Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A histochemical study was carried out on orcein-positive hepatocellular material in 111 cases, 27 of which were stained positively by orcein. Orcein-positive material was very frequently found in protracted viral hepatitis and in chronic active hepatitis, as well as in other liver diseases with or without cholestasis; it was absent in liver cirrhosis. In all the cases considered the orcein-positive material was mainly formed of proteins, rich in amino acids with sulfhydryl and disulphide radicals, tryptophan and, to a lesser extent, of NH2 alpha amino acids. The orcein-positive substance was apparently carbohydrate-free. The presence of copper was also confirmed.
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PMID:Histochemical study of orcein-positive hepatocellular material in paraffin sections of liver biopsy samples in the course of various liver diseases. 9 Nov 88

The clinical picture of liver disease in endemic areas of Schistosomiasis mansoni differs in many ways from that observed in alcoholic and other types of cirrhosis. In hepatosplenic schistosomiasis there is predominance of the clinical manifestations of portal hypertension, e.g., bleeding esophageal varices, while ascites, jaundice, and hepatic precoma or coma are much less common. Ammonia tolerance is usually normal and helps explain the low mortality rate during bleeding. Of special interest is the observation of a high incidence of persistent hepatitis B surface antigenemia among patients with hepatosplenic schistosomiasis, suggesting increased susceptibility of such patients to the development of virus-induced chronic active hepatitis.
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PMID:Clinical aspects of hepatosplenic schistosomiasis: a contrast with cirrhosis. 12 11

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

Hemostasis is intimately related to liver function, because most coagulation factors are synthesized by liver parenchymal cells and the liver's reticuloendothelial system serves an important role in the clearance of activation products. The extent of coagulation abnormalities depends upon the degree of disturbed liver function. Acute or chronic hepatocellular diseases may display decreases in the vitamin K-dependent factors (prothrombin; factors VII, IX, and X; proteins C and S), whereas other parameters remain normal. Patients with hepatic failure may present with the entire spectrum of factor deficiencies and may even develop disseminated intravascular coagulation (DIC). Patients with liver cirrhosis have a wide spectrum of abnormalities. Except for factor VIII:C and von Willebrand factor, all procoagulant and inhibitory factors are decreased, which is a reflection of impaired protein synthesis. Abnormal fibrinogen and prothrombin molecules can be identified. Platelets are quantitatively and qualitatively altered, and most patients develop DIC. Vitamin K deficiency leads to the production of abnormal vitamin K-dependent factors. The factors lack gamma-carboxy glutamic acid residues in the NH2-terminal part of their molecules. Surgery associated with the liver leads to major hemostasis alterations. The LeVeen shunt is invariably related to DIC. Bleeding with partial liver resection is mostly mechanically induced, but chronic DIC may be present. Orthotoptic liver transplantation is associated with severe hemorrhages. These are partly due to the pre-existing hemostasis defects and partly due to DIC with a marked fibrinolytic response. This is especially noted during the anhepatic phase and when the donor liver is perfused by the recipient's blood. Postoperative recovery is quick, provided the graft is not rejected. Postoperatively, there may be an initial hypercoagulable state, which could be related to the thrombosis occasionally encountered.
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PMID:Coagulation abnormalities in liver disease. 133 67

The work was designed to study the effects of a meat meal on glomerular filtration rate (GFR), renal plasma flow (RPF), and plasma concentrations of glucagon, insulin, growth hormone, renin, aldosterone, total amino acids, and NH3 in healthy humans (H) as well as in patients with Child A liver cirrhosis (LC). The meat meal produced renal hyperaemia and hyperfiltration without changes in the filtration fraction. Fractional Na excretion in urine increased significantly after the meat meal only in LC. Hyperinsulinaemia and hyperglucagonaemia were seen at baseline in LC and were not affected by the meat meal, whereas in H glucagon concentration increased significantly over baseline within 30 min from the meat meal and insulin within 60 min. Growth hormone concentration was normal at baseline in LC and increased significantly 120-180 min after the meal, whereas it was not affected in H. Renin and aldosterone were stable in both H and LC. Plasma amino acid concentration began to increase 60 min after the meat meal, when hyperfiltration was present. The data indicate that in human Child A cirrhosis of the liver renal haemodynamic response to a meat meal is independent of changes in glucagon.
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PMID:Glucagon-independent renal hyperaemia and hyperfiltration after an oral protein load in Child A liver cirrhosis. 155 40

