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La desnutrición es una complicación frecuente que influye negativamente en el pronóstico del enfermo con cirrosis hepática. La disminución de la ingesta junto con la aparición de diversas alteraciones endocrino-metabólicas condicionan un estado hipercatabólico que precisa de un mayor aporte energético. Una de las complicaciones que puede aparecer en la fase de cirrosis descompensada es la encefalopatía hepática. El reconocido papel del amonio en la patogenia de la encefalopatía hepática ha condicionado durante muchos años una restricción en el aporte de proteínas de estos enfermos. Sin embargo, no existe evidencia de que una dieta baja en proteínas mejore el curso de la encefalopatía hepática y sí de que empeore el estado nutricional y favorezca la aparición de distintas complicaciones relacionadas con la desnutrición. En este trabajo, se revisa el uso de aminoácidos ramificados y de proteínas de diferente origen, probióticos y simbióticos, antioxidantes, L-Ornitina-L-Aspartato, acetil-L-carnitina en enfermos con encefalopatía hepática.Protein calorie malnutrition is frequently a complication in the chronic liver disease patient and is considered to be a negative prognostic factor. Anorexia and several other endocrine metabolic complications produce an hypermetabolic state that needs more caloric intake. Hepatic encephalopathy is one of the developments possible in patients with descompensated cirrhosis. The wellknown role of ammonia in the pathogenesis of hepatic encephalopathy has determined a restriction in dietary protein along many decades. Nevertheless, there is no evidence about a low protein diet being better in the outcome of hepatic encephalopathy, it worsens, moreover, the nutritional status and helps in the development of many nutritional related complications. This article reviews the use of oral branched-chain amino acids and proteins of different sources, probiotics, synbiotics, antioxidants, oral L-Ornithine L-Aspartate and acetyl-L-carnitine in patients with hepatic encephalopathy.

La cirrosis representa el estadio final de muchas enfermedades crónicas del hígado y se asocia con malnutrición en mayor o menor grado, con independencia de su etiología, sobre todo en los estadios avanzados. Su origen es multifactorial, pudiendo señalarse tres factores que contribuyen a ella: a) la limitación o disminución de la ingesta; b) la alteración de la digestión y absorción de nutrientes; c) la interferencia en el metabolismo de los nutrientes. Un pobre estado nutricional se asocia con un peor pronóstico de supervivencia. Si la malnutrición calórico-proteica (MCP) es un predictor independiente de mortalidad o solo un reflejo de la severidad de la insuficiencia hepática, es algo que está sujeto a controversia. No hay consenso sobre cuales son los mejores criterios diagnósticos de MCP en la cirrosis. La evaluación de la malnutrición es extremadamente difícil puesto que muchos de los parámetros utilizados se afectan tanto por la enfermedad en sí como por los factores desencadenantes o etiológicos. Las alteraciones metabólicas remedan un estado hipercatabólico. Estos pacientes tienen una disminuida utilización y capacidad de almacenamiento de carbohidratos y un aumento del catabolismo proteico y graso, que conduce a la depleción de las reservas proteicas y lipídicas. Estas anormalidades, combinadas con un descenso en la ingesta y en la absorción de nutrientes, constituyen las bases de la MCP. La alteración metabólica más importante de los pacientes con enfermedad hepática avanzada es el cambio en el metabolismo de los aminoácidos. Los niveles plasmáticos de los aminoácidos de cadena ramificada (AARR) están disminuidos y los niveles de aminoácidos aromáticos (AAA) elevados, lo que tiene implicaciones terapéuticas. Entre las consecuencias de las alteraciones estructurales en la cirrosis, destaca el desarrollo de encefalopatía hepática, definida como una alteración en la función del sistema nervioso central que refleja una serie de manifestaciones neuropsiquiátricas, neuromusculares y de conducta. Se debe a la incapacidad del hígado enfermo para la metabolización de las neurotoxinas que se acumulan en el cerebro y que afectan a los neurotransmisores, atribuido al efecto tóxico del amonio sobre el tejido cerebral. El tratamiento nutricional reporta beneficios en los diferentes estadios de la enfermedad. A corto plazo, mejoría del balance nitrogenado, descenso en la estancia hospitalaria y mejoría de la función hepática. A largo plazo, disminución de la incidencia y severidad de la encefalopatía y mejoría de la calidad de vida. La suplementación con nutrición enteral puede mejorar el aporte proteico, descender la frecuencia de hospitalización, mejorar el estado nutricional, la función inmune y la severidad de la enfermedad. La restricción proteica no está indicada en la cirrosis compensada. Se recomienda una dieta conteniendo alrededor de 30 kcal/kg/d y 1,2 g de proteínas/kg/d. En la encefalopatía aguda puede necesitarse una restricción proteica temporal que no debe superar las 48 h y que debe minimizarse ya que, incluso en pacientes con EH, se obtienen mejores resultados sin una restricción proteica severa. La suplementación oral con AARR a largo plazo enlentece la progresión de la enfermedad hepática y prolonga la supervivencia y la calidad de vida. Se recomienda la suplementación con fibra o dietas con proteínas vegetales, que aportan alto contenido en fibra y menos AAA, o bien con proteínas lácteas además de una elevada relación calorías/nitrógeno.Cirrhosis represents the final stage of many chronic liver diseases and is associated to more or less pronounced hyponutrition, independently of the etiology, particularly at advanced stages. Its origin is multifactorial, with three factors contributing to it: a) limitation or decrease of intake; b) impairment in nutrients digestion or absorption; and c) the interference with nutrients metabolism. A poor nutritional status is associated with a poor survival prognosis. Whether caloric-protein malnourishment (CPM) is an independent predictor of mortality or only a marker of the severity of liver failure is subject to controversy. There is no consensus on which are the best diagnostic criteria for CPM in cirrhosis. Assessment of hyponutrition is extremely difficult since both the disease itself and the triggering or etiologic factors affect many of the parameters used. Metabolic impairments mimic a hypercatabolic state. These patients have decreased carbohydrate utilization and storage capacity and increased protein and fat catabolism leading to depletion of protein and lipid reserves. These abnormalities together with decreased nutrients intake and absorption are the bases for CPM. The most important metabolic impairment in patients with advanced liver disease is the change in amino acids metabolism. The plasma levels of branched amino acids (BAA) are decreased and of aromatic amino acids (AAA) are increased, which has therapeutic implications. Among the consequences of the structural impairments taking place in cirrhosis, we may highlight hepatic encephalopathy, defined as impaired central nervous system functioning that manifests as a series of neuropsychiatric, neuromuscular, and behavioral symptoms. These are due to the inability of the diseased liver to metabolize neurotoxins that accumulate in the brain affecting neurotransmitters and are attributed to the toxic effect of ammonium on the brain tissue. Nutritional therapy brings benefits in the different stages of the disease. In the short term, it improves nitrogen balance, decreases the hospital stay, and improves liver function. In the long term, it decreases the incidence and severity of encephalopathy and improves quality of life. Supplementation with enteral nutrition may improve protein intake, decrease the frequency of hospitalization, and improve the nutritional status, the immune function and the disease severity. Protein restriction is not indicated in compensated cirrhosis. A diet containing about 30 kcal/kg/d and 1.2 g of protein/kg/d is recommended. In acute encephalopathy temporary protein restriction may be needed, which should not last longer than 48 h and be minimized since even in patients with liver disease better outcomes are obtained without obtaining severe protein restriction. Oral supplementation with BAA slows the progression of liver disease and improves survival and quality of life. Supplementation should be done with fiber or diets with vegetable proteins, which bring high fiber content and less AAA, or either with dairy proteins in addition to a high ratio/nitrogen ratio.

