Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hepatic encephalopathy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1976

Insulin, glucagon, aminoacid imbalance, and hepatic encephalopathy.

Hepatic encephalopathy (H.E.) is associated with and perhaps caused by changes in plasma-aminoacid patterns--decreased branched-chain aminoacids (B.C.A.A.) and increased aromatic aminoacids (A.A.A.). The decreased B.C.A.A. may be in part secondary to hyperinsulinaemia, but the B.C.A.A. are catabolised by both fat and muscle. The increase in A.A.A. may reflect a "catabolic stimulus" reflected in hyperglucagonaemia, particularly in severe hepatic failure and H.E., and a decreased insulin/glucagon ratio. Endogenous protein, lean body-mass, or liver then releases large amounts of A.A. and the A.A.A. cannot be catabolised by the failing liver, and thus accumulate in the circulation. With decreased plasma-B.C.A.A., the molar ratio of B.C.A.A. and A.A.A. decreases allowing the toxic A.A.A. to penetrate the blood-brain barrier in increased amounts and encephalopathy develops. Appropriate therapy for H.E. must include reversal of the "catabolic state" by providing sufficient B.C.A.A. and calories to decrease the flux of A.A.A. from muscle and liver, and the restoration of the normal molar ratio of B.C.A.A. and A.A.A.

Amino Acids↗
PubMed1977

Octopamine and ammonia plasma levels in hepatic encephalopathy.

It has been recently proposed that hepatic encephalopathy could be due to the accumulation of octopamine acting as a false neurotransmitter, and the increase of ammonia might reflect this accumulation. The simultaneous determination of octopamine and ammonia was performed in 88 cases with or without encephalopathy. The correlation between the two substances appeared to be good (P less than 0.01; r = 0.5), except in shunted patients. All the cases with low octopamine and high ammonia were patients who had been submitted to surgical portal-systemic anastomosis. This finding does not seem to be coincidental; in this type of patients, the mechanism of hepatic encephalopathy could involve other beta-hydroxyphenylethanolamines in addition to octopamine. The presence of the inhibition of the reaction of transmethylation constantly observed during octopamine plasma assay is in favour of this hypothesis.

Ammonia↗
PubMed1976

The contingent negative variation and psychological findings in chronic hepatic encephalopathy.

Early diagnosis of chronic hepatic encephalopathy (CHE) in the latent stage before the appearance of clinical signs, should reduce both morbidity and mortality as deterioration is often preventable by treatment. Since existing diagnostic procedures are inadequate, we have investigated a test in which morphine is used as a provocative agent and any resulting change in cerebral function assessed by measurement of the CNV in conjuction with a psychological trail test. Twenty six patients were studied, 6 of whom had clinically overt CHE. A significant correlation (P less than 0.05) between the change in CNV amplitude with morphine and the initial CNV amplitude, consistent with the theoretical model of Tecce (1972), was found. However, the CNV and trail test results taken as a whole did not allow even those patients with overt CHE to be distinguished and we conclude that it is unlikely that differing degrees of latent CHE could be detected.

Chronic Disease↗
PubMed1976

The effect of normalization of plasma amino acids on hepatic encephalopathy in man.

Previous work from this laboratory has suggested that the plasma amino acid pattern, known to be deranged in hepatic encephalopathy, may be related causally. In order to test this hypothesis, 23% dextrose and a special amino acid solution whose components were calculated to normalize the plasma amino acid pattern were infused in 11 patients, eight with chronic cirrhosis and acute exacerbation (Group 1) and three patients with fulminant hepatitis (Group 2), in amounts of up to 120 Gm. of protein equivalent per 24 hours. Plasma amino acids were abnormal but different in both groups. In Group 1 (cirrhosis) changes in plasma amino acid pattern including elevated phenylalanine, tyrosine, glutamate, aspartate, and methionine and decreased valine, leucine, and isoleucine. In Group 2 all amino acids were elevated, with the exception of the branched chains which were normal. Hepatic encephalopathy improved in all patients in Group 1 and in one of three patients in Group 2 following the infusion. The ratio (see article) showed an excellent correlation with a grade of encephalopathy. When this ratio, previously 1.0 in the presence of encephalopathy, returned to the normal value near 3.0 to 3.5, encephalopathy improved. An excellent correlation was obtained between the ratio and the grade of encephalopathy and was dose related as well. The results suggest that different amino acid patterns in hepatic encephalopathy of differing etiologies require treatment modalities which may differ for the two types of encephalopathy. Whereas amino acid infusion appears to be a valuable, efficacious way of providing nutrition in treating hepatic encephalopathy in patients with cirrhosis and acute deterioration and coma, other means of therapy such as plasms "laundering" appear to be necessary in patients with fulminant hepatitis.

