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)

12 g of albumin are synthesized daily by the bound polyribosomes of all human liver cells together, corresponding to 10% of the intravascular albumin mass. The cell is producing a precursor albumin. During secretion albumin is liberated by splitting of a small peptide. Only 40% of the total body albumin is located intravascularly. 12g of albumin are degraded or excreted daily, 30% of it by the liver, the kidneys and the gastrointestinal tract. The main site of albumin catabolism is unknown. Albumin with a half-life of about 20 days is degraded at a constant fractional catabolic rate. The absolute rate of degradation varies depending on the plasma content. This mechanism allows an effective regulation of the serum albumin level. The fractional catabolic rate, however, is not completely fixed. It is slowly reduced if the serum albumin content is markedly reduced as in protein deficiency, the blind loop syndrome, cirrhosis, nephrosis, and diseases of the gastrointestinal tract. Infusion of albumin increases the fractional catabolic rate slowly. This must be taken in consideration substitution albumin in chronic diseases. The shift from the extravascular to the intravascular compartment is a short-term regulatory mechanism. The regulation of synthesis and degradation are independent from each other. The molecular mechanism of regulation of synthesis and degradation are unknown, partially due to inadequate methods.
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PMID:[The regulation of serum albumin in physiological and pathological conditions (author's transl)]. 87 Jul 44

40 patients with infectious hepatitis, 25 with chronic aggressive hepatitis, 25 with compensated liver cirrhosis, and 10 with decompensated liver cirrhosis were submitted to examination. The following abnormalities depending upon the stage and severity of hepatic diseases were found: a) disturbances of total lipids, cholesterol, phospholipids, beta-lipoproteids, glycerin, glycerides and neutral fats concentrations; b) marked disorders of glucose tolerance as indicated by the difference between plasma and erythrocyte glucose levels increasing in proportion to the degree of liver damage; c) a fall in plasma and erythrocyte magnesium reflecting the degree of hepatic parenchyma damage; d) a decrease of the albumin/gamma-globulin ratio in proportion to the degree of the impairment of hepatic cells. The presented fat, carbohydrate, magnesium and protein balance indices yield better criterions for the differential diagnostics of hepatic diseases than the routine investigations, and they also make possible objective prognosis.
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PMID:Disturbances of fat, carbohydrate, magnesium and protein balance in liver diseases. 88 63

The blood levels of zinc, lead, copper and albumin and the activity of erythrocyte delta-aminolevulinic acid dehydratase (ALA D), with and without addition of zinc in vitro, were measured in healthy subjects and in patients with cirrhosis. In cirrhosis there was a decrease, of zinc (-40%) albumin (-38%) and of activity of ALA D (-48%) and an increase in blood lead (+80%). Correlation between these results has been studied. The increase of blood lead is probably the result of zinc decrease. Moreover, as the urinary excretion of zinc is enhanced by chelation therapy, the prescription of zinc in lead intoxication is to be recommended. The activity of ALA D in patients with cirrhosis is less enhanced by addition of zinc in vitro than is the activity in patients intoxicated with lead. Probably in cirrhosis there is especially a decrease in the synthesis of ALA D, and lead intoxication the enzyme is inhibited.
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PMID:[The relationship between zinc levels in blood and the activity of delta-amino-levulinic acid dehydratase in human erythrocytes (author's transl)]. 88 56

