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PubMed1978

Decarboxylation to tyramine: an important route of tyrosine metabolism in dogs with experimental hepatic encephalopathy.

Tyrosine metabolism via decarboxylation to tyramine was evaluated in dogs with functional end-to-side portacaval shunt. It was found that the endogenous plasma levels of both tyrosine and tyramine increased steadily after the construction of the shunt. These elevations became more pronounced when the dogs manifested symptoms of hepatic encephalopathy. In encephalopathic dogs, average endogenous plasma tyrosine and tyramine concentrations were 110.1 mumoles per liter and 7.6 ng per ml as compared to 55.4 and 1.2 in control dogs, respectively. The pattern of plasma concentrations of tyrosine and tyramine after an oral dose of L-tyrosine (50 mg per kg) was also investigated in control and shunted dogs. There was a progressive rise in peak levels of tyramine (to about 50-fold increase, at 6 weeks) after the construction of the shunt, as compared to levels obtained in pre- and at 1 and 4 weeks postoperatively (70.6 versus 1.20, 3.9, and 8.11 ng per ml). Similar observations were made with levels of plasma tyrosine. Six weeks after portacaval shunt, mean peak levels of plasma tyrosine, achieved at 5 hr after dose administration, were 450 as compared to 85 mumoles per liter obtained in preshunted dogs. These studies demonstrated a correlation between abnormalities in tyrosine metabolism and postshunt hepatic encephalopathy.

Amino Acids↗
PubMed2024

The causal effect of gut microbiota on hepatic encephalopathy: a mendelian randomization analysis.

BACKGROUND: There is growing evidence for a relationship between gut microbiota and hepatic encephalopathy (HE). However, the causal nature of the relationship between gut microbiota and HE has not been thoroughly investigated. METHOD: This study utilized the large-scale genome-wide association studies (GWAS) summary statistics to evaluate the causal association between gut microbiota and HE risk. Specifically, two-sample Mendelian randomization (MR) approach was used to identify the causal microbial taxa for HE. The inverse variance weighted (IVW) method was used as the primary MR analysis. Sensitive analyses were performed to validate the robustness of the results. RESULTS: The IVW method revealed that the genus Bifidobacterium (OR = 0.363, 95% CI: 0.139-0.943, P = 0.037), the family Bifidobacteriaceae (OR = 0.359, 95% CI: 0.133-0.950, P = 0.039), and the order Bifidobacteriales (OR = 0.359, 95% CI: 0.133-0.950, P = 0.039) were negatively associated with HE. However, no causal relationship was observed among them after the Bonferroni correction test. Neither heterogeneity nor horizontal pleiotropy was found in the sensitivity analysis. CONCLUSION: Our MR study demonstrated a potential causal association between Bifidobacterium, Bifidobacteriaceae, and Bifidobacteriales and HE. This finding may provide new therapeutic targets for patients at risk of HE in the future.

Mendelian Randomization Analysis↗
PubMed1977

Plasma amino acid patterns in hepatic encephalopathy of differing etiology.

Plasma amino acids were measured in 18 patients with hepatic encephalopathy on a protein-restricted diet of 20 g or less daily. Plasma aminograms tended to group into two distinct patterns depending on the etiology of the patients' hepatic pathology. Patients with chronic liver disease with superimposed acute insults, i.e., gastrointestinal bleeding, infection, alcoholic hepatitis, had elevated levels of the aromatic amino acids, phenylalanine, tyrosine, and tryptophan, as well as methionine, glutamate, and aspartate, whereas levels of the branched chain amino acids, valine, leucine, and isoleucine, were consistently depressed. Those patients with previously normal livers and acute hepatic necrosis, i.e., "fulminant hepatitis," had grossly elevated levels of all amino acids except the branched chain amino acids, which were normal. Elevations of amino acid levels in this patient group tended to correlate with extent of hepatic necrosis and hence had prognostic significance. Additionally, the different patterns seen in these two groups tend to suggest the indicated therapy as well as predict its efficacy.

Acute Disease↗
PubMed1977

Treatment of acute hepatic encephalopathy with L-dopa.

A clinical report of a 30-year-old woman who developed acute hepatic failure in the fifth month of pregnancy is presented. L-dopa administration resulted in a marked improvement in both level of consciousness and electroencephalogram. The literature dealing with L-dopa therapy in hepatic encephalopathy is reviewed.

