurements were similar in compensated (17 ± 6 mmHg) and decompensated (18 ± 4 mmHg) patients. Over follow-up for 33 months, 8/20 compensated patients had a decompensating event and neither MELD (8 and 8, respectively) nor HVPG (17 mmHg and 18 mmHg, respectively) differentiated patients who remained compensated vs. those that decompensated. Serum albumin at the time of HVPG measurement was significantly higher in patients who remained compensated than those with a decompensating event (3.5 g/dL vs. 2.6 g/dL, respectively, P = 0.05).
UNASSIGNED: A small, unique, population of cirrhotic patients with substantially elevated HVPG appear to remain free of complications over long term follow-up.
摘要：
■门静脉高压是肝硬化的主要并发症。肝静脉压力梯度（HVPG）似乎是临床结果的最佳替代指标之一。然而,HVPG升高在预测后续临床失代偿中的效用尚不清楚.
■我们分析了2014年至2018年间接受HVPG评估的410例患者。其中,我们确定并分析了20例HVPG>12mmHg且无临床代偿证据的患者（定义为腹水，非出血食管静脉曲张或出血食管静脉曲张，肝性脑病,肝肺综合征,或肝性胸水)。此外,我们将该组与40例随机选择的HVPG>12mmHg且有临床代偿失调征象的肝硬化患者进行了比较.随后在HVPG测量后评估临床事件(平均=33个月)。
■与失代偿患者相比，无临床失代偿证据的高HVPG患者的终末期肝病模型（MELD）评分（8±4）显着降低（13±8，P=0.05）。在补偿（17±6mmHg）和失代偿（18±4mmHg）患者中，HVPG测量值相似。随访33个月，8/20代偿患者发生失代偿事件，既没有MELD（分别为8和8）也没有HVPG（17mmHg和18mmHg，分别)保持补偿的分化患者与那些失代偿的。在HVPG测量时的血清白蛋白在保持补偿的患者中明显高于患有失代偿事件的患者（3.5g/dLvs.2.6g/dL,分别,P=0.05)。
■一个小的，独特,在长期随访中,HVPG显著升高的肝硬化患者群体似乎仍无并发症.
■我们分析了2014年至2018年间接受HVPG评估的410例患者。其中,我们确定并分析了20例HVPG>12mmHg且无临床代偿证据的患者（定义为腹水，非出血食管静脉曲张或出血食管静脉曲张，肝性脑病,肝肺综合征,或肝性胸水)。此外,我们将该组与40例随机选择的HVPG>12mmHg且有临床代偿失调征象的肝硬化患者进行了比较.随后在HVPG测量后评估临床事件(平均=33个月)。
■与失代偿患者相比，无临床失代偿证据的高HVPG患者的终末期肝病模型（MELD）评分（8±4）显着降低（13±8，P=0.05）。在补偿（17±6mmHg）和失代偿（18±4mmHg）患者中，HVPG测量值相似。随访33个月，8/20代偿患者发生失代偿事件，既没有MELD（分别为8和8）也没有HVPG（17mmHg和18mmHg，分别)保持补偿的分化患者与那些失代偿的。在HVPG测量时的血清白蛋白在保持补偿的患者中明显高于患有失代偿事件的患者（3.5g/dLvs.2.6g/dL,分别,P=0.05)。
■一个小的，独特,在长期随访中,HVPG显著升高的肝硬化患者群体似乎仍无并发症.
