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)

Grossly raised levels of tumour related vitamin B12 binding protein, reflected by rises in serum vitamin B12 and unsaturated vitamin B12 binding capacity (UBBC), were found in three of 44 patients with hepatocellular carcinoma. All three were HBsAg negative and had normal serum alpha fetoprotein levels. The patients did not have underlying cirrhosis and the tumours contained characteristic intracellular inclusions. In the first patient the UBBC level fell during a partial remission induced by adriamycin therapy and in the second patient UBBC levels rose with progression of her disease. In the third patient serum B12 binding protein levels fell after tumour resection. Assay and subsequent monitoring of serum vitamin B12 and UBCC may prove valuable in the assessment and follow-up of some patients with hepatocellular carcinoma whose alpha fetoprotein levels are normal.
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PMID:Vitamin B12 binding protein as a tumour marker for hepatocellular carcinoma. 8 76

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 consecutive series of 24 cases of primary carcinoma of the liver in Malawi has been investigated. Histologically, all were hepatocellular carcinomas (HCC). All patients were African Bantus, the average age was 42.7, and the sex ratio was men 3.5:women 1. The duration of symptoms attributable to HCC was about 5 months previous to admission to hospital and was in no case preceded by clinically manifest cirrhosis. The clinical picture was rather uniform with pain in the region of the liver, emaciation and nodular hepatomegaly as the most important features. One of the patients had repeated attacks of hypoglycaemic coma. Sera from 11 out of 13 patients contained alpha-feto-protein. Hepatitis-associated antigen and antibody in the serum were found in 7 and 6 out of 16 and 14 cases respectively. Serum B12 and serum unsaturated B12 binding capacity were moderately raised in most patients. The prognosis was poor, the average time of survival was 4.8 weeks after admission. The cause of death was most frequently hepatic coma. HCC in the African Bantu shows some different features from the same disease in the Western Hemisphere: The incidence is much higher; the patients are younger. The neoplasm commonly develops in a clinically latent cirrhosis. The latter is not caused by alcohol, but is presumably a sequel of hepatitis. It is possible that aflatoxin is the carcinogenic factor, acting more readily in a cirrhotic than in a normal liver.
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PMID:Primary carcinoma of the liver in Malawi: a review of 24 cases. 19 21

The influence of dietary protein content and dietary vitamin B12 supplement on the hepatotoxicity and carcinogenicity of aflatoxin in rat liver was studied. In animals fed a low-protein diet, aflatoxin induced extensive toxic and carcinogenic effects. Cirrhosis was significantly prevented to a certain level by vitamin B12 administration, but the incidence of cholangiofibrosis and hyperplastic nodules was unchanged. No toxic effect was observed in animals receiving high-protein diet with no vitamin B12 supplement in this study (33 weeks). Only one rat bearing a hepatoma was observed in this group. However, hepatoma and hyperplastic nodules were found in the group receiving high-protein diet plus vitamin B12. Cholangiofibrosis and cirrhosis were not observed in the high-protein group regardless of vitamin B12 administration.
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PMID:Influence of dietary protein and vitamin B12 on the toxicity and carcinogenicity of aflatoxins in rat liver. 20 26

A Hungarian family with four heterozygotes for Hb Lepore Washington is described. One, a 43-year-old male, had high levels of serum iron, saturated iron-binding capacity, and ferritin, and normal levels of folic acid and vitamin B12. Liver biopsy showed slight cirrhosis and marked iron deposition in parenchymal cells and in cells of the reticuloendothelial system. Heavy iron deposition was also found in the bone marrow. The patient is not an alcoholic and has no disease that requires blood transfusion. The hemochromatosis thus seems to be of idiopathic nature.
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PMID:Hemoglobin Lepore Washington and hemochromatosis in a Hungarian patient. 47 79

Serum vitamin B12 and vitamin B12 binding proteins (transcobalamins, TCS) were determined in patients with malaria, amoebic liver abscess, carcinoma of the liver, infectious hepatitis, cirrhosis and chronic myelocytic leukemia (CML) as well as in 60 blood donor subjects. Serum vitamin B12 in patients with infectious hepatitis, cirrhosis and CML were higher than that of the normal subjects. The values of unsaturated vitamin B12 binding capacity (UBBC) in patients with carcinoma of the liver, infectious hepatitis, cirrhosis were lower while that of patients with CML were higher than that of the normal subjects. A markedly increased TCI and decreased TCII was observed in patients with CML while these changes was much less in patients with other liver diseases. The difference was possibly due to a flooding of vitamin B12 from damaged liver cells into the circulation and the decreased synthesis of transcobalamins in patients with liver diseases while the increased granulocytes, the source of TCI, was much increased in patients with CML.
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PMID:Vitamin B12 and vitamin B12 binding proteins in liver diseases. 60 23