Adult↗
PubMed1975

The role of plasma amino acids in hepatic encephalopathy.

The dog with an end-to-side portacaval shunt has a plasma amino acid pattern similar to that in man with chronic liver disease and encephalopathy. When dogs with end-to-side portacaval shunts manifested symptoms of hepatic encephalopathy, superior caval catheters were placed and one of three solutions was infused. Whereas almost all animals given a commercially available synthetic amino acid mixture died, a special mixture formulated to normalize plasma amino acids was associated with 100 percent survival and few neurological symptoms. The results suggest that manipulation and normalization of plasma amino acids in animals with hepatic failure may be efficacious in providing adequate nutrition while minimizing hepatic encephalopathy. Moreover, these experiments may shed some light on the mechanism of human hepatic encephalopathy.

Albumins↗
PubMed1979

Chronic hepatic encephalopathy. Long-term therapy with a branched-chain amino-acid-enriched elemental diet.

Therapy of chronic hepatic encephalopathy is often frustrating, limited as it is by the ability to adequately nourish such patients. Protein is needed for repair, but such patients are intolerant of protein. Previous work from this and other laboratories has suggested that the distorted plasma amino acid pattern may be causally related to hepatic encephalopathy. A single, well-studied, long-term patient received therapy with a branched-chain amino-acid-enriched elemental diet that not only enabled adequate nutrition with protein but resulted in improvement in hepatic function as well as reversal of some aspects of hepatic encephalopathy that heretofore have been deemed irreversible. The results confirm that branched-chain-enriched amino acid diets previously successful in the intravenous mode may be successfully used in chronic long-term support of patients with protein intolerance, with improvement in hepatic function secondary to improvement in nutrition.

Administration, Oral↗
PubMed1977

A patient with recurrent hepatic encephalopathy and chronic renal failure treated successfully with long-term hemodialysis.

A 38-year-old man suffering from chronic recurrent hepatic enchephalopathy due to liver cirrhosis complicated with chronic renal failure had been maintained well by regular hemodialysis treatment for 14 months. Only four episodes of hepatic encephalopathy occurred in that period. Each of four episodes of disturbed consciousness was accompanied by slightly elevated blood ammonia levels. Energetic serial dialysis for 5-7 days was necessary for its recovery. The factors causing hepatic encephalopathy did not appear to be easily dialysable as compared with those of uremic coma. It is concluded that the hemodialysis is quite an effective treatment for the recurrent type of hepatic encephalopathy.

Adult↗
PubMed1978

Plasma amino acids in hepatic encephalopathy.

In 75 cases of histologically verified liver cirrhosis the plasma amino acids were determined by ion exchange chromatography and the results were correlated with different liver function tests as prothrombin time, pseudocholinesterase, serum albumin, GOT, bilirubin and venous ammonia. Out of these parameters prothrombin time, pseudocholinesterase and serum albumin significantly correlated with the sum of branched-chain amino acids and with the Fischer's quotient (molar ratio of branched-chain and aromatic amino acids). Methionin and aromatic amino acids inversely correlated with these parameters, additionally methionin positively correlated with bilirubin and GOT. By comparing plasma amino acid levels in cirrhotics without and with hepatic encephalopathy (grade 3 or 4) no significant differences were found. "Fischer's quotient" showed an overlap in patients with and without encephalopathy. Therefore the precipitation of hepatic encephalopathy is not fully explained by the changes in plasma amino acids. Therapeutic administrations of specially mixtures of amino acids with a high content in branched-chain and a low content in aromatic amino acids correct the plasma amino inbalance for a short time and improves hepatic encephalopathy.

