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)

Using cytochemical methods the authors studied the activity of certain lysosomal enzymes and cytochrome oxidase in peripheral blood leucoytes in 22 patients with Wilson's disease. The control group comprised 50 healthy blood donors. It was found that the activity of acid phosphatase in the lymphocytes of patients was higher than in controls, the mean indices being respectively 90.50 +/- 8.95 and 60.38 +/- 3.95. The activity of beta-glucuronidase was found to be lower in the lymphocytes of patients, the mean value was 25.10 +/- 8.59 in patients and 64.91 +/- 5.78 in controls. The activity of cytochrome oxidase was lower in the granulocytes of patients with Wilson's disease than in controls, the mean values being 54.5 +/- 12.14 and 156 +/- 15.41 respectively. The activity of acid phosphatase in granulocytes as well as that of non-specific esterase in lymphocytes was similar in both groups. Decreased antigen degradation in Wilson's disease may be due not only to liver cirrhosis but also to disturbances in the metabolism of white blood cells, including, among others, decreased activity of cytochrome oxidase. The rise of the activity of acid phosphatase and reduced activity of beta-glucuronidase indicate chronic antigenic stimulation of lymphoid system.
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PMID:[Cytochemical studies of peripheral white blood cells in Wilson's disease]. 19 62

Pigment gallstones are defined as any dark brown-to-black stone, consisting of calcium salts of bilirubin, phosphate, carbonate and other anions, and can be separated into carbonate- and noncarbonate-containing groups. Pigment stones predominate in the rural Orient, in cirrhosis, and in elderly United States patients undergoing cholecystectomy. Clinical associations include bile duct obstruction, stasis, and possibly hemolysis. Of pigment stones, 50% are radioopaque and account for two-thirds of all opaque stones. The concentrations of bile salts, phospholipids,, cholesterol, and total bilirubin in bile are similar to normal levels, but the concentration of unconjugated bilirubin is increased in the bile of some patients. Increased unconjugated bilirubin in bile may be caused by increased hydrolysis of excreted conjugated bilirubin. Unconjugated bilirubin is solubilized by bile salts, but the interaction is primarily nonmicellar. Ionized calcium and pH are important determinants of solubility. Sulfated glycoproteins, excreted in increased amounts in patients with cholelithiasis, may be the site of pigment stone precipitation because these compounds bind calcium salts tightly. E coli is frequently cultured from pigment stones in Japan but not in the United States; thus, bacterial beta-glucuronidase may be important in stone formation in Japan but probably not in the West. Stasis leads to increased calcium secretion and to increases in the concentration of sparingly soluble compounds that may then precipitate. Incomplete emptying of the gallbladder may result in the same concentration process. Unsaturated fats and chronic vagal stimulation cause pigment stone formation in animals. At present, surgery is the only treatment for pigment lithiasis.
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PMID:Pigment gallstones. 31 81

An enzyme-linked immunosorbent assay (ELISA) was developed for human beta-glucuronidase, using a specific polyclonal antibody raised against the purified enzyme. beta-Glucuronidase from human liver consisted of three subunits with molecular mass of 76, 64 and 18 kDa. The assay offered a specific, sensitive and convenient means of measuring immunoreactive beta-glucuronidase in human sera. beta-Glucuronidase activity determined by the conventional method appeared to be extremely low, indicating that in human sera beta-glucuronidase exists in an enzymatically inactive form. The sensitivity of the assay permitted the detection of 1-100 ng of purified beta-glucuronidase. A mean serum level in normal subjects was 108 +/- 25 ng/ml (mean +/- S.D.). A high level of beta-glucuronidase was found in sera of patients with severe hepatocellular necrosis, including liver cirrhosis (152 +/- 130 ng/ml) and chronic active hepatitis (220 +/- 99 ng/ml), whereas no significant increase of the enzyme protein was observed in chronic persistent hepatitis (102 +/- 42 ng/ml). beta-Glucuronidase was also increased in sera of patients with primary hepatoma (156 +/- 125 ng/ml). The immunoreactive beta-glucuronidase determined in this assay was thought to be a supplementary serological indicator for hepatocellular necrosis.
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PMID:Serum immunoreactive beta-glucuronidase determined by an enzyme-linked immunosorbent assay in patients with hepatic diseases. 163 57

