Effects of Proteins in Patients With Cirrhosis and Prior Hepatic Encephalopathy
The purpose of this study is to compare a normal-protein diet containing branched-chain amino acids to a low-protein diet in patients with non-terminal cirrhosis (MELD < 25) who have developed an episode of hepatic encephalopathy within two months prior to inclusion.
Hepatic encephalopathy is a major complication of cirrhosis associated with poor prognosis and poor quality of life. Appearance of HE occurs in the setting of precipitating factors that increase plasma ammonia. The gastrointestinal tract is the primary source of ammonia, which is produced by enterocytes from glutamine and by colonic bacterial catabolism of nitrogenous sources, such as ingested proteins. This is the rationale for proposing low-protein diet as strategy to reduce ammonia production and as standard diet in patients with cirrhosis and hepatic encephalopathy. However, low-protein diet could cause wasting muscle and predispose to recurrence of hepatic encephalopathy, since muscle is an important site for extrahepatic ammonia removal.
Branched-chain amino acids have shown beneficial effects on mental state of patients with chronic hepatic encephalopathy. The possible mechanism of action may be improvement of nutritional status through induction of protein synthesis. However, role of branched-chain amino acids in treatment and prevention of acute hepatic encephalopathy is not established.
Administration of a normal-protein diet containing oral branched-chain amino acids may reduce recurrence of hepatic encephalopathy as compared to a low-protein diet.
Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Caregiver, Investigator), Primary Purpose: Prevention
Branched-chain amino acids, Maltodextrin
Corporació Sanitària Parc Taulí
Hospital Universitari Vall d'Hebron Research Institute
Results (where available)
- Source: http://clinicaltrials.gov/show/NCT00955500
- Information obtained from ClinicalTrials.gov on July 15, 2010
The purpose of this study is to determine whether Branched chain Amino Acids enhances the uptake of ammonia in muscle tissue.
With aging, there is a decrease in muscle mass and function especially in the energy storehouses of cells called mitochondria. Amino acids, the building blocks of protein, and insulin hav...
The aims of this study are (1) to study the benefit of branched-chain amino acids enriched nutrient-mixture by analyzing a variety of clinical parameter, including laboratory data, the dur...
This study will assess the behavioral effects of an amino acid mixture thought to influence serotonin function in individuals who have recovered from anorexia nervosa.
To elucidate the effect of preoperative supplementation of carbohydrate and branched-chain amino acids on postoperative insulin resistance in patients undergoing hepatic resection, we set ...
To investigate the usefulness of branched-chain amino acids (BCAA) before transarterial chemoembolization (TACE) or radiofrequency ablation (RFA).
To validate independent associations between branched-chain amino acids (BCAA) and other metabolites with coronary artery disease (CAD).
Recently, five branched-chain and aromatic amino acids were shown to be associated with the risk of developing type 2 diabetes (T2D).
The presenting symptoms and clinical course of 2 cases of intermittent maple syrup urine disease (MSUD) are described. Intermittent MSUD is a potentially life-threatening metabolic disorder caused by ...
Total Parenteral Nutrition (TPN) is necessary in patients unable to receive oral or enteral feeding for a period of at least 7 days. Branched-chain amino acids (BCAA): valine (Val), leucine (Leu), a...
Medical and Biotech [MESH] Definitions
Amino acids which have a branched carbon chain.
An autosomal recessive disorder of fatty acid oxidation, and branched chain amino acids (AMINO ACIDS, BRANCHED-CHAIN); LYSINE; and CHOLINE catabolism, that is due to defects in either subunit of ELECTRON TRANSFER FLAVOPROTEIN or its dehydrogenase, electron transfer flavoprotein-ubiquinone oxidoreductase (EC 184.108.40.206).
An autosomal recessive inherited disorder with multiple forms of phenotypic expression, caused by a defect in the oxidative decarboxylation of branched-chain amino acids (AMINO ACIDS, BRANCHED-CHAIN). These metabolites accumulate in body fluids and render a "maple syrup" odor. The disease is divided into classic, intermediate, intermittent, and thiamine responsive subtypes. The classic form presents in the first week of life with ketoacidosis, hypoglycemia, emesis, neonatal seizures, and hypertonia. The intermediate and intermittent forms present in childhood or later with acute episodes of ataxia and vomiting. (From Adams et al., Principles of Neurology, 6th ed, p936)
A PYRIDOXAL PHOSPHATE containing enzyme that catalyzes the reversible transamination of branched-chain AMINO ACIDS to 2-oxoglutarate.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.