Protein calorie malnutrition is frequently a complication in the chronic liver disease patient and is considered to be a negative prognostic factor. Anorexia and several other endocrine metabolic complications produce an hypermetabolic state that needs more caloric intake. Hepatic encephalopathy is one of the developments possible in patients with descompensated cirrhosis. The well-known role of ammonia in the pathogenesis of hepatic encephalopathy has determined a restriction in dietary protein along many decades. Nevertheless, there is no evidence about a low protein diet being better in the outcome of hepatic encephalopathy, it worsens, moreover, the nutritional status and helps in the development of many nutritional related complications. This article reviews the use of oral branched-chain amino acids and proteins of different sources, probiotics, synbiotics, antioxidants, oral L-Ornithine L-Aspartate and acetyl-L-carnitine in patients with hepatic encephalopathy. [ABSTRACT FROM AUTHOR]

Cirrhosis represents the final stage of many chronic liver diseases and is associated with more or less pronounced hyponutrition, independently of the etiology, particularly at advanced stages. Its origin is multifactorial, with three factors contributing to it: a) limitation or decrease of intake; b) impairment in nutrient digestion or absorption; and c) interference with nutrient metabolism. Poor nutritional status is associated with a poor survival prognosis. Whether caloric-protein malnourishment (CPM) is an independent predictor of mortality or only a marker of the severity of liver failure is subject to controversy. There is no consensus on which are the best diagnostic criteria for CPM in cirrhosis. Assessment of hyponutrition is extremely difficult since both the disease itself and the triggering or etiologic factors affect many of the parameters used. Metabolic impairments mimic a hypercatabolic state. These patients have decreased carbohydrate utilization and storage capacity and increased protein and fat catabolism leading to depletion of protein and lipid reserves. These abnormalities together with decreased nutrients intake and absorption are the bases for CPM. The most important metabolic impairment in patients with advanced liver disease is the change in amino acid metabolism. The plasma levels of branched amino acids (BAA) are decreased and those of aromatic amino acids (AAA) are increased, which has therapeutic implications. Among the consequences of the structural impairments taking place in cirrhosis, we may highlight hepatic encephalopathy, defined as impaired central nervous system functioning that manifests as a series of neuropsychiatric, neuromuscular, and behavioral symptoms. These are due to the inability of the diseased liver to metabolize neurotoxins that accumulate in the brain, affecting neurotransmitters, and are attributed to the toxic effect of ammonium on the brain tissue. Nutritional therapy brings benefits in the different stages of the disease. In the short term, it improves nitrogen balance, decreases the hospital stay, and improves liver function. In the long term, it decreases the incidence and severity of encephalopathy and improves quality of life. Supplementation with enteral nutrition may improve protein intake, decrease the frequency of hospitalization, and improve nutritional status, immune function and disease severity. Protein restriction is not indicated in compensated cirrhosis. A diet containing about 30 kcal/kg/d and 1.2 g of protein/kg/d is recommended. In acute encephalopathy temporary protein restriction may be needed, which should not last longer than 48 h and be minimized since even in patients with liver disease better outcomes are obtained without obtaining severe protein restriction. Oral supplementation with BAA slows the progression of liver disease and improves survival and quality of life. Supplementation should be done with fiber or diets with vegetable proteins, which bring high fiber content and less AAA, or with dairy proteins in addition to a high ratio/nitrogen ratio. [ABSTRACT FROM AUTHOR]