Excretion of oxalic acid in urine was measured in 28 healthy and 97 patients with gastrointestinal diseases. We found significantly higher values in the following groups: patients after resection of parts of the small intestine, patients with sprue and other diseases with malabsorption, patients with M. Crohn of the small intestine, colitis ulcerosa and granulomatosa, patients with chronical diseases of the pancreas gland and patients with cirrhosis of the liver. In 4 patients after resection of parts of the small intestine or pancreas urolithiasis could be verified. Reduction of fat and food without ballast reduced the excretion of oxalic acid in urine. Hyperoxaluria correlied significantly with the following parameters: excretion of fat in feces, exhalation of 14CO2 in the glykocholate breath test, resorption of vit. B12 and the length of resected small intestine. This form of hyperoxaluria is caused by hyperresorption of oxalic acid from food. The mechanism of this hyperresorption is not clarified yet, an important factor seems to be ill resorption of fat.
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PMID:[Hyperoxaluria in intestinal and liver diseases]. 83 13

Since transcobalamin II is the plasma binder of vitamin B12(cobalamin) that mediates delivery of cobalamin to tissues, we measured circulating levels of transcobalamin II after intravenous injection unlabeled cyanocobalamin in 12 control subjects and, because the liver is a major source of transcobalamin II, in eight patients with decompensated cirrhosis. Thirty minutes after injection of cyanocobalamin (200 ng per kilogram of body weight), total transcobalamin II (unsaturated plus cobalamin bound) declined in all 20 subjects to levels that averaged (+/- S.E.) 53.5 +/- 4.6 per cent of initial values. Subsequently, unsaturated transcobalamin II rapidly increased so that by eight hours, total transcobalamin II approached preinjection levels. Rates of regeneration of transcobalamin II were similar in control subjects and patients with liver disease. Unlike total transcobalamin II, total transcobalamin I was unaltered by injection of cyanocobalamin. Moreover, addition of cyanocobalamin to plasma in vitro did not alter measurements of total transcobalamin II. The rapid response of circulating transcobalamin II to cyanocobalamin injection strongly supports a dynamic role for this polypeptide during transport of a relatively large load of cobalamin.
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PMID:Changes in circulating transcobalamin II after injection of cyanocobalamin. 86 12

Toxepasi Complex (UDPG, glutathione and vitamin B12) was administered to patients with aggressive chronic hepatitis and a second group with severe cirrhosis. Changes in laboratory enzymological data indicative of the overall extent of liver damage due to cell necrosis, cholostasis and impairment of protein synthesis were evaluated. Decreases tending to normalisation were noted two weeks after the commencement of treatment, particularly in the first group. The results suggest that the complex may be usefully employed in the management of aggressive chronic hepatitis and cirrhosis of the liver.
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PMID:[Evaluation of the changes in some laboratory parameters in liver disease patients treated with Toxepasi Complex]. 96 62

A controlled clinical trial comparing 2-Mercapto-Priopionyl-Glycine (2-MPG) plus B12 vitamin with B12 vitamin alone in chronic liver disease has been conducted in seven hospitals in Italy. Patients were divided into two groups on the basis of liver histology; group I included 26 patients showing histological evidence for chronic persistent hepatitis (C.P.H.) (according to De Groote et al.) whereas group II consisted of 54 patients with chronic aggressive hepatitis (C.A.H.) or compensated liver cirrhosis. Patients of each group were randomly allocated to 2-MPG plus B12 vitamin, or to placebo plus B12 vitamin, in a double-blind way. The drug (or placebo) was diluted in 500 ml of 10% Levulose, and administered intravenously; 1000 gamma of B12 vitamin were added to each bottle. Patients in the 2-MPG group received 2.5 gms of the drug daily; the treatment lasted for 30 days. The following parameters were checked in all patients on admission, and repeated at the end of treatment: Serum bilirubin, serum Cholesterol, A.P., BSP retention, Prothrombin time, S-GOT, S-GPT, Gamma-GT, Total serum Protein, serum electrophoresis, Immunoglobulins. Patients given 2-MPG showed significant decreases of serum transaminases, and improvement of BSP retention.
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PMID:[Controlled clinical trial of 2-mercapto-propionyl-glycine in chronic hepatopathies]. 125 87


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