Amino Acids↗
PubMed1976

[Present-day therapy of hepatic encephalopathy (author's transl)].

The ammonia hypothesis is the most likely explanation for the pathogenesis of hepatic encephalopathy in cirrhosis patients. Reduction of hyperammonemia is therefore the most consistent therapy. From this point of view, the antibiotics have a central significance for the reduction of ammonia formation in the intestinal tract. Equally important is the correction of the hypopotassemia, which may lead to a renally induced hyperammonemia. At the same time, disorders which favor the cerebral toxicity of ammonia, especially anemia and hypoxias, must be compensated. These various measures have improved the prognosis for hepatic encephalopathy of the cirrhosis patient, but were without effect on the course of the coma in severe toxic hepatitis. During the last toxic hepatitis. During the last 10 years, many treatment methods have been reported whose efficacy, however, could not be proved.

Acid-Base Imbalance↗
PubMed1978

Plasma phenylethanolamine in hepatic encephalopathy.

It has been suggested that amines other than octopamine may be involved in the pathogenesis of hepatic encephalopathy. Plasma phenylethanolamine has been determined by a radioenzymatic method in twenty-six biopsy-proven cirrhotics with or without encephalopathy and in seven normal adults. Phenylethanolamine plasma levels correlated statistically with the presence of liver cirrhosis and severe coma. These results are consistent with the false neurotransmitter hypothesis of hepatic encephalopathy.

2-Hydroxyphenethylamine↗
PubMed1979

Hepatic encephalopathy precipitated by fecal impaction.

Two episodes of hepatic encephalopathy developed in a 64-year-old man with cirrhosis during the course of hospitalization. The first event was precipitated by spontaneous bacterial peritonitis; the second occurred four weeks later and was associated with a massive fecal impaction, an unreported precipitant. No other potential causes were demonstrated. Symptoms promptly resolved following disimpaction.

Fecal Impaction↗
PubMedDate not supplied

[Changes in the level of erythrocyte phosphorylated compounds in patients with hepatic encephalopathy].

Automated ion exchange chromatography was used to compare red cell phosphorylates in clinically healthy subjects and 6 patients with hepatic encephalopathy. Significant changes in the distribution of these compounds were noted, including a marked increase in total acid-soluble content (particularly 2.3 DPG, R5P, 3MPG and G16DP) and a sharp fall in ATP. Increased 2.3 DPG explained the rightward shift of the haemoglobin dissociation curve seen in cirrhosis of the liver, but does not seem to fit in with enhanced blood ammonia. Deep-seated changes in red cell energy metabolism may have the same pathogenesis as the CNS metabolic change observed in hepatic encephalopathy.

Adenine Nucleotides↗
PubMed1978

Sources of serum [14C]-octanoate in cirrhosis of the liver and hepatic encephalopathy.

Serum octanoate levels of patients with liver cirrhosis and hepatic encephalopathy have been shown to be three to 15 times higher than those of controls. Assays for octanoate have been modified to permit isolation of pure octanoate after GLC. Patients with these conditions were given intravenously differently labeled [14C]-palmitates; serum [14C]-octanoate was isolated in each case and shown by mass spectrometry to be authentic octanoate. [1-14C]-oleate and [1-14C]-stereate were also shown to serve as precursors of serum [14C]-octanoate. When differently labeled palmitates (1-[14C]; omega [14C]; and [14C]-uniformly labeled) were used, different yields of serum [14C]-octanoate were recovered. Octanoate samples were chemically degraded to yield individual carbons or groups of carbons. In this manner it was possible to determine the percentage distribution of the [14C] label within the octanoate carbon chain. The data obtained from these studies suggest that 60% to 80% of the serum octanoate was obtained from the incomplete beta-oxidation of long-chain fatty acids and that 20% to 40% of the octanoate may have been formed de novo.

Caprylates↗
PubMed1978

Brain monoamines in hepatic encephalopathy and other types of metabolic coma.

