Sarcopenia in cirrhosis: a clinical practice review

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.