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 aim of the study was to investigate the serum selenium concentration in patients with liver cirrhosis and hepatocellular carcinoma. A total of 59 patients, 49 with liver cirrhosis and 10 with liver cirrhosis and coexistent hepatocellular carcinoma, as well as 202 healthy volunteers entered the study. In the patients with liver cirrhosis and in those with liver cirrhosis and coexistent hepatocellular carcinoma, serum selenium concentrations were significantly lower (39.28 +/- 13.99 and 42.00 +/- 10.59 g/L, respectively), when compared to the group of healthy volunteers (66. 79 +/- 9.13 g/L) (p < 0.001). There was no significant difference in serum selenium concentrations between the two patient groups. In the group of patients with liver cirrhosis positive correlation was found between serum selenium and albumin concentrations, and negative correlation between serum selenium and bilirubin (p < 0.05 and p < 0.01, respectively). There was no correlation of serum selenium concentration with fibrinogen and prothrombin time. Results of the study suggested the possible important nutritive and protective role of selenium in the patients with liver cirrhosis and coexistent hepatocellular carcinoma, as well as the potential need of selenium supplementation in these patients.
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PMID:Serum selenium concentration in patients with liver cirrhosis and hepatocellular carcinoma. 877 9

The effect of thioacetamide-induced liver cirrhosis on plasma and tissue manganese levels and the protective role of selenium, zinc and allopurinol supplements was investigated in rats. Control plasma and liver manganese (Mn) levels were found to be (mean +/- SD): 8.4 +/- 2.4 mg/L and 5.7 +/- 1.5 mg/g wet weight respectively. Plasma manganese levels were significantly increased (p < 0.001) whereas liver manganese levels were significantly reduced (p < 0.05) in the cirrhotic rats. Treatment with selenium, zinc and allopurinol reversed this trend and restored the manganese levels close to the normal values. Lung, spleen, and kidney manganese levels under control conditions were considerably lower than that of the liver tissue. However, these levels registered a significant increase (p < 0.05) in cirrhotic rats and this change was normalized after selenium, zinc and allopurinol treatment. There were no significant differences in the comparative efficacy of each of these protective agents. Zinc supplement considerably increased the plasma zinc levels and plasma Zn/Mn ratio had a good correlation with plasma zinc concentration. This ratio was significantly reduced in cirrhotic rats, but returned to the control level after zinc, selenium and allopurinol treatment. The results of this study indicate that the trace element, manganese, plays an important role in stabilizing cell structure and that this effect is mediated possibly by preserving the antioxidant activity of the tissues.
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PMID:Effect of dietary selenium, zinc and allopurinol supplements on plasma and tissue manganese levels in rats with thioacetamide [correction of thiocetamide]-induced liver cirrhosis. 927 62

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.
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PMID:Plasma selenium in patients with cirrhosis. 950 Jul 9

Neonatal haemochromatosis is a disorder which affects foetuses and newborns. It is characterized by hepatocellular insufficiency, often appearing on the first day of life in the form of coagulopathy, hypoalbuminemia, hypoglycemia and jaundice. While spontaneous recovery has been reported, most of these infants die, and the diagnosis was previously often made during autopsy. With the help of MRI and salivary gland biopsies, plus increasing awareness of this disorder, the diagnosis is now often made quite early, and successful liver transplantations have been reported. Recently, there have also been encouraging preliminary reports of successful intervention with antioxidant and chelation pharmacotherapy, using a combination of selenium, vitamin E, N-acetylcysteine, deferoxamine, and prostaglandin E. We describe two patients with neonatal haemochromatosis who were both treated with this new "cocktail", one of whom died at five days of age, while the other survived, but needed a liver transplant at 2 1/2 months of age. The pathology of this condition is characterized by hepatic cirrhosis with giant cell transformation, and by siderosis of extrahepatic tissues. The prognosis is poor, and our experience with antioxidant treatment has been disappointing. Liver transplantation is a therapeutic option, but its use is limited by the scarcity of donor organs and the small size of many of the patients.
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PMID:[Neonatal hemochromatosis]. 954 1