The intrasplenic injection of 99mTc-labeled albumin microspheres, followed 30 sec later by an injection of 99mTc-labeled red blood cells with recording of the progression of the two tracers, were performed in 110 patients. This also enabled the plotting of activity versus time curves on splenic, hepatic, cardiac, and pulmonary areas of interest, there by giving access to several hemodynamic variables. Scintillation image demonstrated splenoportal obstruction in 8 cases. Intrahepatic obstruction with reflux via collaterals were observed in 53 cases, 14 with umbilical reflux. In 13 cases, the patency of surgical portacaval anastomoses were verified. The splenoportal blood flow velocity was not significantly different in patients with cirrhosis (V = 10.1 cm per sec +/- 3.0 SD) and in normal subjects (V = 13.2 cm per sec +/- 5.8 SD). The fraction of shunted splenic flow in the case of cirrhosis varied from 0 to 100%; there was no relationship between this percentage and the seriousness of the clinical status. In 3 cases, the presence of intrahepatic shunts was detected. There was a very significant difference between mean transit time (MTT) of red blood cells in patients with cirrhosis (t = 12.2 sec +/- 4.4 SD) and those without cirrhosis (t = 19.9 sec +/- 3.7 SD). Among patients with cirrhosis, those with a history of jaundice had a shorter MTT than those without such a history. On the other hand, the MTT was not significantly different whether the patients with cirrhosis had or did not have hemorrhage, ascites or encephalopathy. There was a positive correlation (P less than 0.01) between MTT and plasma albumin concentration,and between MTT and prothrombin (P less than 0.01). Finally, there was a high negative correlation (P less than 0.001) between MTT and total serum bilirubin. Scintillation splenoportography is a useful technique for assessing hepatic hemodynamics and for demonstrating abnormalities of the intrahepatic circulation.
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PMID:Scintillation splenoportography: hemodynamic and morphological study of the portal circulation. 98 35

The electrophoretic mobility of renin substrate in human plasma was determined by electrophoresis of the plasma on a cylinder of polyacrylamide gel, followed by slicing the gel, incubation of each slice with human renin, EDTA, and BAL in saline, and determination of the angiotensin formed by radioimmunoassay. With this modified technique 5, and possibly 8, electrophoretically dissimilar renin substrates have been found in human plasma. Significant variations in the patterns of renin substrates in the blood plasma of pregnant women and of those taking oral contraceptives were shown. In normal plasma from male or female subjects there was a single large peak of renin substrate with a mobility slightly less than that of albumin, and there were a series of very small peaks of renin substrate with lesser mobilities than the major peak. Increasing the sample size and prolonging the period of incubation with renin made the smaller peaks more apparent. In women using oral contraceptives, a distinctly different pattern of renin substrates was found. Early smaller peaks were increased. The major peak was sometimes increased also. Pregnancy produced a strikingly different pattern of renin substrates. There was an increase in all slow-moving peaks and their bases ran together without a return to the baseline. The absence of peaks when renin was omitted indicated that they were renin substrates. In 2 of 4 patients having cirrhosis of the liver with ascites, the amount of major substrate peak was greatly diminished and minor peaks were somewhat reduced. In 3 bilaterally nephrectomized patients, the major peak was not increased and the pattern of minor peaks was normal.
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PMID:Heterogeneity of renin substrate in human plasma: effect of pregnancy and oral contraceptives. 99 64

Although chemistry and physiology of bile acids have been elucidated during the last two decades, tests concerning bile acid metabolism are still rarely used in clinical medicine. The aim of this study therefore was, to investigate bile acid metabolism in patients with liver diseases and to find prognostic valuable parameters which can be recommended for clinical use. Following an introducing review of biosynthesis and kinetics of bile acids, normal values are presented for pool size and synthesis of the two primary bile acids, for bile lipid composition, plasma bile acid concentration and for clearance and conjugation of intravenously injected 14C-cholic acid, which have been measured in healthy subjects. Bile acids were determined by thin-layer-chromatography, gas-liquid-chromatography and by an enzymatic and fluorimetric method. In all patients investigated with acute hepatic necrosis, plasma disappearance of radioactivity was greatly prolonged after intravenous injection of 14C-cholic acid. By estimating free 14C-cholic acid and 14C-cholic acid conjugates in plasma individually, two groups of patients could be distinguished: in patients who survived hepatic coma, the clearance of free 14C-cholic acid was significantly more rapid and the percentage of glycine and taurine conjugates of 14C-cholic acid in plasma was significantly higher than in patients who died in coma. This prognostic significant differentiation was possible by measuring the relationship of conjugated: unconjugated radioactivity in one single plasma sample taken three hours after injection. In patients with cirrhosis of the liver the plasma disappearance rate of radioactivity during 60 minutes following injection of 14C-cholic acid was significantly correlated with serum-bilirubin, SGOT, serum-albumin, prothrombine-time, plasma bile acids, and a clinical scoring. 14C-deoxycholic acid was found in plasma of only a few patients 24 hours after injection of the labelled cholic acid, and was related to the relatively good liver function in these patients. It is concluded that the following tests of bile acid metabolism are of clinical interest: 1. Measuring plasma bile acid concentration may serve as a sensitive liver function test. 2. Estimation of the conjugation of intravenously injected 14C-cholic acid is of prognostic value in patients with fulminant hepatic failure. 3. Determination of the initial plasma disappearance rate of 14C-cholic acid injected intravenously and its transformation to 14C-cholic acid injected intravenously and its transformation to 14C-deoxycholic acid may help to classify patients with cirrhosis of the liver.
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PMID:[Aspects of bile acid metabolism in liver diseases(author's transl)]. 106 81

