Nutrición y alcoholismo crónico / Nutrition and chronic alcohol abuse

Muchos pacientes con etilismo crónico presentan un cuadro clínico de malnutrición, ya sea porque reducen la ingestión habitual de nutrientes esenciales o porque el alcohol impide la adecuada digestión y absorción de los distintos principios inmediatos, vitaminas y minerales. Un ejemplo común es el déficit de vitamina A en estos enfermos. Además, los propios procesos metabólicos del etanol (vía de la ADH y sistema MEOS) generan productos intermediarios tóxicos (acetaldehído, radicales libres)que interfieren con el metabolismo normal de los principios inmediatos, principalmente lípidos, originando daño celular a través de fenómenos de preoxidación lipídica y alteraciones de la fluidez de membranas, depósitos grasos (esteatosis hepatocelular), inflamación secundaria a estrés oxidativo y síntesis de citoquinas proinflamatorias, activación de células estrelladas y fibrogénesis, etc. Los soportes nutricionales pueden ser eficaces para mejorarla enfermedad hepática alcohólica. Se aconseja el aporte de una dieta equilibrada, suplementos vitamínicos y tratamiento farmacológico con antioxidantes para reponerlos depósitos de glutatión reducido exhaustos. Es imprescindible que estos pacientes tengan una aproximación clínica multidisciplinaria para solucionar su problema de dependencia del alcohol

Many patients with chronic alcohol abuse present a clinical picture of malnourishment either because of reduced usual intake of essential nutrients or because alcohol precludes an appropriate digestion and absorption of the different essential elements, vitamins, and minerals. A usual example is vitamin A deficiency in these patients. Besides, ethanol metabolic pathways themselves (through the ADH and the MEOS system) generate toxic intermediate products (acetaldehyde, free radicals) interfering with normal metabolism of essential elements, mainlylipids, leading to cellular damage through lipid peroxidation mechanisms and impairment of the membrane fluidity, fat deposits (hepatocellular esteatosis), inflammation secondary to oxidative stress and proinflammatory cytokines, activation of stellate cells, fibrogenesis, etc. Nutritional supports may be effective to improve alcoholic liver disease. A balanced diet, vitamin supplements, and pharmacological therapy with antioxidants in order to recover depleted glutathione deposits are recommended. It is paramount that these patients have a multidisciplinary clinical approach to resolve the problem of alcohol dependency

Cirrosis y encefalopatía hepáticas: consecuencias clínico-metabólicas y soporte nutricional / Liver cirrhosis and encephalopathy: Clinical and metabolic consequences and nutritional support

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 quese acumulan en el cerebro y que afectan a los neurotransmisores, atribuido al efecto tóxico del amonio sobre el tejido cerebral. (...)

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 differentstages 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

Dietary saturated fatty acids reverse inflammatory and fibrotic changes in rat liver despite continued ethanol administration.

We investigated the potential of dietary saturated fatty acids to reverse alcoholic liver injury despite continued administration of alcohol. Five groups (six rats/group) of male Wistar rats were studied. Rats in groups 1 and 2 were fed a fish oil-ethanol diet for 8 and 6 weeks, respectively. Rats in groups 3 and 4 were fed fish oil and ethanol for 6 weeks before being switched to isocaloric diets containing ethanol with palm oil (group 3) or medium-chain triglycerides (MCTs, group 4) for 2 weeks. Rats in group 5 were fed fish oil and dextrose for 8 weeks. Liver samples were analyzed for histopathology, lipid peroxidation, nuclear factor-kappaB (NF-kappaB) activation, and mRNAs for cyclooxygenase-2 (Cox-2) and tumor necrosis factor-alpha (TNF-alpha). Endotoxin in plasma was determined. The most severe inflammation and fibrosis were detected in groups 1 and 2, as were the highest levels of endotoxin, lipid peroxidation, activation of NF-kappaB, and mRNAs for Cox-2 and TNF-alpha. After the rats were switched to palm oil or MCT, there was marked histological improvement with decreased levels of endotoxin and lipid peroxidation, absence of NF-kappaB activation, and reduced expression of TNF-alpha and Cox-2. A diet enriched in saturated fatty acids effectively reverses alcohol-induced necrosis, inflammation, and fibrosis despite continued alcohol consumption. The therapeutic effects of saturated fatty acids may be explained, at least in part, by reduced endotoxemia and lipid peroxidation, which in turn result in decreased activation of NF-kappaB and reduced levels of TNF-alpha and Cox-2.

Influence of liver failure, ascites, and energy expenditure on the response to oral nutrition in alcoholic liver cirrhosis.