beta-Glucuronidase, a lysosomal hydrolase, was purified from human liver tissue, and an enzyme-linked immunosorbent assay was developed using specific antibody against the enzyme. Using the assay procedure, the serum immunoreactive beta-glucuronidase (beta-glucuronidase) was determined in 190 patients with various liver diseases and in 53 healthy controls to examine whether or not the serum level of beta-glucuronidase would successfully reflect the degree of histological hepatic cell necrosis. beta-Glucuronidase was also determined at regular intervals in 28 patients with chronic hepatitis to investigate the clinical usefulness of serial measurement of the enzyme to predict the histological progression of hepatitis. These 28 patients could be subdivided into three groups, "continuously low type", "labile type" and "elevated type" according to the profiles of fluctuation of serum beta-glucuronidase values. Serum beta-glucuronidase was significantly increased in patients with hepatoma, liver cirrhosis and chronic active hepatitis compared with normal controls. There was significant positive correlation between the beta-glucuronidase and the degree of hepatic cell necrosis determined by histological observation, on the other hand, there was no statistical correlation between the transaminase activities and the degree of hepatic cell necrosis. It was confirmed in immunohistochemical study that the increased beta-glucuronidase in serum has been released from necrotic hepatic cells into blood stream. It was speculated that the elevation of serum transaminase activities had resulted from the alteration in the membrane permeability of hepatic cells rather than from hepatocellular necrosis. Histological progression of hepatitis was found in 8 of 10 patients (80%) of "labile" and "elevated type", while it was found only 3 of 18 patients (16.7%) of "continuously low type". These results suggested that the serial measurement of beta-glucuronidase could be used for an indicator to predict the histological progression of hepatitis.
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PMID:[Measurement of serum immunoreactive beta-glucuronidase: a possible serological marker for histological hepatic cell necrosis and to predict the histological progression of hepatitis]. 165 3

Black and brown pigment gallstones are morphologically, compositionally, and clinically distinct. Black stones form primarily in the gallbladder in sterile bile and are associated with advanced age, chronic hemolysis, alcoholism, cirrhosis, pancreatitis, and total parenteral nutrition. Brown stones form not only within the gallbladder but also within the intrahepatic and extrahepatic ducts; they are uniformly infected with enteric bacteria and are usually associated with ascending cholangitis. Brown stones are related to juxtapapillary duodenal diverticula and are the predominant type of de novo common bile duct stones. Cholecystectomy is usually curative in black pigment stone disease, whereas stones often recur after cholecystectomy for brown stone disease. The pathogenesis of black stones is probably related to nonbacterial, nonenzymatic hydrolysis of bilirubin conjugates. At the pH of bile, this results in two monohydrogenated bilirubin anions that precipitate with calcium ions. Bilirubin monoconjugates that are increased in several conditions, such as Gilbert's syndrome and chronic hemolysis, may play a pivotal role in black stone formation as a source of unconjugated monohydrogenated bilirubin and as a possible co-precipitant with calcium. The precipitation of calcium carbonate and phosphate is influenced by local gallbladder factors. Brown pigment stones are formed in bile infected with enteric bacteria that elaborate hydrolytic enzymes: beta-glucuronidase, phospholipase A, and conjugated bile acid hydrolase. The resulting anions of bilirubin and fatty acids form insoluble calcium salts. We used nb/nb mice with a chronic hemolytic anemia as a model of hemolysis-induced black stone disease. The presence of 40% bilirubin monoconjugates in mouse gallstones indicated the importance of this moiety in the pathogenesis of black stones. Other data obtained by marrow transplantation experiments in mice revealed the relative importance of genotype versus the hemolytic anemia on determinants such as biliary bile acid composition and mucin secretory glands in the mouse gallbladder neck. Additional physical chemical studies of the interaction of unconjugated bilirubin in model bile solutions will be helpful in further delineating the pathogenesis of both black and brown pigment gallstones.
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PMID:Pigment gallstone disease. 202 17

Two methods of inducing liver cirrhosis in the rat were studied. Intragastric administration of CCl4 for 16 weeks according to Proctor and Chatamra was compared to the administration of thioacetamide in the drinking water (0.3 g/l) for the same period. CCl4 administration induced micronodular cirrhosis in 6/8 animals with a 27% mortality. Thioacetamide induced cirrhosis in 6/8 animals without mortality. The histologic pictures differed somewhat in that the CCl4 group exhibited more necrosis and cellular swelling while the thioacetamide group had more nuclear atypias and proliferation. Biochemically both groups had elevated plasma levels of aspartate aminotransferase. The lysosomal enzyme beta-hexosaminidase (beta-NAG) showed a transient increase in the thioacetamide animals, while beta-glucuronidase decreased. CCl4-induced cirrhosis led to an increase in beta-NAG. Plasma zinc decreased in both groups as well as liver zinc content in the CCl4 group, while there was a continuous elevation of liver zinc in the thioacetamide group. We conclude that oral administration of thioacetamide is a simple and reliable method of inducing experimental liver cirrhosis. The differences in histological appearances and some biochemical parameters may be caused by the different mechanisms of action of thioacetamide and CCl4.
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PMID:Thioacetamide- and carbon tetrachloride-induced liver cirrhosis. 276 88