Erythrocyte-membrane fatty acid composition and cholesterol content were evaluated along with serum selenium in 33 patients with liver cirrhosis and in 40 normal subjects. Thirteen patients were suffering from post-viral (group V) and 20 from alcoholic (group A) cirrhosis. The aim of the study was to elucidate whether membrane lipid abnormalities in cirrhosis were linked to the aetiology of the disease or whether they were the results of the cirrhotic process itself. The patients presented a significant increase in membrane cholesterol, palmitic acid (C16:0) and saturated fatty acids (SFA), and a decrease in polyunsaturated fatty acids (PUFA) and polyunsaturated/saturated fatty acids ratio (P/S) compared with the control group. Serum selenium levels were significantly reduced. When patients were subdivided according to aetiology, the alcoholic patients showed greater lipid composition abnormalities than the viral cirrhotics (higher levels of SFA and lower PUFA and P/S), while pathologic palmitic acid, membrane cholesterol and serum selenium values were confirmed in both groups of patients. In conclusion, low serum selenium and a series of erythrocytes membrane lipid composition abnormalities would appear to be features peculiar to cirrhosis. Alcoholic cirrhotics, on the other hand, show a more deranged erythrocyte membrane lipid profile.
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PMID:Erythrocyte membrane lipids and serum selenium in post-viral and alcoholic cirrhosis. 954 51

Effects of selenium deficiency, induced by thioacetamide, were investigated in rats. Thioacetamide (0.3 g/L) given in drinking water, as expected, caused a significant loss of selenium from the liver. It was accompanied by liver cirrhosis and a significant increase in the liver weight as well as liver to body weight ratio. A significant loss of selenium from spleen was also accompanied by an increase in its weight. Weights of lungs, testis and kidney, however, were not affected by thioacetamide and there was no change in their selenium content. Plasma levels of selenium were significantly reduced in the thioacetamide treated group. All these changes were confirmed to be due to selenium deficiency caused by thioacetamide, as supplementation with selenium reversed these changes. The mode of action of selenium is unknown but may involve anti-oxidant defense mechanisms.
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PMID:Selenium and liver cirrhosis. 974 5

A great number of epidemiological data have identified chronic alcohol consumption as a significant risk factor for upper alimentary tract cancer, including cancer of the oropharynx, larynx, and the esophagus, and for the liver. In contrast to those organs, the risk by which alcohol consumption increases cancer in the large intestine and in the breast is much smaller. However, although the risk is lower, carcinogenesis can be enhanced with relatively low daily doses of ethanol. Considering the high prevalence of these tumors, even a small increase in cancer risk is of great importance, especially in those individuals who exhibit a higher risk for other reasons. The epidemiological data on alcohol and other organ cancers are controversial and there is at present not enough evidence for a significant association. Although the exact mechanisms by which chronic alcohol ingestion stimulates carcinogenesis are not known, experimental studies in animals support the concept that ethanol is not a carcinogen, but under certain experimental conditions is a cocarcinogen and/or (especially in the liver) a tumor promoter. The metabolism of ethanol leads to the generation of acetaldehyde and free radicals. These highly reactive compounds bind rapidly to cell constituents and possibly to DNA. Acetaldehyde decreases DNA repair mechanisms and the methylation of cytosine in DNA. It also traps glutathione, an important peptide in detoxification. Furthermore, it leads to chromosomal aberrations and seems to be associated with tissue damage and secondary compensatory hyperregeneration. More recently, the finding of considerable production of acetaldehyde by gastrointestinal bacteria was reported. Other mechanisms by which alcohol stimulates carcinogenesis include the induction of cytochrome P4502E1, associated with an enhanced activation of various procarcinogens present in alcoholic beverages, in association with tobacco smoke and in diets, a change in the metabolism and distribution of carcinogens, alterations in cell cycle behavior such as cell cycle duration leading to hyperregeneration, nutritional deficiencies such as methyl, vitamin A, folate, pyrridoxalphosphate, zinc and selenium deficiency, and alterations of the immune system, eventually resulting in an increased susceptibility to certain viral infections such as hepatitis B virus and hepatitis C virus. In addition, local mechanisms in the upper gastrointestinal tract and in the rectum may be of particular importance. Such mechanisms lead to tissue injury such as cirrhosis of the liver, a major prerequisite for hepatocellular carcinoma. Thus, all these mechanisms, functioning in concert, actively modulate carcinogenesis, leading to its stimulation.
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PMID:Alcohol and cancer. 975 43