The influence of liver failure, ascites, and energy expenditure on the response to oral nutrition was assessed in a group of 55 alcoholic cirrhotic patients. Caloric intake, nutritional status, resting energy expenditure (REE), and Child-Pugh score were evaluated before and after 1 mo of oral nutrition. Patients were severely malnourished, 73% had muscular midarm circumference (MMAC) below the 5th percentile of a reference population, 51% had triceps skinfold thickness below the 25th percentile. Eleven patients were in class A of Child, 19 in class B, and 25 in class C. Twenty-six patients were nonascitic, whereas ascites was resolved in 10 ascitic patients by the end of the study and 19 patients had refractory ascites. Liver damage was more pronounced and did not improve during the study in patients with refractory ascites. Caloric intake was approximately 40 kcal/kg of body weight and was in the same range in the three groups according to Child classification. Fat mass (FM) increased, respectively, from 17.4% +/- 1.7% to 19.5% +/- 1.4%, P < 0.01, in Child A patients; from 17.1% +/- 1.4% to 19.3% +/- 1.4%, P < 0.001, in Child B patients; and from 17.6% +/- 1.5% to 18.8% +/- 1.5%, P < 0.05, in Child C patients. The increase in FM was comparable in the three groups, whereas MMAC and the creatinine/height ratio did not change significantly. FM was lower and did not increase in patients with refractory ascites. Child C patients were characterized by an increase in the rate of glucose oxidation (P < 0.02) and a decrease in the rate of lipid oxidation (P < 0.05). High-density lipoprotein cholesterol and apolipoprotein (Apo) A1 were reliable indices of improvement of liver function in patients with severe liver failure, ApoA1 was also a marker of improvement of metabolic impairment. With respect to the measured REE/predicted REE ratio calculated according to Harris-Benedict equation (r), 19 patients were considered hypermetabolic (r < 1.1), 30 normometabolic (0.9 < r < 1.1), and 6 hypometabolic (r < 0.9). An increase in FM correlated with r (P < 0.01) and was more marked in hypermetabolic patients. In contrast to the other two groups, Child-Pugh score and nutritional status remained unchanged in the hypometabolic patients. These results show that severe liver failure did not preclude improvement of nutritional status provided caloric intake was high. In Child C patients, improvement of nutritional status paralleled improvement of liver function and normalization of oxidative metabolism. Refractory ascites had negative effects on changes in nutritional status and liver function. Despite adequate caloric intake to energy requirements, hypometabolism has a poor prognosis regarding both nutritional status and liver function.

Influência do grau de comprometimento hepático sobre a circulaçäo e excreçäo renal do ácido úrico, em pacientes cirróticos / Influence of the degreees of chronic hepatic failure on the circulation and renal excretion of uric acid in cirrhotic patients

A influência do grau de insuficiência hepatocelular (na cirrose hepática) sobre a circulaçäo e excreçäo do ácido úrico foi investigada em 12 pacientes cirróticos, de etiologia alcoólica, classificados em Child A (n=5) e Child B+C (n=7), todos do sexo masculino de 27 a 59 anos de idade, comparativamente ao grupo controle saudável (n=5), pareado por sexo e idade. A excreçäo urinária do ácido úrico e dos demais metabólitos nitrogenados (uréia, amônia e creatinina) foi estudada nas condiçöes de dieta hipoprotéica-hipoenergética (0,4g-20kcal/kg/d) e normoprotéica-normoenergética (1,14g-38kcal/kg/d). Os níveis séricos de ácido úrico, de albumina e alfa-1 antitripsina (alfa 1AT) foram determinados em amostras de sangue obtidas após jejum. A presença da doença hepática resultou na elevaçäo dos níveis de alfa 1AT, e o agravamento hepatocelular, na queda de albuminemia, sem alteraçäo significativa do ácido úrico circulante. A excreçäo urinária do ácido úrico foi semelhante entre os grupos, em ambas as dietas, porém, na dieta hipoprotéica-hipoenergética, o ácido úrico näo acompanhou o padräo de excreçäo da uréia e da creatinina, o que pode ser atribuído às quedas da ureogênese e da massa muscular (creatinogênese), com o agravamento da doença ou a maior capacidade renal em reter ácido úrico, nestas condiçöes. Isto pode ser configurado matematicamente, relacionando-se metabólitos excretados na urina com seus níveis plasmáticos, mostrando hipoexcreçäo de 45 por cento dos hepatopatas, tanto para o ácido úrico como para a creatinina. Assim, a menor produçäo hepática do ácido úrico, pelos pacientes cirróticos, seria compensada pela menor excreçäo renal do metabólito, preservando os níveis plasmáticos. A importância fisiológica deste processo adaptativo estaria fundamentada na participaçäo do estresse oxidativo, na gênese e perpetuaçäo da cirrose pelo álcool, e nas propriedades anti-oxidantes do ácido úrico.

