Acid Liver Disease Research Articles

Clinical use of branched-chain amino acids in liver disease, sepsis, trauma, and burns.

The branched-chain amino acids (BCAAs)--leucine, isoleucine, and valine--share unique biochemical properties that may make them useful in altered physiologic states. They can be metabolized independently of liver function to provide energy, other amino acids, or small nitrogenous compounds. This unique ability makes the BCAAs a desirable supplement in liver disease with encephalopathy and, to a lesser extent, in sepsis with hepatic dysfunction. Furthermore, the BCAAs play a role in the regulation of protein synthesis, suggesting beneficial effects in catabolic states such as postoperative stress, trauma, renal failure, and burns. However, initial studies in these areas have presented equivocal results.

Amino acids in liver disease.

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肝疾患時の胆汁酸とBilirubinに関する研究

The clinical significance of serum bilirubin sulfate, one of the direct bilirubin, was evaluated in various liver diseases with over 2 mg/dl of serum bilirubin concentration. The diagnosis included 25 cases of acute hepatitis, 8 cases of chronic hepatitis, 8 cases of liver cirrhosis and 16 cases of liver cirrhosis with hepatoma. Bilirubin sulfate was fractioned by Yonei's solvent partition method. The clinical significance of bilirubin sulfate was assessed by comparison of bilirubin sulfate with the other bilirubin fractions and with non-specific liver function tests. The results were as follows; 1) The existence of bilirubin sulfate was confirmed in human sera. Bilirubin sulfate concentration correlated with serum total bilirubin and direct bilirubin, and the correlation with direct bilirubin was higher than total bilirubin. 2) The percentage of bilirubin sulfate in total and direct bilirubin increased in the order of acute hepatitis, chronic hepatitis and liver cirrhosis. The percentage of bilirubin sulfate was higher in direct bilirubin than in total bilirubin. 3) Bilirubin sulfate showed the following correlation with non-specific liver function tests; with cholesterol in acute hepatitis, with choline esterase in chronic hepatitis and with GOT, cholesterol and bile acid in liver diseases.

Amino acids in liver disease: a cause of hepatic encephalopathy?

Amino acids in liver disease: a cause of hepatic encephalopathy?

Amino Acids in Liver Disease: A Cause of Hepatic Encephalopathy?

Patients with chronic liver disease often have elevations in plasma levels of aromatic amino acids, including tyrosine, phenylalanine, and tryptophan, as well as methionine, glutamate, aspartate, and ornithine; branched-chain amino acids, leucine, isoleucine, and valine, are usually depressed. 1,2 Fischer et al 3 have focused the interest of clinicians and investigators alike on the pathogenesis and treatment of hepatic encephalopathy by suggesting that the depressed ratio of branched-chain to aromatic amino acids may have etiologic importance in hepatic coma. 4 A corollary of this hypothesis is that restoration of this ratio to normal should not only provide specific treatment for hepatic encephalopathy but should also allow administration of enough protein equivalents of amino acids to attain nitrogen balance without precipitating hepatic coma. Nutritional repletion may also prevent further deterioration of hepatic structure and function. A recent dietary survey reported substantially less protein consumption in patients with alcoholic hepatitis and cirrhosis

Evaluation of fluorimetrically estimated serum bile acid in liver disease

Fasting serum bile acid (SBA) was measured by the enzymic fluorimetric method coupled with the NAD-resazurin system in 23 controls, 35 asymptomatic carriers of HBs antigen including 4 e antigen carriers and 91 patients with various liver diseases. All HBs and e antigen carriers showed SBA within the normal range. SBA was most significantly correlated with serum bilirubin (γ = 0.74) and was a more sensitive index for impaired liver function than bilirubin or alkaline phosphatase in 164 randomly chosen samples from the liver disease group. In serial determinations of SBA with reference to GOT, GPT, changing patterns of these two parameters were classified into the parallel type and the discrepant type. Thirty two out of 40 cases with chronic liver disease belonged to the parallel type. SBA remained abnormal even after the normalization of transaminase in 12 out of 20 resolving episodes in cases of the parallel type, regardless of diagnosis. Since SBA changed according to the stage of the disease activity, serial and simultaneous estimation of SBA and GOT, GPT was found to be helpful in the observation of liver diseases. Maximum values of SBA elevation in an endogenous bile acid tolerance test after eating two egg yolks were higher than controls in 4 out of 7 cases with liver disease, who were associated with normal fasting SBA.

Bile acids in liver disease associated with inflammatory bowel disease.

To investigate the possibility that bowel-related liver disease is due to accumulation of abnormal bile acids in the enterohepatic circulation, bile acids have been measured in gall-bladder bile and portal blood of patients with chronic bowel disease, none of whom had liver disease. There was no difference in the composition and concentration of bile acids in bile and portal blood compared with control patients. In a second study, serum bile acid composition and concentrations were similar in two groups of patients with liver disease, whether they had bowel disease or not. In a further study, post-prandial serum bile acid concentrations were not elevated in a group of patients with chronic bowel disease, making it unlikely that subcliical liver disease was present. No evidence has been found to support the hypothesis that bowel-related liver disease in man results from the action of abnormal bile acids.

Serum bile acids in liver disease

Serum bile acids have been measured in patients with a wide variety of liver diseases using a technique which separates the major individual conjugated and free bile acids. Total serum bile acids may be elevated up to 100 times the normal concentration in patients with liver disease and this increase consists largely of conjugated bile acids. The ratio of glycine-conjugated to taurine-conjugated bile salts is low in all types of liver disease and this is found particularly in the serum of patients with obstructive jaundice. There is a decrease in the ratio of trihydroxy:dihydroxy cholanic acid in patients with cirrhosis.

Plasma Non-esterified Fatty Acids in Liver Disease

Plasma Non-esterified Fatty Acids in Liver Disease

Plasma free fatty acid in liver disease.

The plasma free fatty acid level was raised in the majority of 131 patients with a variety of liver disorders, and included both those with severe liver cell damage and those with relatively good liver cell function and obstructive jaundice. This raised level is probably due to an increased mobilization of depot fat, for glucose, which inhibits peripheral liberation of free fatty acids, caused a fall in the plasma level and obliteration of the femoral venous-arterial difference in patients with liver disease comparable with that in normal persons. In addition, the plasma free fatty acid flux was measured using palmitate-1-C(14) and was found to be increased in patients with liver disease.

Increased Concentration of Free Fatty Acids in Liver Disease.

SummaryFasting plasma FFA concentrations were determined in 34 subjects with cirrhosis and 28 without cirrhosis.Mean fasting FFA concentrations were elevated in subjects with cirrhosis and this was most marked in those subjects with acute hepatic failure or hepatic coma. The increased FFA concentrations were not accompanied by a rise in blood ketone concentrations.

Studies on the Metabolism of Keto Acid in Liver Diseases

Studies on the Metabolism of Keto Acid in Liver Diseases

Estimation of blood pyruvic acid in liver diseases and in pancreatic diabetes

A comparative study of blood pyruvic acid and keto-acids content in health, diabetes, and liver disease, has been carried out, using both the colorimetric and the chromatographic methods. The Chromatographic method gives lower concentrations than does the direct colorimetric method and does not show an increase of blood pyruvic acid in diabetes. The results that have been obtained are compared and discussed.