Lattanzi Barbara, D'Ambrosio Daria, Merli Manuela
Department of Clinical Medicine, Gastroenterology, Sapienza University of Rome, Italy.
J Clin Exp Hepatol. 2019 Jan-Feb;9(1):125-130. doi: 10.1016/j.jceh.2018.04.007. Epub 2018 May 5.
Sarcopenia is an important burden in liver cirrhosis representing a negative prognostic factor for mortality. Moreover, sarcopenia is an independent predictor of complications in patients with liver cirrhosis, including Hepatic Encephalopathy (HE). An association between sarcopenia and HE in liver cirrhosis has been reported in recent studies, indeed both these complications often affect patients with advanced liver cirrhosis and may exert a synergic effect in deteriorating patients' outcome. Episodes of HE occur more often in patients with muscle depletion. The rationale for these finding is based on the role played by muscle in ammonia detoxification due to the inability of urea synthesis in the cirrhotic liver. Consequently, muscle depletion may have relevant implications in favoring hyperammonemia and HE. At the same time hyperammonemia has been found to impair muscle protein synthesis through myostatin down-regulation. From this point of view, modulation of diet and amelioration of nutritional status and muscle mass can be considered a potential goal to prevent this vicious circle and improve the cognitive impairment in cirrhotic patients.
肌肉减少症是肝硬化的一项重要负担,是死亡率的一个负面预后因素。此外,肌肉减少症是肝硬化患者并发症的独立预测因素,包括肝性脑病(HE)。最近的研究报道了肝硬化患者中肌肉减少症与肝性脑病之间的关联,事实上,这两种并发症经常影响晚期肝硬化患者,并可能在恶化患者预后方面发挥协同作用。肝性脑病发作在肌肉消耗的患者中更常见。这些发现的理论依据是,由于肝硬化肝脏无法合成尿素,肌肉在氨解毒中所起的作用。因此,肌肉消耗可能对促进高氨血症和肝性脑病具有重要影响。同时,已发现高氨血症通过下调肌生成抑制素损害肌肉蛋白质合成。从这个角度来看,调整饮食以及改善营养状况和肌肉量可被视为预防这种恶性循环并改善肝硬化患者认知障碍的一个潜在目标。