Compensated liver cirrhosis: Natural course and disease-modifying strategies.

Ramesh Kumar, Sudhir Kumar, Sabbu Surya Prakash
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Abstract

Compensated liver cirrhosis (CLC) is defined as cirrhosis with one or more decompensating events, such as ascites, variceal haemorrhage, or hepatic encephalopathy. Patients with CLC are largely asymptomatic with preserved hepatic function. The transition from CLC to decompensated cirrhosis occurs as a result of a complex interaction between multiple predisposing and precipitating factors. The first decompensation event in CLC patients is considered a significant turning point in the progression of cirrhosis, as it signals a drastic decline in median survival rates from 10-12 years to only 1-2 years. Furthermore, early cirrhosis has the potential to regress as liver fibrosis is a dynamic condition. With the advent of effective non-invasive tools for detecting hepatic fibrosis, more and more patients with CLC are currently being recognised. This offers clinicians a unique opportunity to properly manage such patients in order to achieve cirrhosis regression or, at the very least, prevent its progression. There are numerous emerging approaches for preventing or delaying decompensation in CLC patients. A growing body of evidence indicates that treating the underlying cause can lead to cirrhosis regression, and the use of non-selective beta-blockers can prevent decompensation by lowering portal hypertension. Additionally, addressing various cofactors (such as obesity, diabetes, dyslipidaemia, and alcoholism) and precipitating factors (such as infection, viral hepatitis, and hepatotoxic drugs) that have a detrimental impact on the natural course of cirrhosis may benefit patients with CLC. However, high-quality data must be generated through well-designed and adequately powered randomised clinical trials to validate these disease-modifying techniques for CLC patients. This article discussed the natural history of CLC, risk factors for its progression, and therapeutic approaches that could alter the trajectory of CLC evolution and improve outcomes.

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代偿性肝硬化:自然病程和疾病改良策略。
代偿性肝硬化(CLC)是指伴有一种或多种失代偿事件的肝硬化,如腹水、静脉曲张出血或肝性脑病。CLC患者大多无症状,肝功能正常。CLC向失代偿性肝硬化的转变是多种诱发因素和促发因素之间复杂相互作用的结果。CLC患者的首次失代偿事件被认为是肝硬化进展的一个重要转折点,因为它标志着中位生存率从10-12年急剧下降到仅1-2年。此外,早期肝硬化有可能消退,因为肝纤维化是一种动态状态。随着检测肝纤维化的有效非侵入性工具的出现,目前越来越多的CLC患者被认可。这为临床医生提供了一个独特的机会来正确管理这些患者,以实现肝硬化消退,或者至少防止其进展。有许多新出现的方法可以预防或延迟CLC患者的失代偿。越来越多的证据表明,治疗潜在病因可以导致肝硬化消退,使用非选择性β受体阻滞剂可以通过降低门静脉高压来防止失代偿。此外,解决对肝硬化自然病程有不利影响的各种辅助因子(如肥胖、糖尿病、血脂异常和酒精中毒)和诱发因素(如感染、病毒性肝炎和肝毒性药物)可能有利于CLC患者。然而,必须通过精心设计和充分有力的随机临床试验来生成高质量的数据,以验证CLC患者的这些疾病改良技术。本文讨论了CLC的自然史、其进展的风险因素,以及可以改变CLC进化轨迹并改善结果的治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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