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)

Glutathione peroxidase activity and selenium and vitamin E levels were measured in the plasma and erythrocytes of 25 chronic alcoholic patients without liver cirrhosis before and after 14 days of abstinence from alcohol, and compared with the levels in 25 sex- and age-matched healthy controls. Before abstinence, all three levels were shown significantly depressed in the alcoholic patients compared with the controls, in both plasma (80, 71, and 89% of control values) and erythrocytes (68, 70, and 83% of control values). After a 14-day abstinence period with no dietary supplementation, a trend towards normalization was noted in erythrocyte (vitamin E and glutathione peroxidase 74 and 91% of control values respectively), in whole blood selenium (82%) and plasma in vitamin E (74%). However, plasma selenium and glutathione peroxidase values were lower than pre-abstinence values (76% and 86% of control values respectively). Our results point to a deficiency in the antioxidant defense system of chronic alcoholics before the occurrence of severe liver disease. This lack of protection against lipoperoxides is all the more important in circumstances like chronic alcohol consumption, in which lipid peroxidation is known to increase. However, the present study also demonstrated that during 14 days of a normal diet free of ethanol, a rapid trend occurred towards the normalization of the factors.
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PMID:Effect of abstinence from alcohol on the depression of glutathione peroxidase activity and selenium and vitamin E levels in chronic alcoholic patients. 208 28

The patients were subdivided into 3 groups, in accordance with clinical, echographic, laboratory and laparoscopy criteria: without liver disease, with liver disease and with alcoholic cirrhosis. In alcoholics with liver disease (with or without cirrhosis), we found a constant significant decrease in lead during abstinence, while in patients with cirrhosis zinc has a significant increase. Always lower to normal the blood selenium. The cadmium in the serum increases also after a month.
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PMID:[Changes in blood Zn, Se, Cd, Pb during therapeutic abstinence from alcohol in 101 cases of alcoholism]. 259 87

In 55 patients with alcoholic cirrhosis and in 47 healthy individuals we assayed the concentration of selenium in serum (S-Se) by proton induced X-ray emission, the aminoterminal peptide of type III procollagen (NPIIIP) by RIA and the plasma fibronectin (FN) by immuno-nephelometry, together with routine biochemical tests. S-Se was lower in cirrhosis than in controls (0.57, SD 0.20 vs 0.92, SD 0.16 mumol/l; p less than 0.001) and was more reduced in ascitic than in compensated patients (0.50, SD 0.19 vs 0.66, SD 0.17 mumol/l; p less than 0.001). Regression analysis showed a positive correlation of S-Se with serum albumin and FN, whereas necrotic or inflammatory activity seems unrelated to S-Se; a negative correlation was found between S-Se and NPIIIP, suggesting a protective role of selenium against fibrosis.
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PMID:Serum selenium in liver cirrhosis: correlation with markers of fibrosis. 277 52

Selenium deficiency has been implicated as contributing to hepatic injury in alcoholics. The mechanism by which this occurs is most likely lipoperoxidation secondary to decreased activity of the selenoenzyme glutathione peroxidase. To further assess this relationship, we measured selenium content in autopsy livers in 12 patients with alcoholic cirrhosis compared to 13 patients matched for age and sex dying from other causes, mostly with cardiopulmonary diseases. The mean (+/- SEM) hepatic selenium content in cirrhosis was 0.731 +/- 0.077 microgram/g dry weight versus 1.309 +/- 0.166 microgram/g in controls (P less than 0.005; Student's t test). Clinical and biochemical indices of significant hepatic dysfunction, including encephalopathy, ascites, and elevations of serum bilirubin or prothrombin time, were only present in the cirrhotic group. A significant inverse correlation between hepatic selenium content and the prothrombin time was noted (r = -0.50; P less than 0.02). No significant relationships between hepatic selenium and the abnormalities of bilirubin, albumin, or aspartate aminotransferase were found. We conclude that significantly decreased hepatic selenium stores are present in patients with severe alcoholic cirrhosis compared to controls. The magnitude of that selenium deficit does correlate with some indices of hepatic function, specifically the prothrombin time. These data lend further support to a true selenium deficiency state in alcoholic cirrhosis. It is highly possible that selenium deficiency represents an important link, synergistically joining the nutritional and hepatotoxic backgrounds of alcoholic liver injury and cirrhosis.
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PMID:Decreased hepatic selenium content in alcoholic cirrhosis. 316 92

