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)

The profile of urinary salicylate metabolites was determined after an i.p. administration of acetylsalicylic acid (ASA) to CCl4-cirrhotic rats to rats which in addition to CCl4 received an oral dose of silymarin throughout the CCl4 treatment to produce cirrhosis and to control groups. ASA esterase activity was determined in serum and livers. The time course of plasma concentration of salicylates in similar groups was followed after the i.p. injection of ASA. The cirrhotic animals showed a lack of urinary glucuronides and an increase in urinary gentisic and salicylic acids. The activities of plasma and serum ASA esterase were significantly increased in cirrhosis and the plasma half-life of ASA was reduced. The simultaneous administration of silymarin (50 mg/kg of b.w.) along with CCl4, completely prevented all the alterations. The mechanism by which silymarin prevented those alterations is not completely known but our results establish the potential use of silymarin in cirrhotic patients to prevent disorders in drug metabolism and disposition frequently found in patients with liver diseases.
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PMID:Silymarin improves metabolism and disposition of aspirin in cirrhotic rats. 339 94

The material from 113 point liver biopsies was studied. In 11 biopsy samples hepatic cirrhosis of viral origin was diagnosed, in 15 there was an alcoholic cirrhosis of the liver, and in 23--primary biliary cirrhosis. The comparative group included 8 patients with CPG, 13 with CAG, 32 with alcohol induced fatty dystrophy and 12 with non-alcoholic fatty dystrophy. Twenty six biopsy samples in which there were no inflammatory changes, the hepatic structure was unaltered, were used as controls. Stellate reticuloendotheliocytes were identified by means of acid-alpha-naphthyl-acetate esterase test. Quantitative assessment of stellate reticuloendotheliocytes (SR) was made stereometrically. In cases of primary biliary cirrhosis (PBC), active viral and alcoholic cirrhosis significant SR activation was found (due to hepatic parenchyma necroses) to maintain homeostasis. The biggest SR activation was revealed in PBC which is connected with the involvement of the immune mechanisms in this disease.
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PMID:[Stellate reticuloendotheliocytes in cirrhosis of the liver]. 359 4

Cytocentrifuged preparations of mononuclear cells in blood and pleural fluid were stained for acid alpha-naphthyl acetate esterase (ANAE) in order to characterize the lymphocytes of pleural effusions histochemically. The cellular samples were obtained from 42 patients with pleural effusions caused by tuberculosis, pneumonia, cancer, malignant lymphoma, sarcoidosis, congestive heart failure, hepatic cirrhosis or nonspecific causes. The mean percentage of ANAE-positive lymphocytes from patients with tuberculous pleural effusion was significantly greater (P less than 0.001) in pleural fluid (85.6%) than in peripheral blood (70.0%). Tuberculous pleural fluid also contained a higher mean percentage of ANAE-positive lymphocytes than did pleural fluid from patients with cancer (75.0%), malignant lymphoma (50.0%), pneumonia, nonspecific disease (74.9%) or transudates (59.3%). The findings show that ANAE staining is useful for demonstrating T lymphocytes in pleural effusions. The pathogenetic role of these T lymphocytes and the diagnostic significance of demonstrating ANAE-positive cells in pleural effusions are discussed.
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PMID:Acid alpha-naphthyl acetate esterase staining of lymphocytes in pleural effusions. 617 49

Cholesteryl ester storage disease is a rare disorder if cholesterol metabolism characterized by excessive hepatic storage of cholesteryl esters. The underlying defect probably is decreased activity of alpha-naphtyl-acetatesterase, a lysosomal acid lipase. The leading symptom in the early stage is a pronounced enlargement of the liver without subjective complaints or other changes in the physical status. Diagnosis can be established by liver biopsy, which will yield characteristic findings, and by exclusion of other storage disease. Histologic examination of the biopsy specimen will show lipid droplets in hepatic parenchymal cells, vacuolated Kupffer cells and focal accumulation of foamy cells. Biochemical analysis of the biopsy specimen will show an increased content of cholesteryl esters. Investigation of media of culture fibroblasts will show decreased activity of lysosomal alpha-naphtyl-acetat-esterase. In addition adrenal calcification has to be ruled out, in order to exclude wolman's disease. The prognosis of the disease will depend upon the degree of liver insufficiency, since lympho-histiocytic infiltration as a secondary phenomenon may lead to septal fibrosis and cirrhosis in children or adolescents in most cases. A case report is given of a 13-year old girl suffering from this disease.
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PMID:[Cholesteryl ester storage disease in the liver (author's transl)]. 645 7

