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Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

According to the present studies it is shown that arginine ketoglutarate in sufficiently high dosage (3x3 g daily by mouth) produces a significant lowering of plasma ammonia and free serum phenols with a high-protein diet in patients with liver cirrhosis, compared to a previous day without this substance. The ammonia reduction can be explained by a significant increase in urea synthesis, measured by the urea nitrogen content of the 24-hour urine. The simultaneous lowering of pathologically raised serum levels of free phenols can be explained by an improved oxidative decomposition of these substances. No stimulation of insulin secretion worthy of note occurred after oral administration of 9 g arginine ketoglutarate.
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PMID:[Effect of arginine ketoglutarate on the detoxifying capacity of the liver in cirrhosis of the liver (author's transl)]. 40 72

The tracing of ammonium nitrogen is important in hepatic diseases, especially in liver cirrhosis with hyperammonemia. In this paper, a new convenient method is described for determining stable isotope 15N-labeled ammonia using the Conway apparatus and chemical ionization mass spectrometry. The minimum quantity of ammonia necessary for reliable measure of 15N content was 0.1 muMol. The average error was 5.3%. In clinical application, 4 ml of blood after oral administration of 1 g of 15NH4Cl was sufficient for measurement.
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PMID:Determination of 15N-ammonia by chemical ionization mass spectrometry. 44 91

Following ureterosigmoidostomy, encephalopathy with hyperammonemia may occur in the presence of cirrhosis, and the same complication was also observed in a few patients without liver damage. This suggests overloading of normal liver ureagenisis by an increased portal ammonia supply. To test this hypothesis and to try to produce an experimental model of chronic hyperammonemia without portal or hepatic damage, ureterocolostomies were performed in rats. These rats were compared with sham operated upon rats and with rats having chronic uremia induced by subtotal nephrectomy. Rats having a ureterocolostomy had chronic, but moderate, systemic hyperammonemia without any histologic hepatic damage and without gross behavioral modifications and slight uremia with only inconstant pyelonephretic lesions. In these rats, hyperammonemia results from hepatic overloading by the increased portal ammonia supply which is a consequence of both intestinal absorption of some urinary ammonia and increased intestinal ammoniagenesis induced by hydrolysis of urinary and circulating urea.
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PMID:Hyperammonemia following ureterocolostomy in the rat. 46 48

It will analyse and discuss the influence of fructose-, glucose-, sorbitol- and argininmalat-infusions, of ascorbit acid and vitamin-B-complex as well as of 13 different amino-acids on the determination of ammonia by means of indophenol-reaction. With this the frequent of liver-cirrhosis i.v. administer substances trouble the determination of ammonia just as little (exception: arginin-malat), how amino-acids in physiological and little pathological range.
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PMID:[The influence of infusions and amino-acids on the determination of ammonia by means of indophenol-reaction (author's transl)]. 54 May 66

Ammonia has been known to be an inducing agent of hepatic coma associated with liver cirrhosis. In order to establish a non-invasive method of investigating the portal circulation and the metabolism of ammonia at liver the following studies were performed, by using cyclotron produced 13N-labeled ammonia and delayed line-camera interphased with on-line computer system. 1) Animal experiment. Dynamic scintigraphy of thoraco-abdominal region of a rabbit after intrasigmoidal as well as intravenous administration of 13N-ammonia were performed. 2) Theoretical consideration on the functional image of liver: According to the results of the animal experiments, a model of ammonia metabolism having the minimal complexity necessary to represent data in the case of intrasigmoidal administration was proposed. Starting from the solution to the differential equation describing the model, relevant parameters characterizing the dynamic curve of liver were duded.
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PMID:[Experimental studies on clinical application of 13N-ammonia; a metabolic model and functional image based on animal experiment]. 57 18

1) Clinical application: Dynamic scintigraphy of liver and heart of a patient having liver cirrhosis after intrasigmoidal administration of 13N-ammonia (pH 8.1) were performed. Simultaneously, continuous measurments of radioactivity at the left side abdomen and the left temporal region were done by using a scintillation detector for renography. Successive measurement of radioactivity of blood was also carried out. 2) Comstruction of functional images of liver and heart: By using digital radioisotope image of liver and heart of the patient after intrasigmoidal administration of 13N-ammonia, the maps with respect to parameters described in the pervious paper were constructed.
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PMID:[Experimental studies on clinical application of 13N-ammonia; clinical application of the functional image]. 57 19

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.
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PMID:A patient with recurrent hepatic encephalopathy and chronic renal failure treated successfully with long-term hemodialysis. 60 71

The effect on free plasma amino acids before and after infusion of 1 mg glucagon was studied at rest after an overnight fast in seven patients with compensated liver cirrhosis and in seven healthy controls. Total aminoacidaemia in cirrhotic patients is significantly higher than in controls. Elevated basal levels in cirrhotics are found particularly in tyrosine, citrulline, tryptophane, threonine, phenylalanine, and methionine whereas ornithine and serine levels are decreased. Save for the redox couple cystine-cysteine which increases, glucagon elicits an decrease in most amino acids that is proportionate to their initial level. Total aminoacidaemia decreases in controls and cirrhotics by 14.6 and 9.1 per cent respectively. Serum ammonia level rises significantly in both groups, urea increases only in controls, uricaemia remains virtually unchanged.
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PMID:The effect of glucagon on free plasma amino acids in cirrhotics and healthy controls. 63 37

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.
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PMID:[Changes in the level of erythrocyte phosphorylated compounds in patients with hepatic encephalopathy]. 63 81

To seven healthy volunteers, 12 and 24 g i.v. fructose were administered in the form of 20% solution at a rate of 4 g/min. After both doses, during the 10th min after the completed intravenous administration, a statistically significant increase of serum ammonia and serum uric acid occurred. After 24 g, the rise of the uric acid level remains significant during the 40th min after administration, while ammonia values return to the basal level. Increments of ammonia and uric acid are higher after a larger fructose dose. Under the same set-up and at the same rate, 24 g fructose were administered to eight patients with compensated cirrhosis of the liver. The rise of uric acid was practically the same as in healthy subjects similar to the rise of the ammonia level during the 10th min after administration. 40 min after administration, however, the ammonia level in cirrhotic patients remained significantly raised, as compared with the initial level.
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PMID:Ammonia and uric acid formation after rapid intravenous fructose administration to healthy subjects and patients with compensated cirrhosis of the liver. 78 5


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