In our study alcoholic patients with and without cirrhosis have a decreased serum zinc. They also have increased serum copper and iron with an increase in the serum ferritin. There is no evidence of selenium deficiency in either alcoholic group. Alcohol when given with zinc in a single dose to normal volunteers increases the serum zinc and therefore appears to increase the absorption of zinc.
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PMID:Trace elements and alcohol. 401 73

Serum selenium was evaluated in relation to hepatic structure and function in 46 alcoholics with diagnostic liver biopsy classified into 4 groups by hepatic histology. Their serum selenium concentration varied from 12 to 88 micrograms/l and was lower (p less than 0.001) in all groups of alcoholics, ie patients with normal liver (53.0 +/- 20.7 micrograms/l, mean +/- SD), fatty liver (55.8 +/- 21.2 micrograms/l), alcoholic hepatitis (46.0 +/- 14.1 micrograms/l), and cirrhosis (41.1 +/- 12.8 micrograms/l), than in 25 healthy controls (88.7 +/- 11.0 micrograms/l). Serum selenium level was related to the severity of liver disease, and most reduced in subjects with decompensated alcoholic cirrhosis. Their serum selenium level (29.2 +/- 13.7 micrograms/l) was below (p less than 0.05) that obtained in alcoholics with normal liver and fatty liver respectively. Both inadequate dietary selenium intake and alcohol-induced changes in hepatic structure and function may have contributed to the decrease of serum selenium in the subjects studied.
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PMID:Decreased serum selenium in alcoholics as related to liver structure and function. 401 64

Red blood cell and serum selenium concentrations were investigated to determine normal concentrations for our geographic area and if potential differences existed in patients with selected diagnoses (hepatic, renal, malignant, and chronic diseases). Selenium was quantified in samples of red blood cells, serum and urine by neutron activation analysis. The results were analyzed by comparing 1) pooled data from all ages for each disease with normal values, and 2) normal values with age-matched patients in each disease category. Decreases in red blood cell selenium concentrations (P less than 0.05) occurred in normal subjects over 60 years of age without concurrent significant decreases in serum selenium. Although differential results were noted in age-matched groups, overall results showed that decreased concentrations of selenium in both red cells and in serum occurred with alcoholic cirrhosis, malignancies, and chronic renal failure (P less than 0.025). Red blood cell selenium concentrations also were decreased in patients with stable chronic disease. Decreased serum selenium concentrations were positively correlated with albumin concentrations in patients with cirrhosis. There was no correlation between serum selenium and bilirubin concentrations in patients with liver disease or between serum selenium and creatinine concentrations in patients with chronic renal failure whose urinary excretion of selenium was far below control levels.
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PMID:Red blood cell and serum selenium concentrations as influenced by age and selected diseases. 665 58

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

The liver plays an important role in the metabolism of trace minerals. Hypozincemia has been well documented in cirrhotic patients and multiple mechanisms, including poor intake and depressed absorption, appear to be responsible for it. Of particular interest is a role of zinc deficiency in hepatic encephalopathy and the therapeutic potential of zinc supplementation in patients with liver cirrhosis. Although some reports indicate beneficial effects of oral zinc supplementation in cirrhotic patients with hepatic encephalopathy, not all studies have been positive. Serum selenium concentration depends on the amount of selenium ingested and the decreased levels found in cirrhotic patients should be interpreted with caution.
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PMID:[Zinc and selenium metabolism in liver cirrhosis]. 811 87

The effects of vitamin B12 status on growth and tissue selenium distribution were studied in Sprague-Dawley rats chronically exposed to subtoxic levels of selenite. Vitamin B12 status was monitored by urinary methylmalonic acid excretion and by liver and plasma vitamin B12 levels. Selenite absorption was unaffected by dietary level of vitamin B12. A significant (P < 0.05) interaction of vitamin B12 and selenium was found on growth of rats fed vitamin B12 deficient or control diets. In vitamin B12 depleted rats, there were significant histologic changes in the liver that were characterized by micronodules and regeneration, bile duct reduplication, mild cirrhosis, necrosis of individual hepatocytes and other minor histologic changes. There was no gross or histologic evidence of liver toxicity in rats supplemented with vitamin B12. Rats pair-fed 9 mg/kg selenium with vitamin B12 had significantly lower liver and kidney selenium levels and significantly higher blood selenium levels compared to rats fed the diet without vitamin B12. These results are consistent with the hypothesis that vitamin B12 deficiency limits selenium methylation and excretion, resulting in higher tissue selenium levels and subsequent toxicity.
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PMID:Effect of vitamin B12 on performance and tissue selenium content in rats fed sub-toxic levels of selenite. 830 6


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