Adult↗
PubMed1979

Influence of phenylethanolamine on octopamine plasma determination in hepatic encephalopathy.

Octopamine and phenylethanolamine levels were measured by a radioenzymatic procedure in 30 cirrhotic patients with and without hepatic coma and in 15 normal controls. Octopamine data were obtained either by direct extraction with 40% isoamyl alcohol in toluene according to Molinoff et al. (Molinoff, P.B., Landsberg, L. and Axelrod, J. (1969) J. Pharm. Exp. Ther. 170, 253), or after pre-extraction of phenylethanolamine with 3% isoamyl alcohol in toluene. Phenylethanolamine was statistically correlated with the grade of hepatic encephalopathy. Octopamine levels also appeared to parallel the grade of coma, although the values obtained after pre-extraction were lower and less significant than those obtained with 40% isoamyl alcohol in toluene extraction. The higher values of directly extracted octopamine are due to contamination of other beta-hydroxylated phenylethylamines, among which is phenylethanolamine.

2-Hydroxyphenethylamine↗
PubMed1978

An approach to nutritional therapy of hepatic encephalopathy by normalization of deranged amino acid patterns in serum.

A mixture with essential and nonessential amino acids high in branched chain amino acids and low in aromatic amino acids (Fischer solution), and another synthetic mixture of branched chain amino acids containing 3 amino acids associated with the urea cycle (Hep-OU) were infused to control subjects and patients with severe hepatic disease. Alterations in serum aminograms, blood ammonia levels and electroencephalograms following the infusion were studied and compared with those obtained by a commercially available amino acid mixture. Short-term or continuous infusion of a commercially available amino acid solution to cirrhotic patients caused an increase in methionine, phenylalanine and tyrosine and a decrease in branched chain amino acids. These post-infusion results were similar to the patterns seen in hepatic encephalopathy. In cirrhotic patients, infusion of Fischer solution which contains small quantities of methionine and phenylalanine produced an increase in the concentrations of these 2 amino acids, probably because of impaired utilization by the injured liver. No marked alterations in serum aminograms, however, were observed in cirrhotic patients either immediately after, or 3 h after, the end of the Hep-OU infusion. Reduction of methionine, tyrosine and phenylalanine levels and elevation of the molar ratio of (valine + leucine + isoleucine)/(phenylalanine + tyrosine) were significant. The infusion of Hep-OU to patients with liver cirrhosis or subacute hepatitis resulted in clinical and neurological improvements and the restoration of the molar ratio of branched chain amino acids/aromatic amino acids.

Amino Acids↗
PubMed1977

Chronic hepatic encephalopathy. A psychometrical study.

Psychometric tests were performed in 41 patients with cirrhosis of the liver and suspected hepatic encephalopathy and compared with EEG-examinations and clinical investigations. Marked intellectual impairment was noted frequently even when the clinical investigation was normal. This difference was mainly due to the preserved verbal ability of the patient. The etiology of the cirrhosis did not influence the test results. Male cirrhotic patients with and without alcoholism showed significantly more intellectual impairment then alcoholics without cirrhosis. Patients Patients with constructed porto-systemic shunts showed only slightly reduced intellectual ability compared to those without shunts.

Adolescent↗
PubMed1977

[Hyperammonemia and hepatic encephalopathy in cirrhotics receiving spironolactone (author's transl)].

The aim of this study was to specify the mechanism of hepatic encephalopathy which may occur in some cirrhotics treated by Spironolactone. In 31 cirrhotics with ascite, this diuretic induced a significant increase in arterial ammonemia; 8 patients developed an impending hepatic coma which was associated with ammonemia levels significantly higher than those observed in the patients without encephalopathy at the end of the treatment. Hyperammonemia induced by Spironolactone does not result from a muscular, renal or hepatic ammonia production but seems related to an increased intestinal ammoniagenesis which which is secondary to the bacterial hydrolysis of urea in the colon; indeed, there is a significant correlation between the ammonemia increase and the simultaneous rise in blood urea during treatment.

Adult↗
PubMed1977

[Pathogenesis of hepatic encephalopathy (author's transl)].

