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

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.
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PMID:[Present-day therapy of hepatic encephalopathy (author's transl)]. 82 98

In a survey the trend of the biochemical investigations in hepatology is analysed. Together with the histologic diagnosis the function of the liver parenchyma must be determined, in which cases tolerance tests which do not only determine the function of the liver parenchyma, but also the changed functions of other organs are of importance. On the basis of own findings is shown that the ammonia metabolism in patients with hepatic encephalopathy is also disturbed in musculature. In the serum of patients with decompensated liver cirrhosis a factor could be isolated which apart from the inhibition of the utilisation of glucose has also another metabolic effect. In future we might expect an intensified search for such active metabolites. Investigations concerning the salicylaemia in patients with liver cirrhosis and experimental findings about changes of the O-demethylase activity in the fatty degeneration of the liver show the great significance of the pharmacokinetic analyses in the clinical hepatology.
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PMID:[Perspectives of clinical biochemistry in hepatology]. 85 Oct 12

Hepatic insufficiency is generally caused by active liver cirrhosis with portal hypertension. The final stage is the exogenous hepatic coma. Much rarer is the endogenous hepatic coma caused by fulminant acute hepatitis or severe intoxications. In the treatment of hepatic insufficiency it is first necessary to eliminate all exacerbating factors such as too high protein-intake, gastrointestinal bleedings, abuse of alcohol and diuretics. Because hepatic encephalopathy is mainly produced by toxic intestinal protein metabolites no protein should be adminstered at the beginining of the disease. The production of toxic protein metabolites in the gut can be diminished as well by enemas with sodium acetate buffer (pH 4, 5) as by neomycin (6-8 gm daily). Because long-term treatment with neomycin reduces also the physiological intestinal bacteria combination with lactulose (70-100 gm daily) is better. Treatment with lactulose reduces not only significantly hyperammoniemia but also increases serum phenols. The same effect have so-called ammonia reducing amino acids such as arginine, ornithine and glutamic acid. In endogenous hepatic coma blood exchange transfusions, liver perfusions and charcoal perfusions are necessary. Nevertheless, the prognosis of hepatic insufficiency caused by fulminant hepatitis is very poor in the final stage of the disease. Therefore early diagnosis and treatment in special departments with intensive care is necessary.
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PMID:[Therapy of hepatic insufficiency]. 91 52

Formation of endogenous toxins through protein metabolism and detoxification through liver are described. In chronic hepatic insufficiency (cirrhosis of the liver), with failure of liver metabolism, levels of endogenous toxins in plasma and tissue, i.e. ammonia, phenol-derivatives and free fatty acids, rise. Plasma levels of ammonia and free fatty acids are both dependent on the Krebs cycle. This interaction and mutual dependance was examined clinically through application of amino acids that lower plasma ammonia level. Di-L(+)ornithin-alpha-ketoglutaric acid was able to lower ammonia levels in patients with liver cirrhosis. The difference between pre- and postinfusion levels of ammonia was significant, this corresponds to the observations of other authors. In addition we found a fall in levels of free fatty acids, triglycerides, and cholesterol. This effect on fatmetabolism was also observed in patients with no evidence of incipient or manifest hepatic insufficiency. The biochemical basis and the clinical implications of these findings are discussed.
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PMID:[Influence of ornithin-alpha-ketoglutaric acid on fatmetabolism in patients with cirrhosis of the liver (author's transl)]. 93 1

13N-ammonia, applied rectally, after absorption and transportation visualises the liver. After release of 13N-aminoacids and 13N-urea by the liver, 13N-activity can be measured over other organs. In patients with porta-systemic shunts, 13N-ammonia will appear in the systemic circulation as well. In 16 controls and 26 patients with cirrhosis, activities were measured for 20 minutes over liver, spleen, heart, lungs and forearm. In all subjects, the liver was visualised within a minute, in some patients with cirrhosis faintly, however. Release by the liver of 13N-ammonia metabolites started within a few minutes. Liver/heart activity ratios proved to be more discriminating between the control- and the cirrhosis group than liver/lung and liver/spleen ratios. In the control group, the 20 minutes' liver/heart ratio was most suitable for determining the normal range. The lower normal level was found to be 2.25. Fourteen of the 26 patients with cirrhosis had a normal, 12 an abnormally low 20 minutes' liver/heart ratio.
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PMID:Rectal administration of 13N-ammonia in cirrhosis of the liver. 98 59

