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 sensory modalities of taste and smell were evaluated in eight patients with cirrhosis that was proved by biopsy specimens and in 13 control subjects. Additionally, the following serum levels were determined in these same subjects: zinc, copper, magnesium, calcium, manganese, and selenium. Fourteen concentrations each of sucrose, sodium chloride, urea, and hydrochloric acid were used to evaluate taste acuity. Smell was evaluated with 11 concentrations each of nitrobenzene, thiophene, and pyridine. These studies show that decreased acuity of taste and smell occurred in conjunction with cirrhosis in the patients who were tested. There were no trace element abnormalities that consistently correlated with decreased acuity in perception of the individual test substances.
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PMID:Decreased taste and smell acuity in cirrhosis. 64 37

A 68-year-old man, after having been diagnosed as having hepatic disease at about the age of 41 years, had been hospitalized frequently until his death. Blood sugar, iron, and copper had not increased during his illness. Although the diagnosis of liver cirrhosis had been made and he had been receiving therapy, various neurologic symptoms without disturbances of consciousness appeared six months before his death. Autopsy revealed hemochromatosis, liver cirrhosis, and pancreatic fibrosis. A large amount of iron had accumulated in the liver, the pancreas, and the thyroid gland, while considerable numbers of ceroid and lipofuscin pigment granules had accumulated diffusely in the brain. Abnormal astrocytes of the Alzheimer II type were diffusely distributed in the brain and contained no intranuclear glycogen which stained positive with the carmine stain. No spongy changes were seen in the deeper layers of the cerebral cortex. Chemical analyses for trace metals in the brain, liver, and kidneys revealed a large amount of iron and increased copper in the liver, and considerable quantities of copper, manganese, calcium, and mercury in the brain. Because of changes in the erythrocyte sedimentation rate and marked thymol turbidity seen before and after the occurrence of the neurologic symptoms, this man was suspected of having disorders of the trace-metal binding proteins and/or of their polymers.
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PMID:Hemochromatosis associated with brain lesions--a disorder of trace-metal binding proteins and/or polymers? 92 21

Repeated administration of carbon tetrachloride (CCl4) induces liver cirrhosis, possibly because it involves the production of free radicals. In order to evaluate the effect of free radical scavengers such as superoxide dismutase (SOD) and allopurinol in the pathogenesis of liver cirrhosis, rats were subjected to repeated CCl4 administration with and without scavengers. Four groups of animals were studied: CCl4 plus SOD (group 1), CCl4 plus allopurinol (group 2), CCl4 alone (group 3) and olive oil (group 4, normal controls). Analysis of plasma and tissue concentrations of trace elements was performed and histopathological patterns were studied in all groups after 7 weeks of repeated intraperitoneal administration of the solutions. Plasma levels of zinc and selenium were significantly lower in all experimental groups, with reciprocal elevation of manganese and copper. Copper and manganese content in the liver tissue was significantly higher in all three experimental groups. The zinc content was elevated in groups receiving CCl4 alone (group 3) or with allopurinol (group 2). The liver selenium, however, was significantly lower in these two groups. The copper:zinc ratio for plasma was 0.78 in the control group, 1.6 in the CCl4 group, 1.3 in the allopurinol group and 1.5 in the SOD group. For liver tissue, the ratio was 0.07 for controls, 0.17 for CCl4, 0.11 for allopurinol and 0.28 for the SOD group. The changes in trace element content correlated with the severity of cellular damage observed microscopically in the liver. The higher the copper:zinc ratio, the more advanced and extensive was the microscopic evidence of liver injury after CCl4 challenge.
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PMID:Liver cirrhosis induced by carbon tetrachloride and the effect of superoxide dismutase and xanthine oxidase inhibitor treatment. 157 2

