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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic pathways and toxic effects of long-term selenium exposure in animal models and humans have both similarities and significant differences. In animal models the target organ is the liver, in which chronic cirrhosis develops. In man the target organ appears to be the lung, which manifests acute "rose cold," or, as in our patient, a chronic granulomatous hypersensitivity. Our data indicate not only a different target organ than would have been predicted from animal models, but also a difference in the distribution of selenium in human tissues. Long-term use of selenium favors production of dimethylselenide, which is excreted by the lungs and should be considered a pulmonary toxin. The ramifications of these findings may require a change in the monitoring techniques of long-term industrial exposure and mandate a close follow-up of selenium as a health fad.
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PMID:Long-term selenium exposure. 45 75

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

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

Chronic selenium (Se) toxicosis was diagnosed in two groups of growing pigs. Emaciation, loss of hair, necrotic areas in the skin, lesions of the coronary band and hooves, postnecrotic atrophic cirrhosis of liver, and lumbal poliomyelomalacia were the principal findings. High Se concentrations were detected in blood plasma. Addition of the calculated amounts of sodium selenite directly to the feedstuff instead to mineral premix was the cause of this intoxication.
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PMID:Accidental selenium poisoning of growing pigs. 137 61

The antioxidant status of alcoholic patients was assessed by direct measurement of the plasma antioxidants alpha-tocopherol and beta-carotene and of selenium as a marker of glutathione peroxidase. Overall, the alcoholic group showed significant decreases in the mean plasma values of beta-carotene, zinc and selenium when compared to the control subjects. When the patients were subdivided according to their liver histology, beta-carotene showed a progressive decrease in plasma concentration with increasing liver damage, whereas alpha-tocopherol levels were only depleted in the patients with cirrhosis. There were significant decreases in the plasma concentrations of both alpha-tocopherol and selenium in all patients with alcoholic skeletal muscle myopathy, whereas patients with normal muscle biopsies showed adequate antioxidant status. Such results support a role for free radical-mediated damage in end organ injury, particularly myopathy, in alcohol misusers.
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PMID:The antioxidant status of patients with either alcohol-induced liver damage or myopathy. 141 10

The serum and cyst fluid levels of selenium, zinc and copper were investigated both in patients and sheep with hydatid cysts. Results were compared with those of healthy subjects in both species. The serum values of Se, Zn and Cu in healthy subjects were 60.24 +/- 1.96 micrograms/L, 0.59 +/- 0.07 mg/L, and 1.01 +/- 0.08 mg/L, respectively. The corresponding serum values of the three trace elements in patients with hydatidosis were 41.30 +/- 1.94 micrograms/L, 1.27 +/- 0.08 mg/L, and 0.89 +/- 0.09 mg/L. These results show a decrease in Se and Zn, and a rise in Cu in sera of patients with hydatid disease. Similar results were obtained in infested sheep as related to the healthy control animals. Our results on the three trace elements were found to correlate well with the incidence of cirrhosis, malignant and infectious diseases and arthritis. Se was not detectable in cyst fluid, while Cu and Zn levels were found significantly lower than serum levels. Cu and Zn levels in cyst fluid showed no difference in both species. Variations in serum Cu, Zn and Se levels were insignificant with regard to the genus of the host and the fertile capacity of the hydatid cyst.
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PMID:Trace elements in hydatid disease. 142 83

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

Erythrocyte antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) and reduced glutathione, serum ceruloplasmin, and serum trace elements (copper, zinc, iron, and selenium) related to antioxidant enzymes were assayed in subjects with alcoholic liver disease of different degrees of severity. The erythrocytes of subjects with moderate and severe alcoholic liver cirrhosis had an unbalanced antioxidant system (normal superoxide dismutase, low catalase and glutathione peroxidase activities, and low glutathione content). Serum ceruloplasmin levels were in the normal range. Levels of the serum trace elements zinc and selenium were significantly low in subjects with moderate and severe cirrhosis, whose red cell half-life was also significantly short, as measured by radioactive chromium. These data suggest that the erythrocytes of subjects with moderate and severe alcoholic liver cirrhosis are less protected against oxidant stress. The particular erythrocyte antioxidant system and serum trace element pattern may play a role in the genesis of hemolytic disorders and of alcoholic hepatic damage.
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PMID:Erythrocyte antioxidant activity, serum ceruloplasmin, and trace element levels in subjects with alcoholic liver disease. 837 44

The common denominator of a unique disseminated multi-focal miliary myocardial hyaline necrosis and fibrosis in Keshan disease (KSD) and cystic fibrosis (CF) and a commonality of the affected age groups of fetuses and preschool children led to the review of existing KSD autopsy material to search for pancreatic and hepatic lesions considered pathognomonic for CF. Pancreatic lesions considered pathognomonic for CF were found in 595, or 35% of 1700 documented cases of KSD. The pancreatic lesions were limited to tissues of fetuses and preschool children. Adults dying of KSD had diagnostic lesions limited to the cardiovascular system, liver, and skeletal muscle. Varying degrees of focal biliary cirrhosis were identified in 850, or 50% of the KSD autopsies, and 85, or 5% developed severe lobular cirrhosis. The common denominator in CF and KSD appears to be a primary or induced secondary selenium deficiency in age-susceptible humans, prenatally at or around 22 wk of fetal life, during early postnatal life, or during the rapid-growth preschool years. The basic difference between the natural history of CF and KSD is that the selenium deficiency is totally environmental in KSD and appears to be the result of a maternal malabsorptive syndrome or an abnormality of selenium transfer in CF.
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PMID:Common denominators in the etiology and pathology of visceral lesions of cystic fibrosis and Keshan disease. 170 72

Dietary intake for three essential trace elements: selenium, copper and iron was studied in hospitalized patients receiving either ordinary meals or regimens adapted for liver cirrhosis. The aim of the study was to assess the effects of dietary manipulations: reduction in sodium intake for uncomplicated disease and protein restriction to 40 g per day in patients with hepatic encephalopathy. The meals proposed to these three groups were collected during fourteen days and daily intake for three elements was estimated by direct analysis of the assembled meals of the day. Dietary selenium was greatly affected by the restriction in protein intake contrary to copper and iron which were not significantly reduced. Moreover, overall daily trace element intake was rather low and clearly less than the most recent recommended allowances for these essential elements. Relationships between deficiency in some of these trace elements and worsening of the liver disease have been partly documented. They should encourage studies on the correction of dietary intake.
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PMID:[Intake of essential trace elements (selenium, copper and iron) in the nutrition of patients hospitalized with liver cirrhosis]. 207 93


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