The effect of posture on central blood volume in patients with preascitic cirrhosis on a sodium-restricted diet.

The status of the central blood volume in cirrhosis is controversial. A combination of sodium restriction and upright posture, which redistributes intravascular volume to dependent parts of the body should further aggravate a contracted central blood volume reduction. The aim of this study was to determine the effect of upright posture and sodium restriction on central blood volume (CBV) in preascitic cirrhotic patients, compared with controls. Eight male, preascitic, alcoholic cirrhotic subjects and eight healthy male controls were studied while on a 20-mmol/d sodium diet. Measurements of CBV by radionuclide angiography, and neurohumoral factors were performed on day 7 in both supine and erect positions and cardiac output and systemic vascular resistance (SVR) was calculated. Sodium restriction resulted in less weight loss in the cirrhotic patients (P = .03), with significantly lower plasma renin activity (P = .001). Similar central blood volumes and systemic hemodynamics were observed in both groups in the supine posture. In contrast to the cirrhotic patients, in the control subjects, upright posture resulted in a significant reduction in cardiac output (P = .002) and increase in SVR (P = .005), associated with a decrease in all blood volumes which were significantly less than in the cirrhotic patients. Mean arterial pressure was maintained in both groups in both postures. In conclusion, with sodium restriction, preascitic cirrhotic patients have less intravascular volume contraction than control patients. Erect posture results in redistribution of this relatively expanded intravascular volume to the CBV. Therefore, a low-sodium diet can be safely administered in preascitic cirrhotic patients.

Long-term oral refeeding of patients with cirrhosis of the liver.

A previous study has shown that malnourished, clinically stable patients with liver cirrhosis are in protein and energy balance at their spontaneous dietary intake and that an improvement in nutritional status cannot be anticipated at this intake (Nielsen et al. 1993). In the present study we examined to what extent oral intake could be increased by nutritional support, and to what extent dietary protein would be retained with increased intake. The techniques used for balance studies were also validated since this information is not available for patients with liver cirrhosis. Fifteen malnourished patients with alcoholic liver cirrhosis were given increasing amounts of a balanced ordinary diet for 38 (SE 3) d. Intakes of protein and energy were recorded by weighing servings and leftovers on food trays. Protein intake was calculated from food tables. Total N disposal was calculated after measurement of urinary N excretion, and protein balance was calculated from the N balance. A validation study of protein balance in a subgroup of patients (analysis of N in food by the duplicate portion technique, correction for incomplete recovery of urine by measurement of urinary para-aminobenzoic acid (PABA) after administration of PABA tablets, and measurement of faecal N) did not change protein balance values. Protein intake increased from 1.0 (SE 0.1) g/kg per d to 1.8 (SE 0.1) g/kg per d. With increasing protein intake, 84 (SE 8)% of the increase in intake was retained. The rate of protein retention was not saturated at the intakes obtained in this study. Protein intolerance was only encountered in one patient. Available evidence indicates that the requirement for achieving N balance is increased in these patients but protein retention is highly efficient with increased intake. Protein retention is dependent on energy balance. Energy intake was calculated from food tables and total energy expenditure was calculated by the factorial method. A validation study was performed in a subgroup of patients. The energy contents of food sampled by the duplicate portion technique, and of urine and faeces were measured by bomb calorimetry. Resting energy expenditure (REE) was measured by indirect calorimetry before and at the end of the study, and O2 uptake during bicycle exercise was measured before and at the end of the study. The measured intake of metabolizable energy was on average 13% lower than the value given in food tables. Calculated energy expenditure was not changed by the validation study.(ABSTRACT TRUNCATED AT 250 WORDS)

Postprandial de novo lipogenesis in alcoholic liver cirrhosis: relationship with fuel homeostasis and nutritional status.

