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)

Serum ferritin concentrations were found to be raised, often considerably, in 58 of 76 black patients with primary liver cancer (PLC). No correlation could be demonstrated between the serum ferritin concentration and several other measurements, including the following: hepatic iron stores measured chemically, the size of the tumour, serum transaminase values, and the presence or absence of cirrhosis in the non-tumorous liver. There was, however, a negative correlation between serum ferritin and alpha-foetoprotein concentrations. Ferritin was purified from PLC tissue obtained from three patients at necropsy and the distribution of isoferritins was determined by isoelectric focusing. Acidic isoferritins similar to those previously found in PLC tissue were obtained. Their acidic nature was confirmed chromatographically using DEAE cellulose. Because the serum ferritin in patients with PLC probably consists of a mixture of normal and acidic isoferritins, it is likely that the serum assay used in the present study underestimated the actual concentrations present. With the development of an assay which utlises a specific antibody against acidic PLC isoferritins, serum ferritin may prove to be a second marker for PLC.
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PMID:Serum and tumour ferritins in primary liver cancer. 7 42

36% of a total of chronic liver patients suffered from anaemia and 50.5% of patients affected with liver cirrhosis. In most cases the anaemias were normochrome and hypochrome or hyperchrome only in some cases. In analyzing possible single factors the reductions of vitamin B12 absorption could be made probable by means of the Schilling test and sometimes a folic acid deficiency in macrocyte anaemia with normal vitamin B12 absorption by determining the folic acid content in the serum and by successes of test treatment 82% of patients with liver cirrhosis showed a latent or manifest haemolysis. However, it was only in 1/3 of the patients with liver cirrhosis that the spleen turned out to be the place of an increased degradation of erythrocytes. In some cases an increased erythrocytoclasia into the liver could be identified. Predominantly, however, an increased degradation of erythrocytes in the total RHS had to be assumed. Twice an ineffective erythropoiesis could be found by ferrokinetic examinations. As a whole ferrokinetic examinations cannot be interpreted easily, because their static and dynamic values of iron transport in the plasma volume of liver patients will undergo considerable changes. Patients with disturbances of haematopoiesis and with haemolysis remaining in the latent stage may develop a manifest anaemia because of the influence of additional factors, such as increase of the plasma volume at lowered haematocrit value or microbleedings. The cause of anaemia cannot be concluded with sufficient probability from the type of anaemia; in a single case all pathogenetic factors will rather have to be analyzed. Therapeutic possibilities for hepatogenous anaemia of complex genesis are discussed.
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PMID:[Complex genesis of anemia in chronic liver diseases]. 8 89

A 71-year-old woman showed a highly unusual pattern of iron distribution in the organism which was associated with iron overload. The hallmark of this disease was an extreme hypersiderinemia, the serum iron reaching about 800 mug/100 ml. There was a pigment cirrhosis of the liver, bronzed skin containing hemosiderin, and diabetes mellitus. Paradoxically, hemosiderin was not detectable in bone marrow macrophages, sideroblasts and erythrocytes were reduced, and there was a decrease in radioiron utilization of erythropoiesis, thus indicating insufficient iron supply. The pathogenesis of this disorder based on the formation of an autoantibody with specificity for transferrin thus producing a circulating immune complex which bound the majority of serum iron. Immunosuppression achieved a partial remission including a recovery of the patient's general state, a rise in free transferrin, a decrease in serum iron, disappearance of hemosiderin in the liver, and a rise in erythrocyte production.
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PMID:Transferrin-immune complex disease. 13 71

A patient with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease), treated with ethinyl estradiol, multiple blood transfusions, and iron-dextran, developed hepatocellular carcinoma and acquired hepatocerebral degeneration. In addition to the carcinoma, the liver contained extensive arteriovenous maliformations, telangiectasis, and changes of Osler atypical cirrhosis. The carcinoma possibly had its genesis in the presence of an ocongenic serum hepatitis virus, or the cirrhosis, or both.
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PMID:Hereditary hemorrhagic telangiectasia. A case with hepatocellular carcinoma and acquired hepatocerebral degeneration. 16 31