One year prospective study of 25 cirrhotic patients with portal systemic encephalopathy (PSE) admitted to the Emergency Care Centre in Belgrade was performed in order to investigate the significance of clinical, biochemical and electroencephalographic (EEG) parameters and blood ammonia in the diagnosis, differential diagnosis and prognosis of PSE. 15 cirrhotic patients without PSE (of comparable age, sex, duration and etiology of liver cirrhosis) constituted the control group. Ammonia levels were elevated in 84% of patients with PSE (112 +/- 72 mumol/l) and reached normal range within 3 +/- 0.44 days, but with no correlation to clinical improvement (p greater than 0.1). Ammonia levels correlated with the severity of PSE (p less than 0.05), but not with other biochemical parameters (prothrombin time, bilirubin, albumin, urea, creatinine, potassium). Overall mortality was 44% and was strongly correlated (p less than 0.01) to the severity of PSE. In addition, the mortality in patients with gastrointestinal bleeding and PSE was higher (p less than 0.05), than in PSE precipitated by other conditions. We concluded that the ammonia may be a primary diagnostic parameter for PSE in the absence of the most important diagnostical methods (EEG, psychometric tests). Secondly, ammonia are of great diagnostic importance in patients with coma of unknown origin and can help in deciding admission priorities. The ammonia levels do not appear to be a useful prognostic factor.
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PMID:[Ammoniemia in portosystemic encephalopathy--diagnostic, differential diagnostic and prognostic significance]. 207 39

Ammonia is generated from a large number of metabolically important reactions. Despite its central importance in whole body nitrogen homeostasis excess ammonia is neurotoxic and its concentration must be kept low. Ammonia generated in most extrahepatic tissues is detoxified by incorporation into glutamine (amide). This glutamine may be used in a number of biosynthetic reactions (e.g. in pyrimidine synthesis). Alternatively, as a means of maintaining nitrogen balance, glutamine may be released to the blood. Resting skeletal muscle is particularly important 1) as a "sink" for removal of blood ammonia, and 2) as a major source of circulating glutamine. However, during vigorous exercise skeletal muscle may become a net contributor of ammonia to the blood. A few tissues and cell types (e.g. lymphocytes, macrophages, enterocytes, colonocytes, thymocytes, fibroblasts, bone) and tumors exhibit marked rates of glutamine utilization. In the kidney, glutamine is an important source of urinary ammonia. Ammonia generated from 1) the breakdown of nitrogenous substances in the gut, and 2) from the use of glutamine as a metabolic fuel in the small intestine, is taken up by the liver wherein it is detoxified by conversion to urea and to a lesser extent, glutamine. Some portal vein glutamine acts as a source of urea nitrogen. Ultimately, however, most excess ammonia nitrogen is detoxified indirectly (via glutamine (blood)----glutamine (small intestine)----ammonia (portal vein) or directly in the liver as urea. Portal-systemic shunting of blood, as occurs in chronic cirrhosis of the liver or following the surgical construction of a portacaval shunt results in portal blood bypassing the normal ammonia detoxification machinery of the liver. Under this condition blood ammonia levels rise markedly, increasing the burden on extrahepatic tissues, such as skeletal muscle, brain, and kidney, in maintaining ammonia homeostasis. The most commonly employed animal model of human liver disease is the rat in which an end-to-side portacaval shunt (PCS) has been surgically constructed. Brain glutamine synthetase activity is not increased in PCS rats and in some areas of the brain there may even be a decrease in activity. The brain glutamine synthetase appears to be working at near maximal capacity. Thus, the PCS rats exhibit profound neurological dysfunction when administered ammonium salts in amounts easily tolerated by normal animals. Because of the limited capacity of brain to remove excess ammonia, a rational approach to the treatment of patients with liver disease should include a regimen directed toward lowering the associated hyperammonemia.
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PMID:Ammonia metabolism in normal and portacaval-shunted rats. 210 90

