Serum selenium levels in liver diseases

Aaseth, Jan; Alexander, Jan; Thomassen, Yngvar; Blomhoff, J. P.; Skrede, Sverre

doi:10.1016/s0009-9120(82)96790-x

Cited by 55 publications

(14 citation statements)

References 13 publications

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“…Several groups have reported that patients with cirrhosis have plasma selenium concentrations lower than those of healthy controls. [2][3][4][5][6] The pathogenesis of those depressed selenium levels is unknown; therefore it is not known whether a remediable state of selenium deficiency exists in cirrhotics.Virtually all the selenium in plasma is present in the form of seleno-amino acids in the primary structure of proteins. One of these amino acids is selenocysteine, the physiologically active form of the element, which is synthesized in animal cells and is present in stoichiometric amounts in selenoproteins.…”

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confidence: 99%

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Plasma selenium in patients with cirrhosis

et al. 1998

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Plasma selenium concentration is decreased in patients with cirrhosis and, based on this finding, it has been suggested that patients with cirrhosis are selenium deficient. We measured plasma selenium concentration and the two plasma selenoproteins, glutathione peroxidase (GSHPx-3) and selenoprotein P, in the plasma of patients with cirrhosis of Child classes A, B, and C and in control subjects. Plasma selenium declined in proportion to the severity of the cirrhotic condition, as indicated by the Child class. Selenoprotein P, which originates largely in the liver, declined in a similar manner. Plasma glutathione peroxidase activity increased, and GSHPx-3 originates in the kidney. Selenium in the non-selenoprotein pool, shown by others to be largely selenomethionine in albumin, declined. Thus, although plasma selenium is decreased in patients with cirrhosis, the increase in plasma glutathione peroxidase activity, which occurs in them, suggests that patients with cirrhosis do not have selenium deficiency. (HEPATOL-OGY 1998;27:794-798.) Selenium exerts biological effects as an essential constituent of selenoproteins. 1 Pathological conditions, such as selenium deficiency and organ damage, which are severe enough to alter selenium metabolism, can be expected to affect the concentrations of selenoproteins and to have biochemical and pathological consequences. Several groups have reported that patients with cirrhosis have plasma selenium concentrations lower than those of healthy controls. [2][3][4][5][6] The pathogenesis of those depressed selenium levels is unknown; therefore it is not known whether a remediable state of selenium deficiency exists in cirrhotics.Virtually all the selenium in plasma is present in the form of seleno-amino acids in the primary structure of proteins. One of these amino acids is selenocysteine, the physiologically active form of the element, which is synthesized in animal cells and is present in stoichiometric amounts in selenoproteins. Glutathione peroxidase (isoform GSHPx-3) and selenoprotein P are the only selenoproteins that have been identified in plasma. 7,8 The other amino acid form of selenium in plasma is selenomethionine, 9 an amino acid that is synthesized by plants and is incorporated randomly into animal proteins as a constituent of the methionine pool.Proteins that contain selenomethionine do not contain the element in stoichiometric amounts and are often referred to as selenium-containing proteins to distinguish them from true selenoproteins. Small molecule forms of uncharacterized selenium are involved in homeostasis of the element. Those forms account for approximately 3% of plasma selenium under steady state conditions. 10

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Plasma selenium in patients with cirrhosis

et al. 1998

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“…Evidence of zinc deficiency in alcohol consumers has been published repeatedly (Aaseth et al, 1986;Bjorneboe et al, 1988;Dworkin et al, 1985). Low serum zinc concentration and reduced zinc contents in leukocytes (Lecomte et al, 1994;McClain & Su, 1983;Morgan, 1988) and reduced hepatic zinc content in patients with different stages of alcoholic liver disease (Bode et al, 1988) have mainly been explained by increased urinary zinc losses and not by malabsorption or reduced dietary intake of this trace element.…”

Section: Discussionmentioning

confidence: 99%

“…Nutritional disturbances are assumed to remain among the most relevant medical problems in alcohol consumers (Aaseth et al, 1986;Addolorato, 1998;Suter et al, 1997) but it is still a matter of debate whether chronic alcohol consumption per se results in malnutrition (Italian Multicentre, 1994;Leo et al, 1993; & Lieber,1999;Morgan, 1988;Nicolas et al, 1993;Rissanen et al, 1987, Wheeler, 1990. Both the nutrient intake and the nutritional status of alcohol consumers are markedly influenced by many factors such as severity and duration of alcohol abuse, the presence, type and severity of somatic complications caused by excessive drinking and by economic and social circumstances.…”

Section: Discussionmentioning

confidence: 99%

Nutritional deficiencies in German middle-class male alcohol consumers: relation to dietary intake and severity of liver disease

et al. 2003

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Objective: The purpose of the present study was to compare the nutrient intake and the nutritional status between German middle-class alcohol consumers and non-drinkers. Design: Cross-sectional study using patients with different stages of alcoholic liver disease (ALD) and healthy volunteers. Setting: Southern Germany. Subjects: Seventy-six hospitalized German middle-class alcohol consumers with different stages of alcoholic liver disease (ALD) and 22 healthy control subjects. Methods: Subjects and controls were nutritionally assessed and mineral and vitamin content was measured in blood and urine. Results: When compared with controls, alcohol consumers had significantly higher intakes of total calories, but intake of nonalcoholic calories did not differ between groups (P < 0.05). Among drinkers, there was a decrease in percentage of energy derived from protein and fat and a significant increase in carbohydrates (P < 0.05). With the exception of vitamin E, micronutrient intake of alcoholics was equal to that of controls; however, blood vitamin (vitamin C, retinol, lycopene, a-and g-carotene) and trace element (selenium, zinc) concentrations of alcohol-drinking patients were lower than those of nondrinkers.

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“…In Germany and in most industrialized countries chronic alcohol abuse is not only one of the most important causes of nutritional disorders but also of changes in dietary habits (Aaseth et al 1986;Addolorato, 1998;Suter et al 1997). For instance, studies have reported that increased alcohol consumption is positively associated with an increased consumption of coffee, cheese, eggs, fish, meat whereas negative association was found with the intake of fruits and milk consumption (Kesse et al 2001).…”

Section: Chronic Alcoholics Dietary Pattern and Nutritional Intakementioning

confidence: 99%