Hepatic venous pressure gradient predicts clinical decompensation in patients with compensated cirrhosis
Hepatic venous pressure gradient predicts clinical decompensation in patients with compensated cirrhosis
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DOI：
10.1053/j.gastro.2007.05.024
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发表时间：
2007-08-01
期刊：
影响因子：
29.4
通讯作者：
Bosch, Jaime
中科院分区：
文献类型：
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作者：
Ripoll, Cristina;Groszmann, Roberto;Bosch, Jaime
背景和目标：我们的目的是确定临床失代偿的预测因子（定义为腹水、静脉曲张出血[VH]或肝性脑病[HE]的发展）在代偿性肝硬化和门静脉高压症患者中的应用，通过肝静脉压力梯度（HVPG）确定。我们分析了213例代偿性肝硬化门静脉高压症但无静脉曲张的患者，这些患者被纳入了一项评估β-阻断剂预防静脉曲张。所有人都有基线实验室检查和HVPG。每3个月对患者进行一次前瞻性随访，直至发生静脉曲张或VH或研究结束。为了获得完整的临床失代偿信息（直至研究终止），进行了病历审查。接受肝移植但无失代偿的患者在移植时删失。开发了考克斯回归模型以确定临床失代偿的预测因子。结果：中位随访时间为51.1个月。213例患者中62例（29%）发生失代偿：46例（21.6%）腹水，6例（3%）VH，17例（8%）HE。10名患者接受了移植，12名患者在没有临床失代偿的情况下死亡。基线时的中位HVPG为11 mm Hg（范围：6-25 mm Hg）。在多变量分析中，确定了3个失代偿预测因子：HVPG（风险比[HR]，1.11; 95%置信区间[CI]，1.05-1.17）、终末期肝病模型（MELD）（HP，1.15; 95% CI，1.03-1.29）和白蛋白（HR，0.37; 95% CI，0.22-0.62）。HVPG的诊断能力大于MELD或Child-Pugh score.Conclusions：HVPG，MELD，白蛋白独立预测代偿性肝硬化患者的临床失代偿。HVPG < 10 mm Hg的患者有90%的概率在中位4年的随访中不会发生临床失代偿。
Background & Aims: Our aim was to identify predictors of clinical decompensation (defined as the development of ascites, variceal hemorrhage [VH], or hepatic encephalopathy [HE]) in patients with compensated cirrhosis and with portal hypertension as determined by the hepatic venous pressure gradient (HVPG).Methods: We analyzed 213 patients with compensated cirrhosis and portal hypertension but without varices included in a trial evaluating the use of beta-blockers in preventing varices. All had baseline laboratory tests and HVPG. Patients were followed prospectively every 3 months until development of varices or VH or end of study. To have complete information, until study termination, about clinical decompensation, medical record review was done. Patients who underwent liver transplantation without decompensation were censored at transplantation. Cox regression models were developed to identify predictors of clinical decompensation. Receiver operating characteristic (ROC) curves were constructed to evaluate diagnostic capacity of HVPG.Results: Median follow-up time of 51.1 months. Sixty-two (29%) of 213 patients developed decompensation: 46 (21.6%) ascites, 6 (3%) VH, 17 (8%) HE. Ten patients received a transplant and 12 died without clinical decompensation. Median HVPG at baseline was 11 mm Hg (range, 6-25 mm Hg). On multivariate analysis, 3 predictors of decompensation were identified: HVPG (hazard ratio [HR], 1.11; 95% confidence interval [CI], 1.05-1.17), model of end-stage liver disease (MELD) (HP, 1.15; 95% CI, 1.03-1.29), and albumin (HR, 0.37; 95% CI, 0.22-0.62). Diagnostic capacity of HVPG was greater than for MELD or Child-Pugh score.Conclusions: HVPG, MELD, and albumin independently predict clinical decompensation in patients with compensated cirrhosis. Patients with an HVPG < 10 mm Hg have a 90% probability of not developing clinical decompensation in a median follow-up of 4 years.