Mastocytosis is a disease of mast cell hyperplasia that may involve several organ systems, including liver. Between 1988 and 1991, we conducted a retrospective-prospective study of 41 patients with mastocytosis and found 61% had evidence of liver disease. Hepatomegaly was detected in 24%, splenomegaly in 41%, and elevated serum alkaline phosphatase, serum aminotransaminases, 5'nucleotidase, or gamma-glutamyltranspeptidase (GGTP) in 54% of the patients. Alkaline phosphatase levels directly correlated with GGTP levels, hepatomegaly, splenomegaly, and liver mast cell infiltration and fibrosis. Elevated alkaline phosphatase levels and splenomegaly were observed more frequently in patients with categories II and III mastocytosis. Five patients in combined disease categories II or III developed ascites or portal hypertension and died of complications of mastocytosis; three had hypoprothrombinemia at the time of death. Thirty-five liver biopsy specimens from 25 patients were examined. Mast cell infiltration was commonly observed in the biopsy specimens, more severe in those patients with either category II or III disease, and correlated with hepatomegaly, splenomegaly, alkaline phosphatase levels, and GGTP levels. Mast cells were often only detected by using special stains (toluidine blue and chloracetate esterase). Increased portal fibrosis was seen in 68% of the biopsy specimens and correlated with mast cell infiltration and portal inflammation. Cirrhosis was not observed. Nodular regenerative hyperplasia, portal venopathy, and venoocclusive disease was observed in eight biopsy specimens and may have been the cause of the portal hypertension or ascites in four patients. These findings demonstrate that liver disease with mast cell infiltration is a common finding in patients with mastocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic involvement in mastocytosis: clinicopathologic correlations in 41 cases. 755 67

We studied extrinsic and intrinsic fibrinolysis in 20 patients with cirrhosis (nine mild/moderate, group 1; 11 severe, group 2) and 19 normal controls to define the role of intrinsic (contact factor medaited) fibrinolysis in cirrhosis. Global plasma fibrinolytic activity (fibrin plate lysis) was similar in all groups. Dextran sulphate activated contact factor mediated fibrinolysis was decreased in group 2 (median 95.2%) compared with group 1 (121.0%) and controls (131.7%). Tissue plasminogen activator antigen (t-PA Ag) levels were increased in group 2 (28.2 ng/ml) compared both with group 1 (8.5 ng/ml) and controls (5.9 ng/ml). Plasma t-PA activity was raised in group 2 (5.50 IU/ml) and group 1 (5.25 IU/ml) versus controls (0.82 IU/ml). Plasminogen activator inhibitor-1 (PAI-1 Ag) levels were raised in group 2 (28.0 IU/ml) versus controls (8.5 IU/ml) but PAI activity was similar in all groups. Factor XII activity was decreased in group 2 (48.76 u/dl), but not group 1, versus controls (89.1 u/dl). Prekallikrein activity was decreased both in group 2 (27.27 u/dl) and group 1 (33.01 u/dl) versus controls (108.59 u/dl) and was lower in group 2 than group 1. C1-esterase inhibitor chromogenic activity was decreased in group 1 (102.30 u/dl) and group 2 (58.76 u/dl) versus controls (116.24 u/dl). The normal global fibrinolytic activity despite increased t-PA activity may be due to a concomitant increase in PAI. The decreased intrinsic fibrinolysis in severe cirrhosis, unaccompanied by a rise in C1-esterase inhibitor, may be explained by the decreased factor XII and prekallikrein activity. These changes are probably due to reduced liver cell mass.
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PMID:Decreased contact factor mediated fibrinolysis in cirrhosis. 813 76