The prevalence and nutritional consequences of postprandial de novo lipogenesis were evaluated in 24 stable alcoholic cirrhotic patients. Energy expenditure and the rates of nutrient oxidation were assessed by indirect calorimetry after an overnight fast and 2 h after a standard meal supplying 15 kcal/kg (63 kJ/kg) of body weight. Postprandially, net lipogenesis occurred in 16 patients (group L+) as shown by a respiratory quotient clearly above 1.00 (P < 0.01). The rate of lipid oxidation remained positive in 8 patients (group L-). The main mechanism involved in this metabolic pathway appeared to be a sharp postprandial hyperinsulinaemia. When compared to group L+, patient group L- showed an impaired thermic effect of food (P < 0.05), a lower rate of glucose oxidation (P < 0.05) and a mild hyperketonaemia (P < 0.05) at fasting levels. Muscular and fat masses were lower (respectively P < 0.05 and P = 0.05) and the severity of the disease as assessed by the Child-Pugh classification was more pronounced in this group (P < 0.02). The occurrence of postprandial lipogenesis in stable cirrhotic patients is related to better nutritional status. Such a metabolic pathway may explain the nutritional heterogeneity of cirrhotics and is likely to have an effect on the benefits of refeeding.

[Effect of diet on serum macroelement levels in patients with alcoholic lesions of the liver]. / Vliianie diety na soderzhanie makroélementov v syvorotke krovi u bol'nykh s alkogol'nym porazheniem pecheni.

The content of seven main biometals: sodium, potassium, calcium, magnesium, zinc, copper, iron was studied in the blood serum of patients with alcoholic affection of the liver verified clinically and morphologically. In contrast to literature data, it has been established that the levels of the main elements in the blood serum of patients with alcoholic affections of the liver may be normal, and concentrations of zinc, copper and iron are even elevated. The initial body mass of patients significantly influences the mineral spectrum of the blood serum: the levels of zinc and copper in patients with excessive body mass and obesity were significantly higher than in those with normal body mass. The content of the main elements in the blood serum was not changed in relation to the degree of the liver affection and alimentary therapy.

[The potentials for the dietetic therapy of alcoholic liver lesions]. / Vozmozhnosti dieticheskoi terapii alkogol'nykh porazhenii pecheni.

Most frequent and typical changes of the food status in patients with alcoholic diseases of the liver have been considered by the author. Typical concomitant gastroenterologic disorders in this category of patients have been described. The changes detected have required an adequate dietetic correction to eliminate the imbalance in nutrition and to stimulate the resources of the affected liver. The dietetic correction has proved to be sufficiently effective in most patients. The investigations conducted have shown the necessity of dietotherapy as an important component of the combined treatment of alcoholic affections of the liver.

Nutritional support in hospitalized patients with alcoholic liver disease.

The effects of a nutritional support in hospitalized patients with alcoholic cirrhosis and liver failure were studied in a controlled protocol. Thirty-six patients were included, 17 were randomly assigned to an experimental group and the rest to a control group. Experimentals received a diet aiming at 50 kcal (209 kJ)/kg bodyweight/d and 1.5 g protein/kg bodyweight/d (as proteins of high biological value). Controls received the standard diet prescribed by the attending physician. The severity of liver failure and the nutritional status on admission were similar in both groups. The measured energy intake in controls was 1813 +/- 121 kcal/d (7589 +/- 506 kJ/d) and 2707 +/- 71 kcal/d (1131 +/- 297 kJ/d) in experimentals (P less than 0.001). The protein intake in controls was 47 +/- 3.8 g/d and in experimentals 80 +/- 3 g/d (P less than 0.001). There were seven deaths during the study period (two experimentals and five controls). No differences were observed in the evolution of liver failure, hepatic encephalopathy or nutritional status between both study groups. It is concluded that a higher energy and protein intake in these patients does not have adverse effects and is associated with a non-significant reduction in mortality.

Utilization of alpha-ketoisocaproate for synthesis of hepatic export proteins and peripheral proteins in normal and cirrhotic subjects.

The ratio R, defined as (percent of dose of 14C)/(percent of dose of 3H) in the leucine of plasma fibrinogen, albumin, immunoglobulin G (IgG), red cell globin, and salivary mucin, was measured in 7 normal adults and in 5 cirrhotic patients during continuous intragastric infusion of 1-14C-labeled alpha-ketoisocaproate (KIC) and 3H-labeled leucine. The ratio R measured in whole body protein has been shown in rat experiments to be a measure of the nutritional efficiency of KIC relative to leucine. In normal subjects, R in albumin and fibrinogen became constant (0.63 +/- 0.05) after the third hour and were indistinguishable from one another. The ratio R in IgG was similar and constant. The ratio R in plasma leucine (0.62 +/- 0.06) was significantly lower than R in mucin (0.86 +/- 0.04) or globin (0.73 +/- 0.04), indicating that these latter proteins derive a significant fraction of their leucine from KIC transaminated locally, rather than from circulating leucine. Results in 5 cirrhotic patients were the same, except that R in IgG and R in globin were significantly increased. Thus, cirrhosis does not alter the efficiency, relative to leucine, with which oral KIC is used for synthesis of export proteins by the liver, but increases the efficiency with which it is used for the synthesis of some proteins peripherally.

