In chronic liver disease, hepatic stellate cell activation and degeneration of liver sinusoidal endothelial cells lead to structural changes, which are secondary to fibrosis and the presence of regenerative nodules in the sinusoids, and to functional changes, which are related to vasoconstriction. The combination of such changes increases intrahepatic vascular resistance and causes portal hypertension. The subsequent increase in splanchnic and systemic hyperdynamic circulation further increases the portal blood flow, thereby exacerbating portal hypertension. In clinical practice, the hepatic venous pressure gradient is the gold-standard measure of portal hypertension; a value of ≥10 mm Hg is defined as clinically significant portal hypertension, which is severe and is associated with the risk of liver-related events. Hepatic venous pressure gradient measurement is somewhat invasive, so evidence on the utility of risk stratification by elastography and serum biomarkers is needed. The various stages of cirrhosis are associated with different outcomes. In viral hepatitis-related cirrhosis, viral suppression or elimination by nucleos(t)ide analog or direct-acting antivirals results in recompensation of liver function and portal pressure. However, careful follow-up should be continued, because some cases have residual clinically significant portal hypertension even after achieving sustained virologic response. In this study, we reviewed the current and future prospects for portal hypertension.

中文翻译：

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慢性肝病门静脉高压的发病机制和临床评估的最新进展。

在慢性肝病中，肝星状细胞活化和肝窦内皮细胞变性导致结构变化（继发于纤维化和肝窦中再生结节的存在），并导致功能变化（与血管收缩有关）。这些变化的结合增加了肝内血管阻力并导致门静脉高压。随后内脏和全身高动力循环的增加进一步增加门静脉血流量，从而加剧门静脉高压。在临床实践中，肝静脉压力梯度是衡量门脉高压的金标准；≥10 mm Hg 的值被定义为具有临床意义的门静脉高压，这种情况很严重，并且与肝脏相关事件的风险相关。肝静脉压力梯度测量具有一定的侵入性，因此需要弹性成像和血清生物标志物进行风险分层的实用性证据。肝硬化的不同阶段与不同的结果相关。在病毒性肝炎相关的肝硬化中，通过核苷（酸）类似物或直接作用抗病毒药物抑制或消除病毒会导致肝功能和门静脉压力的重新补偿。然而，应继续仔细随访，因为有些病例即使在实现持续的病毒学应答后仍残留有临床意义的门静脉高压。在这项研究中，我们回顾了门静脉高压症的当前和未来前景。