Hemochromatosis is a disorder characterized by the association of portal cirrhosis with deposition of excess amounts of iron in the parenchymal cells of many organs. Arthralgia and arthritis occur in about 50% of patients. The role of the radiologist is often significant in the recognition of this condition because hemochromatosis may be unsuspected clinically since the hepatic cirrhosis is frequently inactive at the time the arthritis develops. The possibility of hemochromatosis should be considered when the characteristic involvement of the metacarpophalangeal, radiocarpal, and proximal interphalangeal joints of the hand and wrist is present. In addition, articular and fibrocartilage calcification is often noted, particularly in the knee, triangular cartilage of the wrist, hip, elbow, symphysis pubis, and shoulder. Although localized chondrocalcinosis may be seen in association with many disorders, as well as in asymptomatic elderly persons, generalized chondrocalcinosis is a significant finding and is commonly associated with hemochromatosis. Recognition of the typical distribution of the arthropathy plus its characteristic roentgenographic features should aid in the identification of patients with the disorder who do not demonstrate the typical clinical features of hemochromatosis.
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PMID:Hemochromatosis: a disease often silent but not invisible. 17 3

Observations on the clinical effects of venesection therapy in 85 treated, as compared with 26 untreated, patients with idiopathic haemochromatosis showed decreased pigmentation and hepatomegaly together with a return to normal tests of liver function in half the patients who had abnormal tests at presentation. Control improved in 28 per cent of those patients with diabetes mellitus, although some patients developed it during the period of observation, despite venesection. Portal hypertension, testicular atrophy and arthropathy were not improved. In only 12 patients was there sufficient reaccumulation of iron after the initial course of venesection to merit further treatment. Rates of iron accumulation in these patients varied between 1-4 mg and 4-8 mg per day and chelatable iron levels were noted to be inappropriately high in relation to body iron stores during the early stages of the reaccumulation period. Life table data shows that the percentage survival five and ten years after diagnosis was 66 and 32 per cent respectively for the treated patients, and 18 and 6 per cent respectively for the untreated patients, both statistically highly significant differences (p less than 0-01). Possible clinical differences such as age of presentation, the presence of diabetes mellitus, cirrhosis, clinical hepatic failure and hepatoma between the treated and untreated groups that might otherwise have weighted survival in favour of the treated group were corrected by the use of covariant analysis. This gave mean log survival values of 4-15 and 2-88 for the treated and untreated patients respectively, equivalent to 63-4 months and 17-8 months, a highly significant difference (p less than 0-01). Ten patients, all of whom had cirrhosis at the time of diagnosis, died of malignant hepatoma between three and 15 years after completing venesection therapy. There was also a high rate of death from neoplasms in a variety of other sites--22 per cent in the venesected group, strikingly higher than that rate predicted for a similarly aged population using national cancer mortality rates.
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PMID:Long term results of venesection therapy in idiopathic haemochromatosis. 18 63

In human pigmentary cirrhosis nuclear (pseudo-)inclusions of cytoplasmic material, containing less or more degenerated and therefore faintly stained hemosiderin granules, are to be observed. But sometimes there are also finely fibrillar or granular proteinaceous materials, stainable by the Prussian-blue reaction, lying between the chromatin-strands or occupying the whole nucleus and displacing the chromatin to the nuclear envelope (margination of chromatin). Such uncoloured substances may condense into homogeneous masses and nearly hexagonal (0r related) crystals with a diameter up to 14 micron and a yellow-brownish colour, giving a strongly positive PERL's reaction. In contrast to the preceding stages intranuclear crystals of this kind have been observed in one case only. After destruction of the nuclear envelope and the marginated chromatin the crystals are lying free in the cytoplasm and later on, the cytoplasm being destroyed too, they may be ingested by von Kupffer cells. All the iron containing crystals, to be found in the cytoplasm, derive from former intranuclear inclusions. The intranuclear deposits of iron containing protein are interpreted as ferritin-aggregates. It is supposed that ferritin molecules, built up in the cytoplasm, do enter the nucleus via the pores of the nuclear envelope. Such an event not only signalizes a cytopathologic reaction but in turn may give rise to such additional cytopathologic lesions as cell shrinking and cell death.
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PMID:[Iron containing nuclear inclusions in human pigmentary cirrhosis (author's transl)]. 19 46

