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)

Circulation levels of estrone sulfate (E1S) and dehydroepiandrosterone sulfate (DHAS) have been measured in plasma using a radioimmunoassay for estrone and dehydroepiandrosterone following extraction and hydrolysis of the sulfate. The mean +/- SE concentrations of E1S and DHAS in normal men were 458 +/- 25 pg/ml and 1.45 +/- 0.19 micrograms/ml, respectively. In normal women the values for days 5-7 of the cycle were 880 +/- 117 pg/ml and 1.25 +/- 0.12 micrograms/ml which were not different than the values for days 20-22 of 1195 +/- 176 pg/ml and 1.58 +/- 0.29 micrograms/ml. The mean values in post-menopausal women were 250 +/- 33 pg/ml and 0.47 +/- 0.07 micrograms/ml, both lower than the values in young women. In a group of cirrhotic men the mean values were 325 +/- 55 pg/ml and 0.38 +/- 0.12 micrograms/ml, both significantly lower than the normal values. This suggests a defect in sulfurylation in men with hepatic cirrhosis.
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PMID:Estrone sulfate and dehydroepiandrosterone sulfate concentrations in normal subjects and men with cirrhosis. 22 90

Quinidine pharmacokinetics (half-life, volume of distribution, and clearance) as well as protein binding were evaluated following a single 200 mg. oral dose of quinidine sulfate in eight control patients, in eight patients with moderate to severe cirrhosis, and in seven patients receiving 40 to 400 mg./day of propranolol. Patients with cirrhosis had a significantly longer quinidine half-life (9 +/- 1 hr; p less than .01) when compared to control patients (6 +/- 0.5h). This was not related to a reduced quinidine clearance rate but rather to an increase in quinidine volume of distribution (4.1 +/- .4 L./Kg. in cirrhotic patients vs 2.6 +/- 1 L./Kg. in control patients; p less than .01). Abnormal quinidine binding (greater than 25 per cent unbound fraction) was noted in seven of the eight cirrhotic patients. In contrast, patients receiving propranolol had a normal quinidine half-life of 6 +/- 0.5 hr. However, these patients had a significantly reduced quinidine clearance (3.3 +/- .7 ml./min./Kg. vs. 5.3 +/- .5 ml./min./Kg. in controls; p less than .05) and higher peak concentrations (1.25 +/- .20 micrograms/ml. vs. .80 +/- .5 micrograms/ml. in controls; p less than .05). Therefore in patients receiving propranolol, quinidine levels may be higher than expected shortly after dosage, and therefore a potential for transient toxicity exists in these patients. Maintenance quinidine dosage may have to be reduced in patients with moderate to severe hepatic cirrhosis, but not in patients receiving propranolol. Total quinidine concentration measurement underestimate free quinidine concentrations in most cirrhotic patients.
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PMID:Quinidine pharmacokinetics in patients with cirrhosis or receiving propranolol. 26 96

The metabolism of amphetamine was studied in three groups of mice, including normal mice (N), mice given chronic doses of phenobarbital via their drinking water (PB), and mice exposed to carbon tetrachloride vapors daily during the course of chronic phenobarbital consumption (PB/CCl4). Renal and hepatic tissue from animals of each group were examined by electron microscopy. Mice in the PB/CCl4 group demonstrated the classical symptoms of carbon tetrachloride-induced hepatic cirrhosis, and structural damage to the kidney. The PB group presented a normal renal pathology, but ultrastructural changes including swollen mitochondria and dilation of the endoplasmic reticulum were evident in the hepatocytes. The N, PB and PB/CCl4 mice excreted 84.5, 61.5 and 72.3 percent respectively of a dose of 14C-amphetamine sulfate in the 0-72 hour urine. Seven major urinary metabolites were detected in the normal group, 4 in PB group, and 3 in the PB/CCl4 group. Unchanged amphetamine, rho-hydroxyamphetamine and benzoic acid were tentatively identified by combined techniques of gas chromatography and thin-layer chromatography with autoradiography.
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PMID:Amphetamine metabolism in mice exposed chronically to phenobarbital and to phenobarbital with carbon tetrachloride. 44 95

Alkaline phosphatases, which had a unique electrophoretic mobility on polyacrylamide gel electrophoresis, were found in hepatic tissue of a patient with liver cirrhosis. Enzymic and immunological properties of the enzymes examined on electropherogram were similar to those of a fetal intestinal-type alkaline phosphatase in hepatoma with respect to sensitivity to amino acids, heat stability, sensitivity to sodium dodecyl sulfate, and reactivity to anti-intestinal alkaline phosphatase antiserum. The enzymes seem to be a variant of a fetal intestinal alkaline phosphatase. The significance of occurrence of the enzymes in cirrhotic liver is discussed.
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PMID:Electrophoretic variant of fetal intestinal alkaline phosphatase in a patient with cirrhotic liver. 44 73

Liver disease with inclusions of copper was recognized among 30 rural workers with "vineyard sprayer's lung." The pathological findings were varied: focal or diffuse swelling and proliferation of Kupffer cells; histiocytic and sarcoid-like granulomata; fibrosis of variable degree in the perisinusoidal, portal, and subcapsular areas, accompanied by atypical proliferation of the sinusoidal lining cells; micronodular cirrhosis; angiosarcoma of the liver; idiopathic portal hypertension. Abundant deposits of copper were revealed by histochemical techniques within hepatic and pulmonary lesions in these patients. The observations on the human and experimental material suggest an etiological relationship between exposure to copper sulfate and the lesions described. A morphological resemblance was noted between the "liver disease of vineyard sprayers" and the hepatic lesions reported in workers exposed to inorganic arsenic and to vinyl chloride. The identification of the inhaled foreign material within the liver lesions raises important etiological considerations.
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PMID:Liver disease in vineyard sprayers. 55 10