Tyrosine (Tyr), tyrosine hydroxylase (TH), tryptophan (Trp), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) were assayed spectrofluorometrically and radioenzymatically in various regions of post-mortem brains of human patients with hepatic, uremic, and diabetic coma, liver cirrhosis without coma, and hepatic coma treated with parenteral administration of L-valine, a branched-chain amino acid. The results were as follows: In both hepatic and diabetic coma Tyr was increased as compared to non-comatose cirrhosis and controls, while TH acitivity was within normal limits, indicating sufficient oxygen supply of the brain in both types of coma. Brain DA showed a mild decrease in all types of metabolic coma. Brain Trp was not considerably changed in non-comatose cases of liver cirrhosis and after L-valine treatment of hepatic encephalopathy, but was significantly increased in hepatic coma, with highest elevation in the brainstem tegmentum. Both 5-HT and 5-HIAA were not significantly changed in non-comatose cirrhosis, while a general increase with prevalence for the brainstem was obvious in all types of metabolic coma. After L-valine treatment of hepatic coma, 5-HT levels were usually decreased below control values, while 5-HIAA levels were at or below controls. These results in human post-mortem brains confirm previous CSF and brain findings in experimental and human hepatic and uremic encephalopathies, indicating derangement of brain monoamine neurotransmitter metabolism which is attributed to imbalance of aromatic and branched-chain amino acids in plasma and brain. Increased cerebral 5-HT turnover, particularly in the ascending serotonergic brainstem systems, due to derangement of brain uptake of Trp is suggested to represent an important biochemical substrate of disorders of consciousness in hepatic failure and other types of metabolic encephalopathies. Clinical improvement of hepatic encephalopathy and of the underlying neurotransmitter derangements by administration of L-valine and the possible role of this competitive amino acid on intermediary metabolism and ammonia detoxification are discussed.

Aged↗
PubMed1977

[Hepatic encephalopathies; hemodynamic and metabolic study of the influence of ammonia and levodopa].

The authors present the results of a study of cerebral blood flow and energy metabolism carried out in 19 subjects, 12 of whom had hepatic cirrhosis and hepatic encephalopathy (HE). The spontaneous changes and those noted after intravenous administration of ammonium chloride and of L. Dopa, shows that the signs of hepatic encephalopathy are not directly related to the reduction in energy metabolism and that this metabolic disorder does not depend on a blocking of the dopaminergic synopses. The results of this study emphasize the complexity of HE and raise up the hypothesis of the creation of intra-cerebral arterio-venous shunts in cirrhotic patients.

Ammonia↗
PubMed1976

Octopamine plasma levels and hepatic encephalopathy: a re-appraisal of the problem.

An investigation on the blood levels of octopamine was carried out on 70 adult individuals. There was a statistically significant correlation between the levels of octopamine and hepatic encephalopathy. Normal subjects had values below 1 ng/ml, while patients with grade 3 or grade 4 encephalopathy constantly showed values above 3.2 ng/ml. In these two groups the distribution was fairly homogeneous. Through the differences between cirrhotics without neurologic involvement and those with grade 1 or 2 hepatic encephalopathy displayed statistical significance, distribution of values in these groups was rather non-homogeneous. Octopamine levels paralleled variations in mental state in 3 out 4 cases. No difference was found between venous and arterial values. The reaction of transmethylation used in the assay of octopamine was constantly found to be inhibited by the presence of plasma. This inhibition is probably due to the presence of one or more beta-hydroxyphenylethanolamines other than octopamine.

Adult↗
PubMed1979

The role of insulin and glucagon in the plasma aminoacid imbalance of chronic hepatic encephalopathy.

Increased glucagon (IRG) levels have been documented in liver cirrhosis, particularly associated with portal-systemic shunting. In spite of increased insulin (IRI) levels, IRI/IRG are reduced. This alteration has been proposed to have a pathogenic role in plasma aminoacid imbalance which seems to account for hepatic encephalopathy. We studied IRG and IRI/IRG in 13 controls and in 3 groups of cirrhotics, divided on the basis of their mental state. Glucagon was determined by means of 30 K Unger's antibody; insulin by a double antibody technique. Results are expressed in the table as means +/- SEM. (Formula: see text)A progressive increase in IRG secretion is present in cirrhotics and correlates with the mental state; IRI/IRG is not altered in cirrhosis until neurological distrubances are present. A relative fall in IRI which can no more balance the increasing IRG values characterizes hepatic encephalopathy.

Amino Acids↗