Meta‐analysis: oral or enteral nutritional supplementation in cirrhosis

Ney, Michael; Vandermeer, Ben; Zanten, Sander Jo Veldhuyzen van; M., M.; Gramlich, Leah; Tandon, Puneeta

doi:10.1111/apt.12252

Cited by 69 publications

(57 citation statements)

References 25 publications

(95 reference statements)

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“…An overview of these pathways is shown in Figure 2. A number of clinical studies and metaanalyses have failed to show significant benefit of nutritional supplementation in malnourished cirrhotic patients [18–20, 26]. This may be due to the impaired acetyl CoA generation that necessitates formation of acetyl CoA from non-pyruvate sources including amino acids and fatty acids.…”

Section: Mechanisms Of Skeletal Muscle Loss In Cirrhosismentioning

confidence: 99%

“…Therefore, reversing muscle mass is a priority area for therapeutic interventions in cirrhotic patients. Interventions that focus only on deficiency replacement have generally been ineffective while targeted therapies have the potential to reverse muscle loss[1, 18–20, 26, 66, 87]. The major strategies that have been used to improve muscle mass include supplemental calorie and protein intake, increased physical activity, supplemental hormone therapy, and mechanistic targeted treatments[17, 26, 109–111].…”

Section: Management Strategiesmentioning

confidence: 99%

“…Despite being widely recognized as a major complication of cirrhosis, most therapies to date have focused on the principle of “deficiency replacement” rather than targeted treatments and have generally been ineffective[17]. Therapies have focused on nutritional supplementation because reduced dietary intake was believed to be the major cause of malnutrition and sarcopenia but these approaches have been frequently inadequate in improving survival[18–20]. An integrated metabolic-molecular approach in a comprehensive array of models has shown that hyperammonemia is a mediator of the liver muscle axis[21, 22].…”

Section: Introductionmentioning

confidence: 99%

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Sarcopenia from mechanism to diagnosis and treatment in liver disease

Dasarathy

Merli

2016

Journal of Hepatology

457

520

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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 including survival, quality of life, development of other complications and post liver transplantation survival. Radiological image analysis is currently used 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 as a possible mediator of the liver-muscle axis has recently gained attention 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 TGFβ superfamily member and an increased phosphorylation of eukaryotic initiation factor 2α, mitochondrial dysfunction, increased reactive oxygen species that decrease protein synthesis and increased autophagy mediated proteolysis. 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 evaluation.

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Section: Mechanisms Of Skeletal Muscle Loss In Cirrhosismentioning

confidence: 99%

Section: Management Strategiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Sarcopenia from mechanism to diagnosis and treatment in liver disease

Dasarathy

Merli

2016

Journal of Hepatology

457

520

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“…A critical analysis of the data however suggests that most studies till date focus on increased dietary intake, late evening snack and increased protein intake and have been suggested to have limited improvement in nutritional outcomes in cirrhosis [10, 55, 56]. As discussed above, these interventions have a limited impact in improving the nutritional outcome cirrhosis because multiple molecular abnormalities contribute to a state of anabolic resistance.…”

Section: Introductionmentioning

confidence: 99%

“…However, despite extensive studies spanning decades, there is only very limited evidence that increased feeding via the oral or enteral route can potentially improve nutritional outcome [10, 56]. This can be explained by the molecular changes in the skeletal muscle that induce a state of anabolic resistance.…”

Section: Introductionmentioning

confidence: 99%

Treatment to Improve Nutrition and Functional Capacity Evaluation in Liver Transplant Candidates

Dasarathy¹

2014

Curr Treat Options Gastro

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Opinion Statement Liver transplantation is the definitive therapy for cirrhosis and malnutrition is the most frequent complication in these patients. Sarcopenia or loss of muscle mass is the major component of malnutrition in cirrhotics and adversely affects their outcome. In addition to the metabolic consequences, functional consequences of sarcopenia include reduced muscle strength and deconditioning. Despite nearly universal occurrence of sarcopenia and its attendant complications there are no established therapies to prevent or reverse the same. Major reasons for this deficiency include the lack of established standardized definitions or measures to quantify muscle mass and paucity of mechanistic studies or identified molecular targets to develop specific therapeutic interventions. Anthropometric evaluation, bioelectrical impedance analysis, DEXA scans are relatively imprecise measures of muscle mass and recent data on imaging measures to determine muscle mass accurately is likely to allow well defined outcome responses to treatments. Resurgence of interest in the mechanisms of muscle loss in liver disease has been directly related to the rapid advances in the field of muscle biology. Metabolic tracer studies on whole body kinetics have been complemented by direct studies on the skeletal muscle of cirrhotics. Hypermetabolism and anabolic resistance contribute to sarcopenia. Reduced protein synthesis and increased autophagy have been reported in cirrhotic skeletal muscle while the contribution of the ubiquitin-proteasome pathway is controversial. Increased plasma concentration and skeletal muscle expression of myostatin, a TGFβ superfamily member that causes reduction in muscle mass, have been reported in cirrhosis. Hyperammonemia and TNFα have been reported to increase myostatin expression and may be responsible for sarcopenia in cirrhosis. Nutriceutical interventions with leucine enriched amino acid mixtures, myostatin antagonists and physical activity hold promise as measures to reverse sarcopenia. There is even less data on muscle function and deconditioning in cirrhosis and studies in this area are urgently needed. Even though macronutrient replacement is a major therapeutic goal, micronutrient supplementation specifically, vitamin D is expected to improve outcomes.

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Oral nutrition support to prevent and treat undernutrition

Baldwin

2018

Advanced Nutrition and Dietetics in Nutrition Support

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Meta‐analysis: oral or enteral nutritional supplementation in cirrhosis

Abstract: SUMMARY BackgroundMalnutrition is a common and clinically significant problem in patients with cirrhosis. The impact of nutritional therapy remains unclear.

Cited by 69 publications

References 25 publications

Sarcopenia from mechanism to diagnosis and treatment in liver disease

Sarcopenia from mechanism to diagnosis and treatment in liver disease

Treatment to Improve Nutrition and Functional Capacity Evaluation in Liver Transplant Candidates

Oral nutrition support to prevent and treat undernutrition

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