We studied the significance of urinary enzyme measurements in diagnosing proximal tubular damage in cirrhosis of the liver. Urinary excretion (u-enzyme) and fractional urinary excretion (FEenzyme) of gamma-glutamyltranspeptidase (GGT), leucine aminopeptidase (LAP), alkaline phosphatase (AP) and beta-glucuronidase (B-GLU) were quantified in 14 control subjects (group I), 12 cirrhotics with functional renal failure (group II), 13 cirrhotics with renal tubular damage (group III) and 7 non-liver patients with renal tubular damage (group IV). Urinary enzyme excretion and fractional enzyme excretion were significantly higher in the cirrhotics of group III than in the controls or group II. In group III, these tests usually reached values within the range of group IV. The sensitivity of urinary enzyme excretion was 0.92 and specificity ranged from 0.75 (u-LAP) to 1 (u-GGT; u-B-GLU). The sensitivity of fractional enzyme excretion was between 0.61 (FEB-GLU) and 0.84 (FEGGT; FELAP), while specificity was from 0.91 (FELAP; FEAP) to 1 (FEGGT; FEB-GLU). The results indicate that measurement of urinary enzymes may be very useful in diagnosing renal tubular damage in cirrhotic patients with impaired renal function.
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PMID:Urinary excretion of enzymes in cirrhotics with renal failure. 287 95

Plasma levels of the lysosomal enzymes, beta-hexosaminidase and beta-glucuronidase, were analyzed in rats with carbon tetrachloride induced liver cirrhosis. Out of 22 animals, 15 showed cirrhotic and 4 pre-cirrhotic livers. 4 cirrhotic animals exhibited cholestatic features with increased bilirubin, alkaline phosphatase (ALP) and aspartate aminotransferase (ASAT) in plasma. The remaining 15 pre-cirrhotic and cirrhotic rats showed clear significant changes only in ASAT levels. These 15 rats showed no consistent increase in plasma, spleen or liver lysosomal enzyme activities, whereas the 4 rats with cholestatic features exhibited considerable increases of lysosomal enzymes. The increased activities might be attributed to decreased biliary excretion and/or increased production of lysosomal enzymes by activated macrophages.
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PMID:Lysosomal enzymes in plasma, liver and spleen from rats with carbon tetrachloride-induced liver cirrhosis. 315 68

Activities of alkaline phosphatase (ALP), gamma-glutamyl transferase (GMT), lactate dehydrogenase (LD), beta-glucuronidase (GLU) and cathepsin B-like (CB-like) were determined in blind-coded sera from 50 patients with primary liver carcinoma, liver cirrhosis and acute hepatitis, and from 40 control subjects of comparable age range. CB-like activity averaged 700% (p less than 0.01), 1590% (p less than 0.01) and 1600% (p less than 0.01) of control subjects in liver cirrhosis (n = 30), acute hepatitis (n = 5) and primary liver carcinoma (n = 15), respectively. In acute hepatitis group we have found significant correlation between CB-like and GLU activities (r greater than 0.95). This correlation, however, was not observed in primary liver carcinoma suggesting that alteration in CB-like activity is not due to generalized increases in lysosomal membrane instability. The primary liver carcinoma group exhibited also the modest increments in serum ALP, GMT and LD activities (p less than 0.01). This increment, however, was not detected in any of acute hepatitis or liver cirrhosis patients. For the first time the alkaline-stable form of CB-like in human serum is described. This form representing 40% of overall CB-like activity was present in all primary liver carcinoma patients. This form, however, was not present in sera of any of control subjects or in sera of patients with acute hepatitis and liver cirrhosis with the exception of two men, in whom we have probably dealing with an early stage of primary liver carcinoma. Although the nature of the increment in CB-like activity in cancer remains to be determined, such analyses may help to the early detection of malignant hepatoma (primary liver carcinoma).
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PMID:Serum alkaline-stable acid thiol proteinase--a possible marker for primary liver carcinoma. 614 23

Serum activities of two lysosomal enzymes, beta-glucuronidase and acid phosphatase, were estimated in 66 patients with liver cell carcinoma, 10 with secondary liver cancer, 14 with cirrhosis of the liver, and 9 normal controls. A substantial increase in the enzyme activities was found in patients with liver cell carcinoma but not in those with secondary liver cancer. The degree of the enzyme elevations paralleled the stage of hepatoma. Although the serum activities of both enzymes were also elevated in patients with liver cirrhosis, the elevations were significantly higher in hepatoma than in liver cirrhosis. Possible mechanisms for the elevation of serum lysosomal enzyme activities in hepatoma are discussed, but further studies are necessary to elucidate the biological and clinicopathological significance of estimating serum lysosomal acid hydrolases in patients with primary liver cell carcinoma.
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PMID:Serum activities of lysosomal enzymes in patients with liver cell carcinoma. 617 11


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