Effects of vegetable diets on nitrogen metabolism in cirrhotic subjects.

This study compared the effect of a vegetable diet with an animal protein diet on various aspects of nitrogen metabolism to identify what components of the vegetable diet might be causing beneficial therapeutic effects in hepatic encephalopathy. Vegetable diets contained 4.5-fold greater amounts of fiber (56 +/- 3 g/day) and reduced amounts of methionine, tyrosine, and tryptophan. In 6 stable cirrhotic subjects without encephalopathy, vegetable diets caused a significant reduction in the urea production rate from 106 +/- 5 to 89 +/- 5 mg X kg-1 X 24 h-1 of urea nitrogen. This was mainly accounted for by a fall in urinary urea output. Vegetable diets also caused a fall in total urinary nitrogen, which was accounted for by the fall in urea nitrogen, and a comparable increase in fecal nitrogen from 12 +/- 2 to 28 +/- 5 mg X kg-1 X 24 h-1. The fecal bacterial fraction contained 63% of the increase in stool nitrogen. Most plasma amino acids, including methionine, tyrosine, phenylalanine, as well as total and free tryptophan, were unchanged. The effect of vegetable diets on nitrogen metabolism can be mainly accounted for by the increased intake of dietary fiber and increased incorporation and elimination of nitrogen in fecal bacteria.

Controlled trial of nutritional supplementation, with and without branched chain amino acid enrichment, in treatment of acute alcoholic hepatitis.

Sixty-four patients admitted with acute alcoholic hepatitis, with or without underlying cirrhosis, were randomized regardless of encephalopathy to receive a controlled diet either alone, or supplemented orally, nasogastrically, or intravenously as necessary, with 2000 kCal and 10 g nitrogen daily. Whether this came from a conventional protein source or a branched chain amino acid enriched formulation was also randomly determined. In the absence of renal failure, nitrogen intakes of 10 g or more daily were invariably associated with positive nitrogen balance, but complications of liver dysfunction prevented the attainment of significantly more positive balance in the supplemented groups than in controls. Neither in the series as a whole, nor in any identifiable subgroup of patients, was mortality affected by treatment. Changes in prothrombin time and in measured nutritional parameters during the study did not differ between supplemented and control groups, and the observed changes in midarm muscle circumference appeared to reflect changes in degree of fluid retention. Neither enteral nor parenteral branched chain amino acids showed any consistent effect upon encephalopathy.

Slowly digested carbohydrate food improves impaired carbohydrate tolerance in patients with cirrhosis.

To test whether impaired carbohydrate tolerance in cirrhosis could be modified by dietary means ten cirrhotic patients, five of them taking insulin, took as breakfast either lentils or wholemeal bread and cottage cheese containing the same amount of carbohydrate and protein. Lentils resulted in significantly diminished blood glucose, insulin (in those not on insulin) and gastric inhibitory peptide responses. Enteroglucagon and neutrotensin levels were high with lentils, suggesting that absorption of lentil carbohydrate continued into the ileum with perhaps some malabsorption, so confirming the results of earlier studies in vitro. However, breath hydrogen studies on a separate group of eight healthy volunteers indicated that the difference in carbohydrate malabsorption between lentil, and wholemeal bread was insignificant. It is suggested that slowly digested carbohydrate foods, such as leguminous seeds, may minimize carbohydrate intolerance in patients with cirrhosis.

Branched-chain amino acid-enriched elemental diet in patients with cirrhosis of the liver. A double blind crossover trial.

In 14 patients with cirrhosis of the liver and portal-systemic shunts the effect of a branched-chain amino acid-enriched elemental diet on portal systemic encephalopathy, routine laboratory parameters and plasma amino acids was investigated. In addition to the standard therapy including protein restriction (40 g/day) the patients received 44 g of an amino acid-protein mixture containing 30% of branched-chain amino acids and placebo over 3 months in a crossover regimen. Plasma valine and leucine increased significantly, whereas all other amino acids, including the ratio (formula: see text), remained unchanged. The electroencephalogram, number connection test, clinical state and laboratory parameters were not influenced by therapy with branched-chain amino acids. Thus, orally administered branched-chain amino acids probably have no influence on hepatic encephalopathy but are an adequate source of nitrogen in patients with cirrhosis of the liver.