This contribution presents data from the literature as well as our own results concerning the mechanisms of hepatic encephalopathy (HE). 1. Blood chemistry: In patients with liver cirrhosis, the plasma levels of ammonia, phenylalanine, tyrosine, phenolic acids, and octopamine correlated with the stages of HE. Methionine and free tryptophan concentrations were increased only in stages 2-4. Further, branched chain amino acids were below the normal range. Experimental findings in animals elucidated some mechanisms of these changes. 2. Effects of administered substances: With ammonia, methionine, methanethiol, tryptophan, phenolic substances, and fatty acids central nervous disturbances were observed. 3. Interactions: Anemia, methanethiol, and fatty acids favored ammonia toxicity. Alkalosis diminished cerebral symptoms. 4. Neurotransmitters: HE was accompanied by an enhanced turnover of serotonin and by increased amounts of false neurotransmitters (like octopamine) in the brain. 5. Oxydative brain metabolism: Disorders of cerebral oxygen and glucose utilization were mainly documented in cases of long term HE with EEG alterations. 6. Structural changes of the brain: Most of them are irreversible.

Alkalosis↗
PubMed1977

Dopamine uptake by platelets in hepatic encephalopathy; evidence for a possible depletion of brain dopamine.

A decrease in H3-dopamine uptake was demonstrated in the blood platelets of 22 hepatic encephalopathy (HE) patients when compared to that of patients with liver cirrhosis, but without HE, and controls. There was a direct correlation between the stage of HE and the decrease in H3-dopamine uptake. As blood platelets have characteristics similar to neurons which contain amines, they have been proposed as a model for the study of amine metabolism in neurological, as well as liver diseases. A defective dopamine uptake by the HE platelets suggests that a similar biochemical derangement is, also, present in the nerve cells of the dopaminergic system. This could account for the clinical evidence of extrapiramidal dysfunction and the arousal effect of levodopa in HE. Platelets from 10 cirrhosis, but HE-free, patients had a dopamine uptake which was intermediate between the HE patients and controls. When octopamine was added at the same concentrations as in serum of HE patients, the blood platelets from five controls showed a decrease in dopamine uptake proportional to the concentration of octopamine added. Octopamine may impair dopamine uptake by platelets from HE patients.

Adult↗
PubMed2026

A 7-mm Covered TIPS Reduces Hepatic Encephalopathy Without Increasing Rebleeding in Cirrhotic Patients With Small Liver: A Randomized Study.

BACKGROUND/AIMS: International guidelines recommend initiating transjugular intrahepatic portosystemic shunt (TIPS) placement with an 8-mm stent. However, there is an evident lack of randomized controlled trials evaluating TIPS diameters <&#x2009;8&#x2009;mm in cirrhotic patients with a relatively small liver. The aim of this study was to determine whether 7&#x2009;mm-covered TIPS, compared with 8-mm stents, could achieve comparable shunt function with a lower incidence of hepatic encephalopathy (HE). METHODS: In this multicenter randomized controlled trial, patients with cirrhosis and relatively small liver were randomized 1:1 to receive TIPS with a 7-mm (n&#x2009;=&#x2009;92) or 8-mm (n&#x2009;=&#x2009;92) covered stent to prevent variceal rebleeding. The primary endpoint was the incidence of overt HE after randomization. All-cause rebleeding, orthotopic liver transplantation (OLT)-free survival and a composite of these outcomes, were designated as secondary endpoints. RESULTS: Among the 184 enrolled patients, the predominant etiologies of liver cirrhosis were hepatitis B virus infection (56.0%) and alcohol-related liver disease (20.7%). Over a median follow-up of 26.5&#x2009;months, overt HE occurred in 19 patients (20.7%) in the 7-mm group and 33 patients (35.9%) in the 8-mm group. The 2-year cumulative incidence of overt HE was significantly lower in the 7-mm group than in the 8-mm group (21.4% vs. 37.2%, p&#x2009;=&#x2009;0.02). Stent diameter, post-TIPS portosystemic pressure gradient, pre-covert HE and MELD-Na score were identified as independent risk factors for overt HE. The rates of shunt dysfunction were statistically similar between groups (8.7% vs. 8.7%, p&#x2009;=&#x2009;1.0), as were 2-year rebleeding rates (10.9% vs. 9.8%, p&#x2009;=&#x2009;0.81) and OLT-free survival rates (91.3% vs. 88.0%, p&#x2009;=&#x2009;0.82). CONCLUSIONS: A 7-mm covered TIPS demonstrated comparable shunt function to an 8-mm covered stents, with a significantly lower risk of overt HE. These findings support consideration of 7-mm TIPS stents for preventing variceal rebleeding in cirrhotic patients with a small liver who are undergoing TIPS. TRAIL REGISTRATION: ClinicalTrials.gov, NCT02541825.