Much progress has been made in the understanding of the pathogenesis of alcoholic liver disease, resulting in improvement of prevention and therapy, with promising prospects for even more effective treatments. The most successful approaches that one can expect to evolve are those that deal with the fundamental cellular disturbances resulting from excessive alcohol consumption. Two pathologic concepts are emerging as particularly useful therapeutically. Whereas it continues to be important to replenish nutritional deficiencies, when present, it is crucial to recognize that because of the alcohol-induced disease process, some of the nutritional requirements change. This is exemplified by methionine, which normally is one of the essential amino acids for humans, but needs to be activated to S-adenosylmethionine (SAMe), a process impaired by the disease. Thus, SAMe rather than methionine is the compound that must be supplemented in the presence of significant liver disease. Indeed, SAMe was found to attenuate mitochondrial lesions in baboons, replenish glutathione, and significantly reduce mortality in patients with Child A or B cirrhosis. Similarly, polyenylphosphatidylcholine (PPC) corrects the ethanol-induced hepatic phospholipid depletion as well as the decreased phosphatidylethanolamine methyltransferase activity and opposes oxidative stress. It also deactivates hepatic stellate cells, whereas its dilinoleoyl species (DLPC) increases collagenase activity, resulting in prevention of ethanol-induced septal fibrosis and cirrhosis in the baboon. Clinical trials with PPC are ongoing in patients with alcoholic liver disease. Furthermore, enzymes useful for detoxification, such as CYP2E1, when excessively induced, become harmful and should be downregulated. PPC is one of the substances with anti-CYP2E1 properties that is now emerging. Another important aspect is the association of alcoholic liver disease with hepatitis C: a quarter of all patients with alcoholic liver disease also have markers of HCV infection, with an even higher incidence in some urban areas but, at present, no specific therapy is available since interferon is contraindicated in that population. However, in addition to antiviral medications, agents that oppose oxidative stress and fibrosis should also be tested for hepatitis C treatment since these two processes contribute much to the pathology and mortality associated with the virus. In addition to antioxidants (such as PPC, silymarin, alpha-tocopherol and selenium), anti-inflammatory medications (corticosteroids, colchicine, anticytokines) are also being tested as antifibrotics. Transplantation is now accepted treatment in alcoholics who have brought their alcoholism under control and who benefit from adequate social support but organ availability is still the major limiting factor and should be expanded more aggressively. Finally, abstinence from excessive drinking is always indicated; it is difficult to achieve but agents that oppose alcohol craving are becoming available and they should be used more extensively.
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PMID:Alcoholic liver disease: new insights in pathogenesis lead to new treatments. 1072 99

In the present review different aspects related to the essential element selenium in the human organism are considered. A large number of human studies have been performed in order to improve knowledge on the influence of this element in the origin and development of several degenerative diseases. Selenium deficiencies among human beings as well as animals are being recognized worldwide to be related to a number of pathologies. This element has also the special characteristic that the range between its essential and toxic character is very close, and consequently daily dietary intake should be appropriately monitored in individuals. Nevertheless, nowadays there is still a lot of controversy about the optimum dietary level of this element in order to cure or to prevent the appearance of diseases such as cirrhosis, cancer, diabetes, or cardiovascular pathologies. Results obtained in several animal and epidemiological studies have indicated that Se could constitute a dietary factor with protective action against several degenerative diseases.
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PMID:Essentiality of selenium in the human body: relationship with different diseases. 1081 63

Exposure to thioacetamide is associated with the development of liver cirrhosis in experimental animals. In addition to liver, thioacetamide toxicity has been observed in other organs. In this study, the toxic effect of thioacetamide on the spleen was investigated at 0, 4, 8 and 12 weeks post-treatment durations. The level of tissue copper and selenium increased until the eighth week when a significant drop was observed. The zinc level was also increased but returned back to normal by week 8, thereafter it showed further increase. Calculation of the copper/zinc ratio showed an increase, but, recovered and returned to normal value by week 12. The level of manganese fluctuated until the eighth week. It then increased rapidly. Histological studies of the spleen tissue showed a significant increase in extramedullary haematopoiesis in the red pulp region and marked hyperplasia in the marginal zone and follicles. The results of this study, demonstrate an intimate association between trace element levels and spleen pathology, as observed in studies of other organs.
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PMID:Thioacetamide toxicity and the spleen: histological and biochemical analysis. 1082 Aug 95


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