Nutritional support in patients with advanced cirrhosis is difficult due to protein, fluid and salt restrictions. Successful liver transplantation should improve nutrient tolerance. We randomly assigned 28 hypoalbuminemic cirrhotic patients to receive, immediately after liver transplantation, one of three regimens: group 1, no nutritional support (n = 10); group 2, total parenteral nutrition (TPN) (35 kcal/kg/day) with standard amino acids (1.5 g/kg/day) (n = 8); or group 3, isocaloric isonitrogenous TPN with added branched-chain amino acids (n = 10). Therapy was continued for 7 days posttransplant. Jaundice resolution was unaffected by nutritional support. Nitrogen balance favored both TPN groups. Branched-chain amino acid (BCAA) aromatic amino acid ratios were highest in group 3. Coma scores and serum ammonia levels were similar in all groups. Both TPN groups achieved respirator independence earlier; this difference was not statistically significant. Group 1 patients stayed longest in ICU; the difference was statistically significant. TPN with either standard or BCAA- enriched amino acids is tolerated well immediately after successful liver transplant. Positive nitrogen balance is achieved; large protein loads do not worsen encephalopathy. Nutritional support may improve respiratory muscle function, allowing earlier weaning from ventilatory support. A shortened length of ICU stay justifies the expense of TPN.
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PMID:Nutritional support after liver transplantation: a randomized prospective study. 179 69

This study was conducted to determine whether an amino acid solution enriched with branched-chain amino acids altered protein catabolic rates and plasma ammonia in patients with cirrhosis. Nine stable subjects were given two peripheral intravenous infusions: a standard amino acid solution (solution A) and a branched-chain-enriched solution containing 97% more leucine (solution B). Each solution was given for separate 9-day (group 1, n = 6) or 3-day (group 2, n = 3) periods. Amino acid solutions delivered 0.7 gm protein.kg-1.day-1. Diets provided an additional 0.3 gm protein plus maintenance calories. Protein turnover was assessed by a primed continuous infusion of [1-14C] leucine in six patients (three patients in group 1 and three patients in group 2). Nitrogen balance and urinary 3-methyl histidine excretion were determined in group 1 patients. Compared with solution A, solution B increased leucine flux and leucine oxidation but had no significant effect on protein synthesis or catabolism based on the plasma specific activity of either leucine or alpha-ketoisocaproic acid. The additional leucine infused with solution B was quantitatively oxidized. Nitrogen balance did not differ with the two solutions and there was also no difference in the urinary excretion of 3-methyl histidine, suggesting that muscle protein catabolism was unchanged. Plasma ammonia concentration decreased significantly during the infusion of solution B and was associated with a slight fall in plasma glucagon concentration. The results indicated that a branched-chain-enriched amino acid solution did not alter protein synthesis or catabolism although it did lower the plasma ammonia when compared with a standard amino acid formula in stable cirrhotic patients.
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PMID:Effects of branched-chain amino acids on nitrogen metabolism in patients with cirrhosis. 219 23

A case of a patient with severe liver dysfunction and hyperammonemia undergoing splenectomy and liver biopsy was reported. Preoperative examination revealed that this patient's liver function was severely impaired due to liver cirrhosis (ICG15 = 60%, HPT = 29%, serum NH3 = 110 micrograms.dl-1). Preoperatively, kanamycin 2 g.day-1 and lacturose 60 ml.day-1 were given and FFP 3-5 units.day-1 were infused. With no premedication, general anesthesia was induced with dTc 3 mg, thiopental 200 mg and SCC 80 mg. Anesthesia was maintained with N2O-O2-enflurane and pancuronium. Though N2O concentration was kept at 50% to prevent intraoperative hypoxemia, the necessary enflurane concentration was low (almost 1% or lower). Serum NH3 level during operation was stable (100-110 micrograms.dl-1), and the level decreased (66-90 micrograms.dl-1) postoperatively. Postoperatively, this patient's consciousness level fluctuated with or without flapping tremor. The treatment of hepatic encephalopathy with lactulose, aminoleban EN and maalox were effective. Problems of perioperative and anesthetic management of a patient for upper abdominal surgery with severe liver dysfunction associated with hyperammonemia were discussed.
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PMID:[Anesthetic experience of a patient for splenectomy with severe liver dysfunction and hyperammonemia]. 223 30


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