In 5 patients with cirrhosis of the liver sulfated and nonsulfated [14C]cholic acid and [14C]chenodeoxycholic acid were administered intravenously and the specific activity curves were determined. Specific activities declined exponentially and pool sizes, synthesis rates, and turnover rates of bile acids were calculated on the basis of a one-pool system. The biological half-life of cholic acid was 4.3 +/- 1.6 days (mean +/- SEM) and of chenodeoxycholic acid was 2.8 +/- 1.2 days. The half-life of cholic acid sulfate was 0.7 +/- 0.5 day and of chenodeoxycholic acid sulfate was 0.8 +/- 0.5 day. The pool size of cholic acid was 513 +/- 103 mg, of chenodeoxycholic acid, 477 +/- 77 mg, of cholic acid sulfate, 4.7 +/- 1.0 mg, and of chenodeoxycholic acid sulfate, 38.7 +/- 4.0 mg. The daily synthesis of cholic acid was 90 +/- 14 mg, of chenodeoxycholic acid, 118 +/- 6 mg, of cholic acid sulfate, 7.2 +/- 2.1 mg, and of chenodeoxycholic acid sulfate was 32.6 +/- 3.2 mg. The data indicate that sulfate esters of bile acids are significantly more rapidly excreted than are unsulfated bile acids. More than one-fourth of the chenodeoxycholic acid but less than one-tenth of the cholic acid formed was sulfated. The preferential sulfation of chenodeoxycholic acid is responsible for the more rapid turnover of chenodeoxycholic acid in comparison to cholic acid. Sulfation enhances the excretion and thereby prevents the accumulation of hepatotoxic concentrations of chenodeoxycholic acid in patients with cirrhosis of the liver.
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PMID:Pool size, synthesis, and turnover of sulfated and nonsulfated cholic acid and chenodeoxycholic acid in patients with cirrhosis of the liver. 63 88

A 42-year-old woman had an acquired zinc deficiency. The patient was malnourished, secondary to chronic alcohol (ethanol) abuse and cirrhosis, with associated low serum and urinary levels of zinc. Her acrodermatitis was unresponsive to topically applied triamcinolone acetonide but cleared after oral zinc sulfate therapy.
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PMID:Acrodermatitis and acquired zinc deficiency. 66 32

The question is still open, whether a pathologic formation of fibrinogen or an insufficient stabilized fibrin are causative factors within the complex disorders in hemostasis in patients with liver cirrhosis. Thus, 45 patients with liver cirrhosis, which was proven by liver biopsy, were investigated by means of sodium-dodecyl-sulfate (SDS) polyacrylamidgel-electrophoresis in order to evaluate, whether the liver produces a pathological fibrinogen or whether the formation of fibrin from fibrinogen is defect. The fibrin stabilizing factor (factor XIII) was measured by immunological methods. In order to have a mean of the stage of the disease, 37 patients were subdivided by the extend or their porto-caval collateral circulation and further 8 patients were investigated having bleeding from esophageal varices. By the results evidence accrued that in advanced stages of liver cirrhosis and a marked porto-caval collateral circulation polymerization of fibrinogen was insufficiently, especially, the formation of alpha-chains was altered, whereas the formation of gamma-dimers, the separation of fibrinopeptides from fibrinogen, and the aggregation of fibrinmonomers were normal. This defect in fibrin structure was positive correlated with the stage of liver cirrhosis, which correlated negative with the plasma activity of factor XIII. In vitro, the defect in fibrin formation, from fibrinogen was abolished by adding factor XIII to the assay. Thus, in liver cirrhosis fibrin formation is altered because of factor XIII deficiency, but a normal fibrinogen is synthesized by the liver. In consequence, the administration of factor XIII preparations is suggested as one clinical action among others to benefit the hemostatic disorders, especially in patients with bleeding from esophageal varices.
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PMID:[Fibrinogen and fibrin structure in patients with cirrhosis of the liver (author's transl)]. 70 17

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Large amounts of bile acid sulfate were found in the urine of patients with hepatobiliary diseases. In patients with acute hepatitis, daily excretion of bile acid into urine was 68.24 plus or minus 51.80 mumoles per day, and the percentage of sulfated bile acid was 83.4 plus or minus 16.7%. In patients with chronic hepatitis and cirrhosis, a slight increase of urinary bile acid was observed (2.89 plus or minus 2.69 and 5.27 plus or minus 4.28 mumoles per day, respectively), and the percentage of sulfated bile acid was 73.9 plus or minus 28.6 and 44.6 plus or minus 30.4%, respectively. In patients with obstructive jaundice, a moderate increase of urinary bile acid was found (32.62 plus or minus 18.35 mumoles per day), and the percentage of sulfated bile acid was 58.3 plus or minus 22.6%. In patients with hepatobiliary diseases, the elevation of both levels of sulfated and nonsulfated bile acids in serum was observed. The percentage of sulfated bile acid was 9% in normal serum, and varied from zero to 82.8% in pathological sera. A remarkable increase of sulfated bile acid was found in patients with obstructive juandice and acute hepatitis, while a slight elevation was found in patients with chronic hepatitis and cirrhosis. Sulfated bile acid in bile was nonexistent or below 0.5% of total bile acid. According to these findings, the increased bile acid in serum of patients with hepatobiliary diseases might be more easily excreted into the urine as sulfated bile acid.
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PMID:Sulfated and nonsulfated bile acids in urine, serum, and bile of patients with hepatobiliary diseases. 111 56


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