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)

Lysyl oxidase was partially purified from serum by a diethylaminoethyl batch procedure in the presence of 6 mol/L urea and dialyzed against 3 mol/L KSCN. Using this method, we determined serum lysyl oxidase activity in 52 patients with liver disease and in 14 healthy controls, and we examined usefulness of serum lysyl oxidase in assessing liver fibrogenesis. For this purpose, serum lysyl oxidase activity in chronic liver disease was compared with serum levels of prolyl hydroxylase and laminin P1. As compared with controls, serum lysyl oxidase activity increased 1.6-fold in chronic persistent hepatitis, 4.4-fold in chronic active hepatitis and 11.8-fold in cirrhosis, indicating an increase in concert with the development of liver fibrosis. In hepatocellular carcinoma, the serum activity, although significantly increased, was lower than that in cirrhosis. Serum prolyl hydroxylase was significantly increased in chronic active hepatitis, in liver cirrhosis and in hepatocellular carcinoma. Serum laminin P1 was significantly increased in chronic active hepatitis, in cirrhosis and in hepatocellular carcinoma. Serum lysyl oxidase activity did not correlate significantly with serum levels of prolyl hydroxylase and laminin P1 in any subject or in any subgroup. The magnitude of the increase and the abnormal percentage of serum lysyl oxidase activity were larger than those for serum prolyl hydroxylase and laminin P1. These results suggest that serum lysyl oxidase activity is a more sensitive indicator of liver fibrosis than serum prolyl hydroxylase and laminin P1.
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PMID:Serum lysyl oxidase activity in chronic liver disease in comparison with serum levels of prolyl hydroxylase and laminin. 168 40

In the post-absorptive stage L-alanine is the main source of alpha-amino-nitrogen reaching the liver as glucose precursor. This aminoacid has been used as a measure of urea synthesis capacity in several pathologic conditions, but it has not been employed sistematically in patients with liver cirrhosis. We tried to address this issue by evaluating: a) L-alanine plasma levels, b) urea extraformation (UE), and c) ammoniogenesis after oral L-alanine (0.25 and 0.50 g/kg b wt) in healthy control subjects and in patients with nonalcoholic compensated (Child-Pugh's A class) and decompensated (Child-Pugh's B and C) liver cirrhosis. L-alanine plasma levels after oral load were higher and lasted longer in cirrhotics as compared to controls. Furthermore, after L-alanine oral load, significantly higher ammonia plasma levels were observed in cirrhotics than in controls. Changes in the urea extraformation were comparable in cirrhotics and controls. Both delayed L-alanine elimination from plasma and L-alanine-induced hyperammoniemia were more evident in decompensated cirrhotics and related to L-alanine dose.
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PMID:L-alanine plasma levels after oral loads in non-alcoholic liver cirrhosis: relationship with urea extraformation and ammoniogenesis. 174 21

A group of 207 consecutive patients admitted for decompensated liver cirrhosis of different etiologies (alcoholic, HBsAg-associated and cryptogenic), was studied in order to assess the independent long-term (up to 5 years) prognostic value of 13 clinical, biochemical and etiological factors. These were analyzed by the Cox Regression Model using a step-wise backward procedure. The final model included bilirubin (p = 0.003), HBsAg (p = 0.006), encephalopathy (p = 0.010) and a factor comprising urea and albumin (p less than 0.001). The model was validated by a split-sample testing technique and may be used to predict survival in decompensated cirrhosis. A comparison with Child-Pugh's score in terms of survival prediction was carried out and was favorable to our model. We conclude that this model can be useful for predicting short and long-term survival in the three most common types of liver cirrhosis and that the additional overhead to calculate it seems justified in view of the large availability of microcomputers where simple programs can be run to perform this task and draw the predicted survival curves.
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PMID:[Prognostic factors and survival model for decompensated hepatic cirrhosis]. 176 12

Patients with cirrhosis of liver are more prone to have accompanying diabetes mellitus. The present study was conducted to investigate various biochemical parameters in patients with hepatic cirrhosis without diabetes. In these patients blood pyruvate, total bilirubin and globulin levels were elevated as compared to normal individuals. In contrast serum albumin level declined significantly whereas no significant change was observed in the concentrations of blood glucose, total proteins, total lipids, urea and serum cholesterol. These studies confirm the previous reports that carbohydrate metabolism is deranged in hepatic cirrhosis which may lead to diabetes mellitus.
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PMID:Carbohydrate metabolism in liver cirrhosis. 177 May 58

The functional hepatic nitrogen clearance during amino acid infusion is a measure of liver cell mass. The clinical feasibility of the test has so far been limited by methodological problems. A simplified procedure was used to measure the urea-nitrogen synthesis rate and functional hepatic nitrogen clearance in nine subjects with normal liver function and in nine patients with cirrhosis. The method was based on only four consecutive 2-hr urine collections and five blood samples. Total body water was calculated from a nomogram based on age and anthropometric data, whereas the gut urea hydrolysis was assigned one fixed fraction of synthesis (0.17 in control subjects and 0.26 in patients with cirrhosis). Finally, a solution of a single amino acid, alanine, was infused as substrate for urea synthesis. Urea-nitrogen synthesis rate increased linearly with increasing alpha-amino-nitrogen concentration, and the slope of the regression (functional hepatic nitrogen clearance) was reduced in cirrhosis from 37.5 +/- 7.0 L/hr to 18.4 +/- 6.7 L/hr; p less than 0.005. The hepatic nitrogen clearance was linearly related to the clinical status (Child-Pugh score), to routine liver function tests and to galactose elimination capacity (r = 0.869), a well-established, quantitative, liver function measure. The simplified method makes the measurement of hepatic nitrogen clearance suitable for routine clinical use. The test might prove useful to study the alterations of nitrogen metabolism in cirrhosis, with special reference to hepatic encephalopathy.
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PMID:Hepatic amino-nitrogen clearance to urea-nitrogen in control subjects and in patients with cirrhosis: a simplified method. 199 17