We describe prolinase (EC 3.4.13.8) activity in human plasma for the first time. Optimum activity was obtained with prolylvaline as substrate and 0.02 mmol/L manganese concentration at pH 9.0. Moreover, preincubation with manganese was not required, contrary to prolidase (EC 3.4.13.9) activity. The mean value observed in 106 subjects without liver and renal disorders was 16 U/L +/- 14 (2 SD). We determined this plasma enzyme activity in patients with acute hepatitis and chronic liver disease. Plasma prolinase activity was strongly dependent upon cytolysis because of the high activity in liver and the low activity in plasma. Of 24 patients with chronic liver disease (4 chronic hepatitis and 20 cirrhosis) and without cytolysis, prolinase activity was slightly increased in only three patients, whereas prolidase activity was increased in 13. This could be due to a difference in the activation of these two enzymes in liver during the fibrotic process.
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PMID:Determination of prolinase activity in plasma. Application to liver disease and its relation with prolidase activity. 404 19

The presence of large amounts of copper in the liver in primary biliary cirrhosis has been confirmed; a similar increase is not found in cases of long-standing extrahepatic biliary obstruction. The serum caeruloplasmin levels are raised in primary and secondary biliary cirrhosis, but this increase does not appear to be related to the degree of increase of hepatic copper. The manganese content of the liver is slightly raised in both these conditions.The reason for the increased metal content in these circumstances cannot yet be determined, and the effects are not yet understood.
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PMID:Copper and manganese concentrations in biliary cirrhosis of liver. 566 88

We isolated galactosyltransferase (EC 2.4.1.22) from pleural effusions of a lung cancer patient and a patient with cirrhosis by precipitation with ammonium sulfate, followed by gel filtration on Sepharose 6B, and affinity chromatography on columns of alpha-lactalbumin-agarose and protein A-Sepharose. By this procedure the enzyme from both sources was purified 40 000-fold with approximate yields of 37% and 60%, respectively, and did not contain immunoglobulin. Electrophoresis on polyacrylamide gel of the enzyme from the cancer patient (slower moving) and from the non-cancer patient (faster moving) gave one sharp band for each. Their respective relative molecular masses, 74 131 and 107 151, were estimated by sodium dodecyl sulfate/polyacrylamide gel electrophoresis and gel filtration, respectively. The isoenzymes were active between pH 5 and 8, most active at 7, and showed no activity below pH 4 or above pH 9. Activity was greatest at temperatures between 37 and 40 degrees C. At 30 degrees C or 50 degrees C the activity was more than halved, and was lost completely above 60 degrees C. The isoenzymes had an absolute requirement for Mn2+. Omitting the surfactant Triton X-100 from the buffer resulted in considerable loss in activity of both isoenzymes. Glucose can be used as an acceptor for these isoenzymes if alpha-lactalbumin is present in the assay mixture. These isoenzymes had different Km values for UDP-galactose, N-acetylglucosamine, and Mn2+.
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PMID:Isolation and characterization of cancer-associated galactosyltransferase isoenzyme. 643 1

We describe here an easy method of determining prolidase (EC 3.4.13.9) in plasma after preincubation with Mn2+ for 24 h at 37 degrees C to maximize prolidase activity. The mean activity in 338 patients who were either in hospital or outpatients was 900 U/L +/- 520 (2 SD), unrelated to sex or age. In 25 of these 338 samples tested, prolidase activity was between 1500 and 2000 U/L. It exceeded 2000 U/L in eight, all of whom were patients with chronic liver disease. Plasma prolidase activity was normal in cytolytic syndromes such as liver or heart disease. Of the 27 patients with cirrhosis, only five exhibited prolidase activity greater than 2000 U/L. Plasma prolidase activity was uncorrelated with six biochemical indexes to liver function (the aminotransferases, alkaline phosphatase, glutamyltransferase, total bilirubin, and serum albumin) or with the degree of cirrhotic fibrosis. We believe that plasma prolidase activity may be high only in the early stage of fibrosis. This hypothesis would be consistent with the data on rat-liver collagenolytic activities during CCl4 administration. Monitoring of plasma prolidase activity might be useful in evaluating fibrotic processes in chronic liver disease in the human.
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PMID:Plasma prolidase activity: a possible index of collagen catabolism in chronic liver disease. 669 25

