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

A non-concurrent prospective study was made on deaths from cancer and other causes occurring among 2,675 male workers at a metal refinery from 1949 to 1971. The expected number of deaths computed by applying age- and cause-specific death rates of Japanese males to these workers was compared with the observed number of deaths. Among 839 copper smelters, significantly increased mortalities were noted for lung cancer (SMR = 1,189) and colon cancer, but nor for cancer of the stomach, liver (primary) and biliary passages, pancreas and skin or for leukemia, tuberculosis, cerebrovascular diseases, heart diseases and liver cirrhosis. A dose-response relationship was demonstrated between the mortality from lung cancer and the degree of exposure. A very high excess mortality from lung cancer (SMR = 2,500) was seen among copper smelters who were considered to have been most heavily exposed to arsenic or workers who had engaged in sintering and blast furnace operations for 15 years of more before 1949. The latent period of lung cancer was 37.6 years on average, and not related to level of exposure. Twenty-six of 29 deaths from lung cancer among copper smelters occurred after they had left the refinery. Other production workers and clerical workers showed no significant excess mortality from any kind of cancer.
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PMID:A cohort study on mortality from cancer and other causes among workers at a metal refinery. 125 55

The serum non-caeruloplasmin copper concentrations were measured in normal subjects and patients with various types of liver disease by a sensitive direct method involving complexing the copper and measurement by atomic absorption spectrophotometry. In normal subjects the mean concentration (+/- S.D.) was 10.1 +/- 1.6 mug/100 ml, males having a slightly higher value (10.7 +/- 1.3 mug/100 ml) than females (9.2 +/- 1.8 mug/100 ml). In patients with various non-hepatic diseases concentrations were raised (15.8 +/- 8.9 mug/100 ml), as also in hepatitis (14.7 +/- 4.3 mug/100 ml), cholestasis (16.1 +/- 6.4 mug/100 ml) and cirrhosis (16.3 +/- 8.7 mug/100 ml). Heterozygotes for Wilson's disease and patients treated for Wilson's disease had concentrations (12.9 +/- 5.9 and 9.8 +/- 3.7 mug/100 ml, respectively) which did not differ significantly from normal whereas untreated patients had very significantly raised concentrations (22.9 +/- 4.5 mug/100 ml). Direct measurement of serum non-caeruloplasmin copper is more accurate than indirect measurement and may help in assessing the effect of treatment but it is concluded that measurement of this fraction of serum copper will not enable Wilson's disease to be differentiated from other forms of liver disease.
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PMID:Direct measurement of serum non-caeruloplasmin copper in liver disease. 127 46

While a number of studies investigated iron and copper storage or alpha 1-antitrypsin (A1AT) deficiency in the liver of patients with cirrhosis, we did not find any similar study in schistosomotic patients reported in literature. We investigated the storage of both metals and the A1AT deficiency in the liver of 72 cirrhotic and 27 schistosomotic patients (5 with the hepatointestinal and 22 with the hepatoesplenic form of the disease). Forty-four patients with cirrhosis were also alcoholic, and 28 were not. Iron storage was detected in 23 patients with cirrhosis (31.9%); among these 16 (36.3%) were alcoholic and 7 (25.0%) non-alcoholic (the difference was not statistically significant). Thirteen (56.5%), 5 (21.7%) and 5 (21.7%) patients presented I-grade, II-grade, and III-grade iron storage, respectively. Copperstorage was detected in 24 cirrhotic patients (33.3%), 15 being alcoholic (34.0%) in contrast with 9 non-alcoholic patients (32.1%), a statistically non-significant difference. A1AT deficiency was observed in 2 patients with cirrhosis (2.8%), one with history of alcoholism. HBsAg and HBcAg in hepatic tissue were detected in 5 cirrhotic patients (6.9%), three of them with a history of alcoholism. Iron and copper storage and A1AT deficiency were observed in 3 patients with cirrhosis (12.5%), while iron storage and A1AT deficiency were found in 2 additional patients with cirrhosis (2.8%). The authors underline that neither iron nor copper storage nor A1AT deficiency was found in any schistosomotic patient. The authors discuss the possible importance of these data.
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PMID:Iron, copper and alpha 1-antitrypsin deficiency in the liver of cirrhotic and schistosomotic patients. 130 14