In 31 patients with cirrhosis of the liver undergoing porta-caval shunt surgery, the prognostic value of some liver function tests was studied. The surgical mortality was not correlated with the test results. Serum concentrations of bilirubin, albumin, and prothrombin were not correlated with postoperative encephalopathy, but the mutually correlated preoperative galactose elimination capacity and age of patients were correlated with encephalopathy development. Incapacitating encephalopathy mainly occurred in patients above 60 years of age, and when the galactose elimination capacity was at or less than an arbitrary limit of 225 mg/min. The liver function decreased significantly following operation.
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PMID:Preoperative liver function tests correlated with encephalopathy after porta-caval anastomosis. 107 89

Idiopathic portal hypertension is reported in five cases including one case of chronic arsenical intake and one case of chronic industrial vinyl chloride exposure. In all five cases the patients presented with gastrointestinal bleeding as the chief complaint. Physical examination was within normal limits except for splenomegaly in all. Results of liver function tests were normal, except for the relative clearance of sulfobromophtalein. A surgical liver biopsy specimen was obtained in all cases and showed moderate degrees of portal fibrosis, but no cirrhosis. Combined umbilicoportal, hepatic vein and superior mesenteric artery catheterization was performed in all cases. Hepatoportographies showed distortion of the intrahepatic portal venous system and cut-off of small portal venules. Porto-hepatic gradients ranged from 14.0 to 20.5 mm Hg. The portal hypertension was both sinusoidal and presinusoidal in nature but mainly presinusoidal. Hepatic extraction of indocyanine green and of albumin microaggregates was normal, thereby suggesting normal functional portal blood supply to the liver. The patients with arsenical or vinyl chloride exposure could not be differentiated from the other three patients with idiopathic portal hypertension. These results suggest that idiopathic portal hypertension may be related to domestic or industrial exposure to other hepatotoxins.
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PMID:Idiopathic portal hypertension. 108 57

Among 211 patients undergoing gastroduodenoscopy five had been carriers of Australia antigen. The same instrument had been used on all, and follow-up examination was carried out two and four months after the gastroscopy. Twelve patients died during the follow-up period of their original disease. Two additional patients became Australia-antigen positive. One of these had liver cirrhosis. In the other, surgery with multiple infusions of albumin had been carried out after gastroscopy and could have been the cause of the Australia-antigen transmission. No proven case of hepatitis transmission occurred in this group of patients.
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PMID:[Is there a risk of transmitting hepatitis by gastroduodenoscopy?]. 111 11

Tryptophan was measured in the lumbar CSF and serum of patients undergoing neurological investigation (controls) and in patients with hepatic cirrhosis. Samples were taken from the fasting patients at 8:00 a.m. Under these conditions, in the controls the mean CSF, free )mpm-albumin-bound) and total serum tryptophan were in the approximate ratio 1:4:24. In this cross-sectional study, for the controls, CSF tryptophan was correlated significantly and positively with the total serum but not with the free serum tryptophan. In patients with advanced hepatic cirrhosis the mean CSF tryptophan concentration was greatly elevated. However, the mean total serum tryptophan was unchanged and the free serum tryptophan only slightly elevated. Administration of probenecid, which displaces tryptophan from binding sites on serum albumin, and thereby increases the proportion of serum tryptophan in the free form, did not affect CSF tryptophan.
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PMID:Relationships between tryptophan in serum and CSF, and 5-hydroxyindoleacetic acid in CSF of man: effect of cirrhosis of liver and probenecid administration. 114 19


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