Consecutive liver biopsies in a large general hospital for Blacks over the period 1959 - 1960 were compared with those in the 2-year period 1975 - 1976. Changes were noted in the histological appearances of micronodular cirrhosis. With the liberalization of the liquor laws and the granting of access to hard liquor to Blacks, fatty change, alcoholic hepatitis, alcoholic hyalin and alcoholic cirrhosis are making their appearance in the micronodular cirrhosis of the South African Blacks, features which were never observed when alcohol consumption was confined to homebrewed beverages containing large quantities of iron derived from the metallic containers in which liquor is brewed. No change in the histological picture or incidence of macronodular cirrhosis and hepatocellular carcinoma was observed.
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PMID:The changing pattern of liver disease in South African Blacks. 20 77

Immunologically pure human transferrin type C (TfC) was isolated from the plasmas of 11 individual healthy donors. After conversion into the 2Fe-form, the preparations were analysed by polyacrylamide gel electrophoresis and chromatography on DEAE-cellulose. In all samples studied by either method the presence of three components, designated A, B and C, was observed. Calculations from eight chromatograms yielded the following relative proportions for the components: A:6%, B:62% and C:32%. The quantity of iron bound played no role in this chromatographic resolution. The components were immunologically identical but their sialic acid content increased inthe order of A less than B less than C. The presence of galactose as an ultimate residue of the oligosaccharide chains in TfC component A was confirmed by a biological test. This observation together with the results of earlier analyses for hexose, hexosamine and galactose in the subfractions from Behringwerke human transferrin, suggests that sialic acid is probably the only variable among TfC components A, B and C. Loss of sialic acid from component C during the isolation of TfC was excluded as an explanation for the presence of the other two components. The electrophoretic appearance of TfC samples from five patients with liver disease (chronic active hepatitis, cirrhosis or alcoholic liver) did not noticeably differ from that of TfC FROM HEALTHY PERSONS. Baboon transferrin resembles TfC with respect to sialic acid heterogeneity. This species was therefore studied to decide whether sialic acid is gradually lost from transferrin in the circulation or whether transferrin is not fully sialylated before discharge from the hepatocyte. Using DEAE-cellulose chromatography no difference was found between baboon transferrin molecules which were less than 6h old and those which had a mean age of 8.9 days. By inference it is suggested that the reason for the multiplicity of TfC is also likely to be biosynthetic.
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PMID:The molecular components of human transferrin type C. 40 68

Eleven patients with porphyria cutanea tarda were studied. Biochemical confirmation of the clinical diagnosis required only determination of the total urine porphyrin concentration in a sample of urine voided on rising in the morning. The patients were divided for convenience of discussion into four groups differing in age, sex and etiologic factors. Of the six patients in whom a liver biopsy was done one was shown to have micronodular cirrhosis. Except for a modest elevation in the serum glutamic oxaloacetic transaminase values when the patients were first seen, no evidence was found for liver disease apart from the presence of porphyria cutanea tarda. One patient recovered solely by abstaining from alcohol consumption. Five patients underwent phlebotomy; their iron stores had been found to be between 2 and 3 g. Decreasing urine porphyrin values correlated well with decreasing serum ferritin values during the course of phlebotomy. Porphyria cutanea tarda, which is due to a deficiency of uroporphyrinogen decarboxylase, is manifested in association with alcohol abuse, estrogen therapy, exposure to chlorinated hydrocarbons or increased tissue iron stores, or a combination of these factors. Although relatively uncommon, this condition raises important and unresolved issues regarding the hepatotoxicity of alcohol, estrogens, chlorinated hydrocarbons and iron.
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PMID:Porphyria cutanea tarda: clinical and laboratory features. 42 87


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