The 20 minutes' liver/heart activity ratio after rectal administration of 13N-ammonia was abnormally low (less than 2.25) in 12 of 26 patients with cirrhosis of the liver. An abnormal conventional rectal arterial ammonia test (porta-systemic shunts), an abnormally low urea index (prevailing hepatofugal portal venous flow direction), marked portal hypertension (hepatic sinusoidal pressure greater than or equal to 8 mm Hg), ascites and extreme enlargement of the spleen occurred significantly more often in the patients with an abnormally low 13N-liver/heart ratio than in those with a ratio greater than or equal to 2.25. There was no correlation between the 13N-liver/heart ratio and absence or presence of oesophageal varices. The non-invasive rectal 13N-ammonia test appears to be an easy to perform, informative test in cirrhosis of the liver.
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PMID:Rectal 13N-ammonia test (13N-liver/heart ratio), hepatic sinusoidal pressure and prevailing portal flow direction in cirrhosis of the liver. 98 60

In two cases of hepatic coma following advanced liver cirrhosis exchange transfusions were applied with plasmapheresis. In both cases the general condition of patients improved and consciousness returned. After exchange transfusions with plasmapheresis the serum levels of bilirubin, urea and ammonia decreased. Using appropriately selected fluids for erythrocyte suspension it is possible to affect selectively protein depletion and depletion of plasma blood clotting factors.
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PMID:Exchange transfusion with plasmapheresis in the management of hepatic coma. 98 46

In two groups of patients with liver cirrhosis and normal EEG (Group A) and with pathological EEG (Group B) it was possible to demonstrate a correlation between the severity grade of the EEG changes, the livertypical deviations of serum chemistry and alterations in cerebral oxidative metabolism. The metabolism of the brain showed a reduced oxygen consumption and carbon dioxide output in the patients with pathological EEG changes. All patients showed a raised glucose uptake, an increased lactate release, a raised ammonia uptake and glutamine output. These findings in patients with liver cirrhosis indicate a disturbance of the oxidative energy metabolism of the brain with secondary intensification of glycolysis. Pathological changes in the EEG only appear if the oxygen consumption of the brain is limited (as in the patients of Group B). These EEG changes have a poor prognosis in respect to life expectancy. With consideration of the data from animal experiments and the reported results of cerebral blood flow and oxydative metabolism in patients with liver cirrhosis it might be assumed that liver insufficiency with elevated serum ammonia results in a deranged oxydative cerebral metabolism which might explain hepatic encephalopathy.
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PMID:Comparative studies of the electroencephalogram and the cerebral oxidative metabolism in patients with liver cirrhosis. 120 68

In a control group (n = 50) and in 52 patients with cirrhosis, urea was administered orally and ratios for hepatic venous/arterial increment were determined up to 120 minutes after loading. A complete, hepatofugal diversion of the portal blood flow would result in ratios less than or equal to 1. The best discrimination between controls and cirrhotics was obtained with the 0-15 minute ratio ("urea index") which has a normal lower limit of 1.25. In cirrhosis an urea index less than or equal to 1.2 is correlated with an abnormal ammonia test and with the presence of marked portal hypertension (hepatic sinusoidal pressure greater than or equal to 8 mmHg, N: 0-3 mmHg). Ascites occurs more often in patients with cirrhosis and a low index. Regardless of the urea index value, ascites in cirrhosis is associated with an hepatic sinusoidal pressure greater than or equal to 8 mmHg. The urea index procedure may easily be conducted together with the measurement of hepatic sinusoidal pressure.
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PMID:The "urea index" as a marker of portal flow direction in cirrhosis of the liver. 127 21

Crystalline lactulose (Laevolac Cristalli, CAS 4618-18-2), a pure form of the disaccharide widely employed in the therapy of complications of liver cirrhosis, was administered, after a pharmacological wash-out of 10 days and following a randomized design, to 10 cirrhotic patients for 30 days at the dosage of 60 g/d, while another 10 subjects with similar characteristics received no treatment. Besides the parameters usually monitored for the evaluation of liver function and state of hepatic encephalopathy, immunological patterns such as lymphocyte subpopulations CD3, CD4, CD8, CD16(NK), CD25 and antibacterial activity against Ty2 strain of Salmonella typhi were evaluated. At the end of the study (day 30) a significant decrease of blood ammonia was observed, as expected, only in the group treated with lactulose with respect to the control group, as well as a significant increase of CD16 and antibacterial activity (1/3); an enhanced level of CD25, although not significant, was also noticed in the treated group with respect to the control group. These findings seem to show an effect of activation on cell-mediated immune system depressed during liver cirrhosis, produced by lactulose. Further studies are needed to confirm these data and to clarify the possible mechanisms involved.
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PMID:Crystalline lactulose in the therapy of hepatic cirrhosis. Evaluation of clinical and immunological parameters. Preliminary results. 141 64


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