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

Concentrations of iron, copper and zinc were measured in postmortem specimens of liver, muscle and brain tissue by atomic absorption spectrophotometry. Concentrations varied markedly in normal liver specimens from person to person, but not in other organ specimens. Copper concentrations in specimens from cirrhotic livers were normal in most cases, however at the upper limit of normal in about 20% of the cases evaluated. Concentrations of zinc and iron were lower than normal in cirrhotic livers. Mineral concentrations were higher by a factor of 10-20 in liver specimens of patients with hemochromatosis or M. Wilson than in normals. Iron overloading as a consequence of therapy (secondary hemochromatosis) and liver changes due to longtime artificially elevated plasma copper levels may imitate the adult form of the "classic" mineral storage diseases mentioned. Thus "athrocytotic" liver cirrhosis, being caused or accompanied by metal excess has to be considered as a polyetiological syndrome.
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PMID:[Minerals in normal and cirrhotic liver. The pathology of mineral dependent athrocytic liver cirrhosis]. 73 12

Disturbances in the iron metabolism can quite frequently be observed in patients with porphyria cutanea tarda. Studies on 10 patients with porphyria cutanea tarda indicate that elevated iron levels are correlated with decreased latent and normal total iron binding capacity in the serum. Morphological examinations of the liver showed alterations as can be found in fatty liver up to cirrhosis, which -- in most instances -- were associated with iron deposits in the hepatocytes.
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PMID:[Clinical findings in porphyria cutanea tarda]. 84 65

Evaluation of stored iron by means of DFOX-induced sideruria in 101 subjects with various degree of hyposideraemia with or without anaemia, is reported. Three groups were examined: 49 patients with chronic loss of blood and malabsorption and urinary iron values up to 1 mg/24hr; 43 with non-bleeding neoplasia, collagen disease, lymphoma, cirrhosis of the liver etc. and values of 1-2mg/24 hr; 9 with rheumatoid arthritis and cirrhosis of the liver and values over 2 mg/24 hr. The reasons why hyposideraemia may accompany incipient of frank tissue hypo-, normo- or hypersiderosis are discussed.
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PMID:[Desferrioxamine in the diagnosis of hypo-, normo-, and hypersiderotic hyposideremia]. 84 86

Idiopathic hemochromatosis is an iron-storage disease more common in men than in women. It is characterized clinically by diabetes mellitus, cirrhosis of the liver, pigmentation of the skin and cardiac failure. The diagnosis may be overlooked when the presenting symptoms do not follow the pattern. A case is reported which was diagnosed after an onset that featured neurologic symptoms.
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PMID:Idiopathic hemochromatosis: case report of a patient presenting with neurologic symptoms. 86 79

A 68-year-old man, after having been diagnosed as having hepatic disease at about the age of 41 years, had been hospitalized frequently until his death. Blood sugar, iron, and copper had not increased during his illness. Although the diagnosis of liver cirrhosis had been made and he had been receiving therapy, various neurologic symptoms without disturbances of consciousness appeared six months before his death. Autopsy revealed hemochromatosis, liver cirrhosis, and pancreatic fibrosis. A large amount of iron had accumulated in the liver, the pancreas, and the thyroid gland, while considerable numbers of ceroid and lipofuscin pigment granules had accumulated diffusely in the brain. Abnormal astrocytes of the Alzheimer II type were diffusely distributed in the brain and contained no intranuclear glycogen which stained positive with the carmine stain. No spongy changes were seen in the deeper layers of the cerebral cortex. Chemical analyses for trace metals in the brain, liver, and kidneys revealed a large amount of iron and increased copper in the liver, and considerable quantities of copper, manganese, calcium, and mercury in the brain. Because of changes in the erythrocyte sedimentation rate and marked thymol turbidity seen before and after the occurrence of the neurologic symptoms, this man was suspected of having disorders of the trace-metal binding proteins and/or of their polymers.
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PMID:Hemochromatosis associated with brain lesions--a disorder of trace-metal binding proteins and/or polymers? 92 21

The author examined the influence of abnormal amounts of iron on the development of early fibrosis (14th day), early and advanced cirrhosis (45th and 90th day) in liver esperimentaly damaged by carbon tetrachloride by means of morphological and histochemical methods. On the basis of the obtained data she could suggest that while at early stages iron did not have significant influence on the rate of development and gravity of the pathologic process, later (advanced cirrhosis) the changes were less manifested. She asumed that three valence iron, administered in the organism of the animals intoxicated by carbon tetrachloride, improved the course of the metabolic processes in the damaged liver cells, a manifestation of which was later and weaker development of the cirrhotic process.
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PMID:[Morphologic characteristics of carbon tetrachloride poisoned liver in the presence of iron loading]. 101 8