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

Two cases of acute hepatic failure are reported in which the diagnosis of Wilson's disease was considered because of low serum ceruloplasmin, low serum copper levels and high 24 h urinary copper. Case 1 had Kayser-Fleischer rings, haemolysis and a high 24 h urinary copper, and so Wilson's disease was confidently diagnosed. Case 2 had high urinary copper excretion, but [64Cu] study indicated a 24:2 h ratio of 0.7 and made the diagnosis of Wilson's disease uncertain. Both patients underwent orthotopic hepatic transplantation, and multiple biopsies were taken from the resected specimen in order to estimate hepatic copper levels. In both cases, hepatic copper levels revealed considerable variation: 0.8-5.2 mumol/g dry wt (case 1) vs 0.02-12.65 mumol/g dry wt (case 2). In case 1, only two of 14 levels were within the diagnostic range for Wilson's disease (greater than 4 mumol/g dry wt), whereas hepatic copper levels in case 2 were in the Wilsonian disease range in three of 16 specimens. These results were in contrast to uniformly high hepatic copper levels in one patient with established cirrhosis secondary to Wilson's disease and two cases of primary biliary cirrhosis. This report indicates that hepatic copper levels vary greatly in acute liver failure, and that estimates from a single biopsy specimen may be misleading as to the cause of the underlying liver disease.
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PMID:Striking variability of hepatic copper levels in fulminant hepatic failure. 151 66

Indian childhood cirrhosis is a fatal liver disease characterized by a striking accumulation of copper-containing granules within hepatocytes. A two-year-old American boy, the product of a third-cousin marriage, with clinical, biochemical, and histological signs of Indian childhood cirrhosis was studied. Liver biopsies at 22 and 30 months of age revealed a rapid progression from fibrosis to micronodular cirrhosis, with many of the remaining hepatocytes staining strongly for copper and copper-binding proteins. Electron microscopy showed characteristic dense granules containing copper and sulfur by electron probe analysis. Hepatic copper content was 1500 micrograms/g dry weight (normal, 20-50). Urinary copper was 3.6 mumol/d (229 micrograms/24 hours; normal, 15-20), and serum ceruloplasmin was 352 mg/L (normal, 150-320). The case suggests that both genetic and environmental components contribute to the manifestations of Indian childhood cirrhosis, and that the diagnosis of Indian childhood cirrhosis should be considered even in non-Indian infants with progressive liver disease.
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PMID:Indian childhood cirrhosis in an American child. 142 97

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

Primary sclerosing cholangitis is a condition of unknown cause. It is recognized by liver dysfunction and its characteristic radiologic appearance, which is related to portal tract inflammation, bile duct proliferation, and periductal fibroses involving small intrahepatic and large extrahepatic ducts. The disease lasts about 10 years from the time of diagnosis. Primary sclerosing cholangitis is recognized by abnormal results on routine liver function tests or by the development of clinical jaundice. An autoimmune cause has been suggested because of its strong association with inflammatory bowel disease, certain antigens, AIDS, and immunoregulatory abnormalities. Results of medical management of sclerosing cholangitis have been disappointing. Immunosuppressive drugs, copper chelating agents, and antibiotics have failed to alter progression of the disease. Colectomy in patients with inflammatory bowel disease also has no influence. The judicious use of dilations of strictures, bypass procedures, or resection can palliate jaundice in patients with primary sclerosing cholangitis, but liver transplantation is the definitive treatment. Because palliative operations increase the hazards of liver transplantation, percutaneous dilations and stentings are preferred initially. Cirrhosis and portal hypertension are indications for transplantation. In the future, transplantation may be indicated earlier in the course of the disease.
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PMID:Primary sclerosing cholangitis. 158 51

Wilson disease is due to a genetically determined impairment of copper excretion from liver into bile resulting in copper overload of the organism. The chromosomal defect and the primary defect of copper metabolism is not yet defined. When during the course of the disease the cytoplasmatic copper binding sites of hepatocytes are saturated, excess of "free" copper is accumulating. It induces liver cell damage and necrosis followed by the development of fibrosis and cirrhosis. The accumulation process of excess free copper in hepatocytes is accompanied by a redistribution into the lysosomal compartment of the cells as well as by release of free copper into blood. This increase of the free serum copper concentration leads during the course of the disease to an elevated copper burden of other organs. This results in a variety of symptoms, of which liver disease and neurologic disturbances are of major significance in regard to clinical presentation and prognosis of the patients.
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PMID:[Pathogenesis of Wilson's disease]. 159 17


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