1,721,425 research outputs found
Muscle mass vs. adipose tissue to predict outcome in cirrhosis: Which matters and in which patients?
Body composition is definitely different in men and women. Fora similar body mass index, women have a higher proportion ofadipose tissue and men have a higher proportion of lean (mus-cle) mass. Major changes in body composition can be observedin patients with advanced cirrhosis: the depletion of adipose tis-sue is more frequent in females while muscle loss is more char-acteristic of males
Sarcopenia from mechanism to diagnosis and treatment in liver disease
Sarcopenia or loss of skeletal muscle mass is the major component of malnutrition and is a frequent complication in cirrhosis that adversely affects clinical outcomes. These include survival, quality of life, development of other complications and post liver transplantation survival. Radiological image analysis is currently utilized to diagnose sarcopenia in cirrhosis. Nutrient supplementation and physical activity are used to counter sarcopenia but have not been consistently effective because the underlying molecular and metabolic abnormalities persist or are not influenced by these treatments. Even though alterations in food intake, hypermetabolism, alterations in amino acid profiles, endotoxemia, accelerated starvation and decreased mobility may all contribute to sarcopenia in cirrhosis, hyperammonemia has recently gained attention as a possible mediator of the liver-muscle axis. Increased muscle ammonia causes: cataplerosis of α-ketoglutarate, increased transport of leucine in exchange for glutamine, impaired signaling by leucine, increased expression of myostatin (a transforming growth factor beta superfamily member) and an increased phosphorylation of eukaryotic initiation factor 2α. In addition, mitochondrial dysfunction, increased reactive oxygen species that decrease protein synthesis and increased autophagy mediated proteolysis, also play a role. These molecular and metabolic alterations may contribute to the anabolic resistance and inadequate response to nutrient supplementation in cirrhosis. Central and skeletal muscle fatigue contributes to impaired exercise capacity and responses. Use of proteins with low ammoniagenic potential, leucine enriched amino acid supplementation, long-term ammonia lowering strategies and a combination of resistance and endurance exercise to increase muscle mass and function may target the molecular abnormalities in the muscle. Strategies targeting endotoxemia and the gut microbiome need further evaluatio
Dietary and nutritional indications in hepatic encephalopathy
The restriction of dietary protein has long been considered a main stay in the therapy of hepatic encephalopathy. More recently it has been recognized that protein energy malnutrition is frequent in advanced liver disease and may adversely affect the patients'outcome. Moreover studies on inter-organ ammonia exchange in liver cirrhosis have shown that the muscle may have a crucial role in ammonia detoxification. In light of these evidences nutritional guidelines have proposed that protein restriction should be avoided in patients with hepatic encephalopathy as protein requirement is even increased in cirrhotic patients. Survey about the current clinical practice show that protein restriction is still considered advisable in patients with hepatic encephalopathy, however a recent trial evidenced that a low protein diet in patients hospitalized for acute hepatic encephalopathy exacerbates protein breakdown without inducing any specific clinical benefit when compared to a normal protein regimen. The relevance of an adequate protein intake and possible strategies to implement protein tolerance are also discussed. © 2008 Springer Science+Business Media, LLC
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