Cirrhosis of the rat liver was induced by a 12 week individualized CCl4/phenobarbital treatment. After treatment, all surviving animals (81%) showed cirrhosis of the liver. The cirrhosis induced was irreversible when evaluated 24 weeks after cessation of treatment. Quantitative liver function measurements were reduced in a differentiated manner. Ranked according to the most pronounced changes they are: capacity of urea-N synthesis (CUNS), galactose elimination capacity (GEC) and antipyrine clearance (APC). Hepatic glutathione concentrations were only slightly decreased after the CCl4 treatment. It is possible to produce a high incidence of irreversible cirrhosis with differentiated functional impairment in the rat.
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PMID:CCl4 cirrhosis in rats: irreversible histological changes and differentiated functional impairment. 200 67

An attempt was made to estimate noninvasively portal pressure (PP) in patients with chronic liver disease, using the theory of quantification, a kind of multivariate analysis. Forty-one patients with liver cirrhosis and 22 patients with chronic hepatitis in whom hepatic venous catheterization had been performed were studied. Seventeen parameters (age, sex, mean blood pressure, red blood cell count, platelet count, prothrombin time, lactate dehydrogenase, alkaline phosphatase, total bilirubin, albumin, gamma-globulin, indocyanine green retention at 15 min, blood urea nitrogen, hepatomegaly, splenomegaly, ascites and edema) were selected for the estimation of PP. The estimated PP correlated significantly with the data obtained by hepatic venous catheterization with a high correlation coefficient of 0.835 (p less than 0.01). An investigation using the theory of quantification was also undertaken to determine which of the 17 parameters selected above was most useful in estimating PP. Among the 17 parameters indocyanine green retention at 15 min, red blood cell count, prothrombin time, hepatomegaly and splenomegaly seemed to contribute significantly to the estimation of PP. When the formula was applied to 31 successive patients with chronic liver disease (external samples), the correlation between the estimated and measured PP was 0.455 (p less than 0.01). These results indicate that the formula is clinically useful in estimating PP in patients with chronic liver disease.
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PMID:[Estimation of portal pressure using the theory of quantification]. 201 41

This case describes a patient with cholesteryl ester storage disease who underwent liver transplantation for progressive cirrhosis, portal hypertension, ascites, and uncontrollable gastrointestinal bleeding. Four and one-half years posttransplant, her growth improved, cholesterol levels have returned to normal, and she is clinically well except for mild hypersplenism and an elevated blood urea nitrogen (BUN) and creatinine. Serum triglycerides remain elevated, but there have been no signs of progressive renal, intestinal, vascular, or pulmonary disease.
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PMID:Liver transplantation for cholesteryl ester storage disease. 207 31

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

Dietary measures have achieved mixed results in the management of liver disorders. Although a high energy diet may shorten the course of viral hepatitis by a relatively small amount, dietary restriction is usually of no benefit in compensated cirrhosis. Restriction of sodium intake to 22 to 60 mol/day leads to resolution of cirrhotic ascites in approximately 20% of patients, and reduces the requirement for diuretics in the remainder. In advanced liver disease, diet plays an important role in the avoidance of portal-systemic encephalopathy (PSE), with the tolerance of most nutrients, most importantly protein, being sharply reduced. Despite the frequent presence of carbohydrate intolerance in liver disease, carbohydrate supplementation may be required to ensure adequate utilisation of the reduced dietary protein intake. Zinc supplementation may also be required in liver cirrhosis to compensate for a deficiency. Bed rest is an important component of the management of acute and chronic liver disorders, together with the avoidance of fatigue. Abstinence from alcohol is required in alcoholic liver disease patients, who should receive parenteral thiamine 100 mg and other vitamin and mineral supplementation as required. Agents acting on the ascending loop of Henle [such as furosemide (frusemide)] or the distal tubule (such as spironolactone) are the diuretics most frequently employed to mobilise ascites in cirrhosis, the latter drug being the more effective in nonazotaemic patients. In the absence of oedema, the diuresis should be restricted to a maximum of 750 ml/day; however, patients with oedema may safely undergo a diuresis of less than or equal to 1.5 L/day. Diuretic therapy is often associated with renal complications, such as azotaemia (usually reversible) and severe hyponatraemia in cirrhotic patients with ascites; spironolactone may produce antiandrogenic adverse effects. Lactulose, used in the treatment of acute and chronic PSE, acts by inhibiting gastrointestinal absorption of ammonia and other toxic nitrogenous substances, and by reducing urea degradation. Other pharmacological treatments, such as branched-chain amino acids and benzodiazepine antagonists have a limited role in the management of PSE. Chronic cholestasis has been treated with cholestyramine and fat-soluble vitamins, whereas ursodeoxycholic acid appears to be a promising agent in the treatment of primary biliary cirrhosis. In chronic hepatitis, the prevention of development of cirrhosis is a primary treatment goal which has been attempted with variable success using antifibrotic drugs such as penicillamine and colchicine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Traditional management of liver disorders. 208 80


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