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Safe and successful gut-restricted adsorbent strategy against cirrhosis and acute-on-chronic liver failure
Gut ( IF 23.0 ) Pub Date : 2024-10-26 , DOI: 10.1136/gutjnl-2024-332457
Schalk Willem Van der Merwe, Maite G Fernandez-Barrena

Cirrhosis marks the advanced stage of chronic liver disease characterised by sustained inflammation leading to the loss of hepatocytes and the progression of fibrosis. These structural and functional alterations profoundly impact blood flow within the hepatic microcirculation, potentially culminating in portal hypertension over time. Traditionally, the evolution of cirrhosis has been divided into two clinical phases: An initial asymptomatic stage known as compensated cirrhosis followed by decompensated cirrhosis, marked by the emergence of complications such as ascites, variceal bleeding, hepatic encephalopathy, jaundice, coagulopathy and bacterial infections. Decompensated cirrhosis typically signals a more aggressive disease course with patients susceptible to hepatic and extrahepatic organ dysfunction, complications or necessitating liver transplantation.1 It is imperative to recognise that decompensated cirrhosis transcends hepatic manifestations representing a systemic disorder. Recent observational studies in Europe, including chronic liver failure acute-on-chronic liver failure (CANONIC) and PREDICTing Acute-on-chronic liver failure (PREDICT), have further classified decompensated cirrhosis into non-acute and various forms of acute decompensation, potentially leading to acute-on-chronic liver failure (ACLF). However, the precise factors determining the trajectory towards decompensation in cirrhosis remain elusive. Accumulating evidence suggests that specific preceding events play pivotal roles in this progression. Notably, clinically significant portal hypertension, systemic inflammation and failure of the intestinal barrier leading to bacterial product translocation through the portal circulation are key events interdependently influencing each …

中文翻译:


针对肝硬化和慢加急性肝衰竭的安全成功的肠道限制性吸附剂策略



肝硬化标志着慢性肝病的晚期,其特征是持续炎症导致肝细胞丢失和纤维化进展。这些结构和功能改变深刻影响肝脏微循环内的血流,随着时间的推移可能最终导致门静脉高压症。传统上,肝硬化的演变分为两个临床阶段:最初的无症状阶段称为代偿期肝硬化,然后是失代偿期肝硬化,其特征是出现腹水、静脉曲张出血、肝性脑病、黄疸、凝血病和细菌感染等并发症。失代偿期肝硬化通常预示着病情的侵袭性更强,患者易患肝和肝外器官功能障碍、并发症或需要肝移植。必须认识到失代偿期肝硬化超越了代表全身性疾病的肝脏表现。欧洲最近的观察性研究,包括慢性肝衰竭慢加急性肝衰竭 (CANONIC) 和预测慢加急性肝衰竭 (PREDICT),将失代偿期肝硬化进一步分为非急性和各种形式的急性失代偿,可能导致慢加急性肝衰竭 (ACLF)。然而,决定肝硬化失代偿轨迹的确切因素仍然难以捉摸。越来越多的证据表明,特定的先前事件在这一进展中起着关键作用。值得注意的是,具有临床意义的门静脉高压症、全身炎症和导致细菌产物通过门静脉循环易位的肠道屏障衰竭是相互依赖影响每个的关键事件......
更新日期:2024-10-26
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