In this study, serum Zn(2+) content was determined by a new enzymatic method. The method depends on the reactivation of apocarbonic anhydrase proportional to the Zn(2+) content of the sample. Carbonic anhydrase was purified from bovine erythrocytes by affinity chromatography. The Zn(2+) in its structure was removed by dialysis against pyridine 2,6-dicarboxylic acid, resulting in a pure apoenzyme with a yield of 100%. The activity of the enzyme was determined by its esterase effect on 4-nitrophenyl acetate. Zn(2+) levels were determined in the serum samples obtained from 100 healthy subjects, 10 patients with cirrhosis, 12 diabetic patients and 15 patients with chronic renal failure by this enzymatic method and by atomic absorption for comparison. There was a good correlation between the two methods in all patients and controls and intraassay CV% was 2.4 and 4.2 for enzymatic and atomic absorption methods, respectively and interassay CV% as 3.9 and 6.1 respectively.
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PMID:An enzymatic method for zinc determination in serum. 834 75

An autopsy case of systemic mast cell disease (SMCD) without primary skin lesions in a 57-year-old Japanese male is described. Initially the patient was suspected of having liver cirrhosis or malignant lymphoma because of hepatomegaly and lymph node enlargement on admission. However, a lymph node biopsy and bone marrow aspiration conducted on his third admission indicated a SMCD because of the existence of metachromatic cell aggregates stained with toluidine blue. At autopsy, the diagnosis was confirmed because the proliferating cells were histochemically proven to be mast cells by naphthol AS.D chloroacetate esterase, Giemsa and alcian blue, in addition to toluidine blue staining. The intra-abdominal and retroperitoneal lymph nodes were replaced by mast cell aggregates, which caused the splenic infarction and bilateral hydronephrosis, with infiltration of mast cells into the spleen and kidneys also being apparent. Mast cell infiltration was similarly found in the bone marrow, liver, ileum and ascending colon. Immunohistochemically, the mast cells were positive for antibodies of alpha 1-antichymotrypsin, CD45 (LCA), CD43 (MT-1), CD45R (MB-1) and the oncoprotein c-kit. Electron microscopic examination using formalin-fixed tissue gave supportive evidence of a mast cell origin for the lesions.
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PMID:Systemic mast cell disease with splenic infarction: a case report. 970 48

The activity of the enzymatic activity of the preparations of IgG1, IgG2 and IgG4, isolated from the blood of patients with acute virus hepatitis B and chronic viral hepatitis C resulting in cirrhosis, was studied. The blood samples were found to have DNAase activity significantly exceeding that of immunoglobulins isolated from the blood sera of healthy donors, as well as peroxidase, oxidase and esterase activities, whose level did not significantly differ from those of the donor blood sera. The interaction of IgG preparations with the cations of different metals was studied. The study revealed that the addition of CuSO4 solution at the final concentration of 4.7 x 10(-5) M to the blood samples led to a significant increase in activity in comparison with the initial one (on the average, 7.8 +/- 2.97 times) in all 14 samples. The activity thus observed was partially inhibited by the addition of the solution of staphylococcal protein A. As noted in the course of this study, high DNAase and peroxidase activities of Ig were most frequently observed in patients with cirrhosis of the liver. The difference in the levels of IgG activity between patients with cirrhosis of the liver and patients with virus hepatitis, but no signs of cirrhosis, is not significant.
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PMID:[The enzymatic activity of IgG preparations in viral hepatitis]. 978 8

Eight outpatients with advanced hepatic cirrhosis were tested over 3 months for branched-chain amino acids (BCAA) supplements in the late evening. Serum albumin level (2.8+/-0.3 vs. 3.1+/-0.2 g/dl, P<0.002), serum cholin esterase activity (54+/-13 vs. 67+/-17 IU/l, P<0.02), and plasma Fischer's ratio (1.3+/-0.9 vs. 1.4+/-0.9, P<0.005) increased over the 3 months. The frequency of muscle cramps decreased (7.4+/-2.0 vs. 0.3+/-0.5 times/week, P<0.0001) dramatically. These data suggest that BCAA supplements in the late evening are of benefit to malnourished patients with hepatic cirrhosis. Relief of muscle cramping is an important outcome of BCAA supplements in the late evening.
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PMID:Branched-chain amino acids supplements in the late evening decrease the frequency of muscle cramps with advanced hepatic cirrhosis. 1296 33


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