hepatic encephalopathy/carbohydrate

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Synaptic membrane complex carbohydrates in experimental hepatic encephalopathy.

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To evaluate further the status of synaptic plasma membranes (SPMs) in the brain in the syndrome of hepatic encephalopathy (HE) lipid- and protein-bound sialic acid and ganglioside and protein composition were investigated in SPMs from the brains of six rabbits with galactosamine-induced fulminant

[Effects of neomycin on intestinal digestion, absorption and fermentation of carbohydrates in patients with liver cirrhosis: evidence for an alternative therapeutic mechanism in hepatic encephalopathy].

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BACKGROUND Despite non absorbable antibiotics and neomycin may have antagonistic effects on intestinal bacterial environment, both have synergistic effects in the treatment of hepatic encephalopathy. This could be due to their action on different enteric flora or a neomycin induced carbohydrate

Beneficial effect of carbohydrate maldigestion induced by a disaccharidase inhibitor (AO-128) in the treatment of chronic portal-systemic encephalopathy. A double-blind, randomized, controlled trial.

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BACKGROUND The most widely used treatment of portal-systemic encephalopathy (PSE) is the administration of oral, non-absorbable disaccharides. Theoretically, the inhibition of intestinal disaccharidases should induce malabsorption of disaccharides and increase delivery of undigested carbohydrates to

Lactulose treatment of hepatic encephalopathy: effects on carbohydrate metabolism and colonic hydrogen ion concentration.

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Lactulose and combination therapy of hepatic encephalopathy: the role of the intestinal microflora.

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Lactulose is the most frequently utilized agent in the treatment of hepatic encephalopathy because of its efficacy and the fact that it has few serious side effects. How this nonabsorbable disaccharide works has been a matter of controversy, but evidence suggests that metabolism by the enteric flora

Influence of an orally administered protein mixture enriched in branched chain amino acids on the chronic hepatic encephalopathy (CHE) of patients with liver cirrhosis.

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8 patients with liver cirrhosis and chronic hepatic encephalopathy (CHE) stage I and II on a protein restricted diet and partly on lactulose therapy received in alternate periods of 4 to 8 weeks a) 45 g/day of a protein mixture enriched in branched chain amino acids (BCAA-protein), b) the same

Hepatic encephalopathy syndromes.

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Hepatic encephalopathy (HE) is a neuropsychiatric complication of acute and chronic liver failure. Its clinical spectrum ranges from minimal (subclinical) to overt encephalopathy. Psychometric and electrophysiological tests are helpful in diagnosing minimal HE. However, changes in metabolites in the

[Therapy of hepatic encephalopathy].

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The pathogenesis of the hepatic encephalopathy (HE) in spite of substantial progresses in this field still rests unclear. Actually four main hypotheses of the pathogenesis are discussed: the ammonia-hypothesis, the synergism-hypothesis, the hypothesis of the false neurotransmitters and that one of

Nutritional support in hepatic encephalopathy.

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Hepatic encephalopathy (HE) is a syndrome of global cerebral dysfunction resulting from underlying liver disease or portal-systemic shunting. HE can present as one of four syndromes, depending on the rapidity of onset of hepatic failure and the presence or absence of preexisting liver disease. The

Three cases of adult-onset type II citrullinemia treated with different therapies: Efficacy of sodium pyruvate and low-carbohydrate diet.

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We report three cases of adult-onset type II citrullinemia (CTLN2) treated with different therapies including one case successfully treated with p.o. administration of sodium pyruvate and low-carbohydrate diet. Although recent advances in liver transplantation have enabled successful treatment of

In vivo 13C NMR studies of compartmentalized cerebral carbohydrate metabolism.

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Localized 13C nuclear magnetic resonance (NMR) spectroscopy provides a unique window for studying cerebral carbohydrate metabolism through, e.g. the completely non-invasive measurement of cerebral glucose and glycogen metabolism. In addition, label incorporation into amino acid neurotransmitters

[Therapeutic approaches for patients with adult-onset type II citrullinemia (CTLN2): effectiveness of treatment with low-carbohydrate diet and sodium pyruvate].

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Adult-onset type II citrullinemia (CTLN2) is an autosomal recessive disease characterized by highly elevated plasma levels of citrulline and ammonia due to the urea cycle dysfunction associated with citrin deficiency. Patients with CTLN2 show various neurological symptoms with hyperammonemia closely

Regulation of urea synthesis by diet protein and carbohydrate in normal man and in patients with cirrhosis. Relationship to glucagon and insulin.

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Diet protein increases whereas carbohydrates decrease urea synthesis. Traditionally, these effects have been explained by changes in substrate supply. Diet protein intake increases whereas carbohydrate decreases blood amino acid concentration. However, glucose also decreases urea synthesis by a

Conventional diet therapy for hyperammonemia is risky in the treatment of hepatic encephalopathy associated with citrin deficiency.

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Citrin deficiency caused by SLC25A13 gene mutations develops into adult-onset type II citrullinemia (CTLN2) presenting with hepatic encephalopathy. Recent studies have suggested that excessive loading of carbohydrates is harmful in citrin-deficient individuals. Here we report a CTLN2 patient who

[Lactulose fermentation and lactose absorption in Chilean patients with liver cirrhosis: importance for hepatic encephalopathy therapy].

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BACKGROUND Non-absorbable carbohydrates are widely used in the therapy of hepatic encephalopathy. It has been argued that their effects depend on intestinal fermentation. In some geographic areas other than Chile up to 27% of healthy inhabitants are not able to increase breath hydrogen after a

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