Nutrition and Muscle in Cirrhosis

J Clin Exp Hepatol. 2017 Dec;7(4):340-357. doi: 10.1016/j.jceh.2017.11.001. Epub 2017 Nov 8.


As the cirrhosis progresses, development of complication like ascites, hepatic encephalopathy, variceal bleeding, kidney dysfunction, and hepatocellular carcinoma signify increasing risk of short term mortality. Malnutrition and muscle wasting (sarcopenia) is yet other complications that negatively impact survival, quality of life, and response to stressors, such as infection and surgery in patients with cirrhosis. Conventionally, these are not routinely looked for, because nutritional assessment can be a difficult especially if there is associated fluid retention and/or obesity. Patients with cirrhosis may have a combination of loss of skeletal muscle and gain of adipose tissue, culminating in the condition of "sarcopenic obesity." Sarcopenia in cirrhotic patients has been associated with increased mortality, sepsis complications, hyperammonemia, overt hepatic encephalopathy, and increased length of stay after liver transplantation. Assessment of muscles with cross-sectional imaging studies has become an attractive index of nutritional status evaluation in cirrhosis, as sarcopenia, the major component of malnutrition, is primarily responsible for the adverse clinical consequences seen in patients with liver disease. Cirrhosis is a state of accelerated starvation, with increased gluconeogenesis that requires amino acid diversion from other metabolic functions. Protein homeostasis is disturbed in cirrhosis due to several factors such as hyperammonemia, hormonal, and cytokine abnormalities, physical inactivity and direct effects of ethanol and its metabolites. New approaches to manage sarcopenia are being evolved. Branched chain amino acid supplementation, Myostatin inhibitors, and mitochondrial protective agents are currently in various stages of evaluation in preclinical studies to prevent and reverse sarcopenia, in cirrhosis.

Keywords: (PG) SGA, patient-generated SGA; AMPK, 5′ adenosine monophosphate-activated protein kinase; ASPEN, American Society of Parenteral and Enteral Nutrition; ATP, adenosine triphosphate; Akt/PKB, serine/threonine-specific protein kinase B; BIA, bio-electric impedance analysis; BMC, bone mineral content; BMI, body mass index; CT, computed tomography; DDLT, deceased donor liver transplantation; DRM, disease-related malnutrition; DXA, dual X-ray absorptiometry; ESPEN, European Society of Parenteral and Enteral Nutrition; FFI, Fried Frailty Index; FFM, fat free mass; FFMI, fat free mass index; FM, fat mass; HE, hepatic encephalopathy; LDLT, living donor liver transplant; LST, lean soft tissue; MAC, mid arm circumference; MAMC, mid arm muscle circumference; MELD, model for end-stage liver disease; MNA, Mini Nutritional Assessment; MRI, magnetic resonance imaging; NASH, non-alcoholic steatohepatitis; PCM, protein-calorie nalnutrition; REE, resting energy expenditure; RQ, respiratory quotient (or RQ or respiratory coefficient); SGA, Subjective Global Assessment; SMI, Skeletal Muscle Index; SPPB, Short Physical Performance Battery; TIPS, trans jugular intrahepatic portocaval shunts; TNF, tumour necrosis factor; TSF, triceps skin fild thickness; WHO, World Health Organisation; YPA, total psoas area; aKG, alfa keto glutarate; cirrhosis; mTORC1, mammalian target of rapamycin complex 1; nutrition.

Publication types

  • Review