Radioisotope studies of iron kinetics carried out in patients with chronic hepatitis yielded the following results. Serum iron level and free iron binding capacity showed little difference from the normal mean value. All three types studied (chronic persistent hepatitis, chronic active hepatitis, chronic active hepatitis with cirrhosis) revealed an abnormal distribution of iron in the first 24 hours. Normalization of iron distribution ensued in persistent hepatitis and in chronic active hepatitis with cirrhosis, but in chronic active hepatitis the abnormal distribution persisted, as reflected by a decreased iron utilization and an increased iron storage in the liver. The cause of this is attributed to a transitory accumulation of ferritin in the liver.
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PMID:Iron turnover in chronic hepatitis. 102 35

A group of 8 patients (M) with liver cirrhosis were studied. Each subject was standardized with rest time extending from 22,00 to 05,00 and meals scheduled at 08,00-08,30, 12,00-12,30, 17,30-18,00. Then was sampled at 04,00, 08,00 12,00, 16,00, 20,00, 24,00. In each sample of serum were determined iron, T.I.B.C. and L.I.B.C. All data were analyzed by macroscopic approach (chronograms) and by mean cosinor. A significant circadian rhythm was detected in all parameters, with a statistically valid difference between normal subjects and patients with liver cirrhosis in the mesor of T.I.B.C. and L.I.B.C.
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PMID:[Circadian aspects of iron metabolism. Changes of total iron binding capacity in patients with liver cirrhosis and in apparently healthy persons]. 102 38

During a study of pathogenetic mechanisms in the hepatic cirrhosis of thalassaemia major, 16 liver biopsies were examined by electron microscopy. Previous ultrastructural studies of liver cells during iron overload have shown electron-dense iron as lysosomal haemosiderin, and as lysosomal and cell-sap ferritin. In this study, all biopsies, regardless of the patient's age, showed ferritin molecules within lysosomes in a specific pattern in relationship with regularly arranged lamellae. This membrane-associated lysosomal ferritin is considered to be a stage in the segregation of iron seen in iron overload. The dimensions and electron density of individual ferritin molecules indicate differences between cell sap and lysosomal ferritin. Intracellular ferritin transport and iron-seclusion mechanisms are reconsidered in view of these findings. The liver biopsies of thalassaemic infants also provide information about the causal relationship between iron overload and collagen deposition. Since the collagen deposition precedes any morphological evidence of cellular injury (other than the increased iron content), the primary cirrhotogenic factor in thalassaemia is apparently not cell necrosis but possibly excessive collagen deposition induced by iron.
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PMID:The liver in thalassaemia major: ultrastructural observations. 105 35

A high negative correlation (coefficient similar to 0.9) between increased 59Fe absorption from a diagnostic 0.56 mg 59Fe2+ dose and the depletion of available storage iron was observed in menstruating and pregnant women, fullterm and premature infants, blood donors, patients with infections, inflammations, tumors, hepatic cirrhosis, gastric surgery, increased urogenital or gastrointestinal blood loss. The increased diagnostic 59Fe2+ absorption is a reliable and sensitive indicator of at least depleted iron stores or prelatent iron deficiency as caused by iron malnutrition or maldigestion, increased iron requirement in pregnancy, infancy, urogenital or gastrointestinal blood loss. Although the messenger system which signalyzes the depletion of iron stores to the iron absorbing enterocytes of the duodenal and jejunal mucosa is not yet known available storage iron seems to control intestinal iron absorption under normal and the great majority o pathological condition in humans. Anemia per se or high erythropoietin levels in blood do not influence iron absorption since patients with even severe erythroblastic hypoplasia, aplastic anemia and megaloblastic anemia due to vitamin B12 deficiency absorb iron according to their iron stores. An only mild hyperplasia of the erythropoietic system in the bone marrow does also not effect iron absorption which was still under the control of available storage iron in patients with hereditary spherocytosis, nonspherocytic congenital hemolytic anemia due to glucose-6-phosphate dehydrogenase deficiency, acquired hemolytic anemia and vitamin B12 deficiency induced megaloblastic anemia..
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PMID:Intestinal iron absorption under the influence of available storage iron and erythroblastic hyperplasia. Comparative studies in children with hereditary spherocytosis, nonspherocytic enzymopenic hemolytic anemia, acquired hemolytic anemia, vitamin B12 deficiency induced megaloblastic anemia, erythroblastic hypoplasia and aplastic anemia. 113 Jan 21


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