Humans↗
PubMed1977

Portal vein anomaly and hepatic encephalopathy in a horse.

Periodic episodes of diffuse central nervous system disease occurred in a yearling Thoroughbred gelding that had a history of frequent respiratory tract disease and stunted growth. Hepatic encephalopathy was diagnosed on the basis of history, clinical signs, prolonged bromsulphalein clearance, and increased blood ammonia content. Because of the poor prognosis and recurrent clinical signs the horse was euthanatized. Necropsy revealed an arteriovenous anomaly and thrombosis of the portal vein. Histologically, there was diffuse primary astrocytosis of the brain.

Animals↗
PubMed1979

In vitro adsorption of possible aetiological factors of hepatic encephalopathy.

Four different adsorbents (activated charcoal, XAD-4, a strong base anion and a strong acid cation-exchange resin) were tested in vitro for their capacity to remove substances that may be important in the development of hepatic encephalopathy. Separate columns packed with one of these adsorbents were perfused for three hours with a reconstituted plasma solution containing simultaneously high concentrations of amino-acids, ammoniumchloride, short-chain fatty acids, octopamine and bile salts. Effective removal of all these substances was only obtained when either activated charcoal, or XAD-4, were combined with the cation-exchange resin. Possible implications for the treatment of hepatic coma are discussed.

Absorption↗
PubMed1977

Brain proteins in hepatic encephalopathy.

Brain proteins were analyzed in supra- and infratentorial structures of 6 patients dying from liver failure. An equal number of patients, lacking any evidence of liver disease or neurological disorder, served as controls. The results were related to regional light microscopic findings. Hepatic coma was associated with a marked reduction of soluble brain proteins, particularly in areas of grey matter. The protein loss is probably neuronal and may be secondary to abnormalities in glial function. Implications for the pathogenesis of hepatic encephalopathy are discussed.

Adult↗
PubMed1976

Hepatic encephalopathy and light and electron micrographic changes of the baboon liver after portal diversion.

Six baboons of varying weights and estimated ages had complete portal diversion. All animals became emaciated and lost hair. Five of the 6 developed hepatic encephalopathy so serious that it either killed them or required their sacrifice after an average of 109 days. One exceptional animal which lived for 208 days without encephalopathy had markedly elevated blood ammonia levels. In one brain that was examined, greatly increased numbers of Alzeheimer's Type II astrocytes were diffusely distributed in the cerebral cortex. Changes in liver function tests were similar to those reported by many authors in dogs. The 6 baboon's livers underwent striking atrophy during the 49 to 208 days of postoperative observation. With some variations in degree, the same light and electron microscopic changes were observed that have now also been seen after completely diverting portacaval shunt in rats, dogs and humans. Thru the hepatic injury of Eck fistula is common to all species so far studied although most of the metabolic consequences of the procedure seem to selectively spare rats and man.

Alanine Transaminase↗
PubMed1979

[Hyperoctanoatemia and the hepatic encephalopathy of cirrhosis. 150 dosages in 61 patients (author's transl)].

A new and sensitive method for determination of octanoate in serum by gas-liquid chromatography is described. It was validated by mass spectrometry. Octanoate concentrations were determined in the serum of 61 fasting cirrhotic patients of which 47 also had hepatic encephalopathy. Concentrations in arterial and venous blood were higher in cirrhotic patients with encephalopathy than in those without and higher in the latter than in controls. Arterial concentrations were higher than venous concentrations and octanoate and ammonia varied independently. A predominant endogenous origin is likely. Data obtained from studies using palmitic acid labeled at different loci suggest that recovered serum octanoate was formed mostly by incomplete oxidation of long chain fatty acids. Sodium octanoate infusion to rhesus monkeys studied polygraphically induces a temporary coma.

Adult↗