Repeated administration of carbon tetrachloride (CC1(4)) to the experimental animals not only produces liver cirrhosis but also pathological changes in different organs. The alteration of trace elements in the plasma and in the liver has been documented. Very limited studies were carried out regarding the alteration of trace elements in different organs in experimental animals subjected to CC1(4) toxicity and the influence of scavengers such as superoxide dismutase (SOD) and allopurinol as preventative measurements. Four groups of animals were studied: CC1(4) and allopurinol (group 1), CC1(4) and SOD (group 2), CC1(4) alone (group 3) and olive oil (group 4). Analysis of tissue concentrations of trace elements in different organ's tissues (e.g. lung, spleen and kidneys) were performed. Histopathological assessments were studied in all groups after 7 weeks of repeated administration of the solutions. Copper contents in the spleen and lungs were significantly high in group 2, while kidney copper contents were significantly high in all experimental groups. Selenium contents in the kidneys and lungs were significantly low in group 1, while it was significantly high in group 2 in all organs. Manganese contents in kidneys was significantly low in group 1 and significantly increased in group 2 in the case of spleen and lung. Lung zinc content was significantly increased in group 2. Spleen zinc decreased significantly only in group 3. Histopathological assessment indicated evidence of interstitial pneumonia in the group treated with allopurinol. The low levels of selenium predisposes to the development of interstitial pneumonia.
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PMID:Alterations of trace elements in kidney, spleen and lungs in treated and untreated experimental liver cirrhosis. 761 71

Clinical observations and animal studies have raised the hypothesis that increased concentrations of manganese (Mn) in whole blood might lead to accumulation of this metal within the basal ganglia in patients with end-stage liver disease. We studied ten patients with liver failure (and ten controls) by magnetic resonance imaging (MRI) and measurement of Mn in brain tissue of three patients who died of progressive liver failure (and three controls) was also done. Whole blood Mn concentrations in patients with liver cirrhosis were significantly increased (median 34.4 micrograms/L vs 10.3 micrograms/L in controls; p = 0.0004) and pallidal signal intensity indices correlated with blood Mn (Rs = 0.8, p = 0.0058). Brain tissue samples reveal highest Mn concentrations in the caudate nucleus, followed by the quadrigeminal plate and globus pallidus. Mn accumulates within the basal ganglia in liver cirrhosis. Similarities between Mn neurotoxicity and chronic hepatic encephalopathy suggest that this metal may have a role in the pathogenesis of chronic hepatic encephalopathy. Further studies are warranted because the use of chelating agents could prove to be a new therapeutic option to prevent or reverse this neuropsychiatric syndrome.
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PMID:Manganese and chronic hepatic encephalopathy. 763 Feb 46

9 cases (males) of primary sclerosing cholangitis (PSC) were studied clinico-morphologically. In puncture liver biopsies, sclerosis of walls of big ducts and portal tracts was found in 2 cases only; cell infiltration was minimal. Lobular hepatitis with intralobular fibrosis and moderate sclerosis of portal stroma was found in 3 patients, monolobular inactive liver cirrhosis in 4 patients. In all cases mild intralobular cholestasis was found which was followed with a considerable increase of copper and manganese in the liver and serum. The accumulation of a large amount of collagen of different types was observed around bile ducts which ultrastructurally was seen as fibrillar structures and homogeneous substance similar to the basal membrane. The elements of the epithelium destruction were found in foci of the duct basal membrane alteration, in the absence of cell infiltration. Progressing fibrosis of both portal tracts without inflammation and individual segments of the bile ducts and the intralobular stroma is at the basis of PSC.
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PMID:[Morphological changes in the liver in primary sclerosing cholangitis (a histological and electron microscopic study)]. 794 63


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