2022 年胃肠病学头条新闻：预防代偿性肝硬化患者失代偿

StephenW

2022 年胃肠病学头条新闻：预防代偿性肝硬化患者失代偿

撰写者
     斯科特·科特勒医学博士

Villanueva 等人于 10 月发表在《肝脏病学杂志》上的一项研究提出了预防代偿性肝硬化患者失代偿的重要目标。1 失代偿性肝硬化的定义是腹水、静脉曲张破裂出血或肝性脑病，与高死亡率相关 . 具有临床显着门静脉高压症（CSPH；即肝静脉门静脉梯度 >10 mm Hg）的患者存在肝功能失代偿的风险。 Villanueva 等人进行了一项个体参与者数据荟萃分析，包括四项随机对照试验，这些试验包括代偿性肝硬化和 CSPH 患者，他们接受非选择性 β 受体阻滞剂卡维地洛 (n = 181) 与内窥镜静脉曲张结扎术 (EVL) 或无积极治疗 (n = 171）。 与接受 EVL 或未接受积极治疗的患者相比，接受卡维地洛治疗的患者发生肝功能失代偿的风险较低，这主要是由于腹水的发生减少，死亡率和肝脏相关死亡率较低。

降低代偿期肝硬化患者肝功能失代偿风险的首要考虑是治疗肝病的根本原因。 Villanueva 等人的研究表明卡维地洛在减少 CSPH 患者的肝功能失代偿中发挥作用。 卡维地洛具有抗肾上腺素能血管舒张作用，可降低肝内血管阻力，在降低门静脉压力方面优于普萘洛尔和纳多洛尔。

在临床实践中实施 Villanueva 等人的研究结果的一个实际考虑是识别代偿期肝硬化和 CSPH 患者，因为大多数中心并不常规测量肝静脉门静脉梯度。 CSPH 的替代标志物包括内窥镜检查发现胃食管静脉曲张（包括小静脉曲张）、门体循环影像学检查或多普勒检查门静脉逆流，以及酒精、病毒或非肥胖 NASH 相关患者 肝硬化，瞬态弹性成像显示肝脏硬度 >25 kPa。2,3 需要在这些重要发现的基础上进行前瞻性研究。

StephenW

2022 Top Story in Gastroenterology: Preventing Decompensation in Patients With Compensated Cirrhosis

Written by
    Scott J. Cotler MD

A study by Villanueva et al published in the Journal of Hepatology in October addresses the important goal of preventing decompensation in patients with compensated cirrhosis.1 Decompensated cirrhosis, defined by development of ascites, variceal bleeding, or hepatic encephalopathy is associated with a high mortality rate. Patients with clinically significant portal hypertension (CSPH; ie, hepatic vein portal gradient >10 mm Hg) are at risk for hepatic decompensation. Villanueva et al performed an individual participant data meta-analysis including four randomized controlled trials comprising patients with compensated cirrhosis and CSPH who received the non-selective beta blocker carvedilol (n = 181) versus endoscopic variceal ligation (EVL) or no active treatment (n = 171). Patients who received carvedilol had a lower risk of hepatic decompensation, primarily owing to a reduction in the development of ascites, and lower rates of mortality and liver-related mortality than those who underwent EVL or received no active treatment.

The first consideration in reducing the risk of hepatic decompensation in patients with compensated cirrhosis is to treat the underlying cause of liver disease. The study by Villanueva et al suggests a role for carvedilol in decreasing hepatic decompensation in patients with CSPH. Carvedilol has anti-adrenergic vasodilatory effects that decrease intrahepatic vascular resistance, and it offers an advantage over propranolol and nadolol in reducing portal pressures.

A practical consideration in implementing the findings of Villanueva et al in clinical practice is to identify patients with compensated cirrhosis and CSPH, as measurements of the hepatic vein portal gradient are not routinely taken at most centers. Surrogate markers of CSPH include the findings of gastroesophageal varices (including small varices) on endoscopy, portosystemic collaterals on imaging, or reversal of flow in the portal vein by Doppler, and, in patients with alcohol, viral, or non-obese NASH-related cirrhosis, liver stiffness >25 kPa by transient elastography.2,3 Prospective studies are needed to build on these important findings.