Ghumman Ussama, Lee Brian, Bigham Dakota, Tsai Eugenia
Department of Internal Medicine, UT Health San Antonio, San Antonio, TX, USA.
Department of Hepatology, Texas Liver Institute, San Antonio, TX, USA; Division of Gastroenterology, UT Health San Antonio, San Antonio, TX, USA.
Ann Palliat Med. 2025 May;14(3):255-268. doi: 10.21037/apm-24-173.
Cirrhosis, a leading cause of death in the United States, is a result of chronic liver injury leading to progressive liver fibrosis. Initially asymptomatic, cirrhosis progresses to decompensated forms characterized by jaundice, ascites, gastroesophageal variceal bleeding, and hepatic encephalopathy (HE). Malnutrition, frailty, and sarcopenia are prevalent comorbidities in cirrhosis patients and are often used interchangeably in the clinical setting. Malnutrition is a condition marked by imbalanced nutrient intake and is closely related to the development of frailty and sarcopenia. Frailty is characterized by the decline in physiological reserve and function, while sarcopenia is the generalized loss of skeletal mass. Both are insidious complications of cirrhosis and also significantly influence morbidity, mortality, and transplant outcomes. Major contributing factors include decreased oral intake, poor nutrient uptake and deranged metabolism. Accurate assessment of frailty and sarcopenia in patients with cirrhosis is essential for predicting clinical outcomes. Interventions targeting frailty and sarcopenia could significantly improve patient prognosis. Nutritional interventions and physical activity promote muscle protein synthesis, increase muscle mass and mitigate sarcopenia. A cirrhosis-specific treatment includes ammonia-lowering agents to improve cognitive function and ultimately oral intake, and increase muscle mass. Emerging therapies, such as including L-ornithine L-aspartate, leucine-enriched branch-chained amino acids, hold promise in modulating skeletal muscle. This review explores the definitions, clinical manifestations, and consequences of malnutrition, frailty, and sarcopenia in cirrhosis, emphasizing the importance of early assessment and intervention.
肝硬化是美国主要的死亡原因之一，是慢性肝损伤导致进行性肝纤维化的结果。肝硬化最初无症状，会进展为失代偿期，其特征为黄疸、腹水、胃食管静脉曲张出血和肝性脑病（HE）。营养不良、身体虚弱和肌肉减少症在肝硬化患者中普遍存在，在临床环境中常被互换使用。营养不良是一种以营养摄入不均衡为特征的状况，与身体虚弱和肌肉减少症的发展密切相关。身体虚弱的特征是生理储备和功能下降，而肌肉减少症是骨骼肌质量的普遍丧失。两者都是肝硬化的隐匿性并发症，也会显著影响发病率、死亡率和移植结果。主要促成因素包括口服摄入量减少、营养吸收不良和代谢紊乱。准确评估肝硬化患者的身体虚弱和肌肉减少症对于预测临床结果至关重要。针对身体虚弱和肌肉减少症的干预措施可显著改善患者预后。营养干预和体育活动可促进肌肉蛋白质合成、增加肌肉量并减轻肌肉减少症。一种针对肝硬化的治疗方法包括使用降氨药物来改善认知功能并最终增加口服摄入量和肌肉量。新兴疗法，如L-鸟氨酸L-天冬氨酸、富含亮氨酸的支链氨基酸，有望调节骨骼肌。本综述探讨了肝硬化中营养不良、身体虚弱和肌肉减少症的定义、临床表现及后果，强调了早期评估和干预的重要性。
