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)

Follow-up study of 40 children suffering from chronic hepatitis. The diagnosis was made by liver needle biopsy with the Menghini method, when clinical signs or laboratory data of liver disease had lasted for more than 6 months. 24 patients showed the histological pattern of the aggressiv type of chronic hepatitis according to the definition of the European Association for the Study of the Liver (1968). In this group only 5 children had autoantibodies in the serum (so-called lupoid hepatitis). The HBAg positive courses played the most important part in the chronic persistent group as well as in the aggressive one. According to literature only the patients with the aggressive type have been treated with prednison, because chronic persistent hepatitis has a good prognosis without any treatment. In nearly all cases high transaminases and gammaglobulin levels decreased during the treatment with prednison, whereas the histological signs of inflammation seldom changed. Cirrhosis of the liver has developed in 2 HBAg positive patients of the aggressive group, who had not consequently received their daily dose of prednison.
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PMID:[Studies on juvenile chronic hepatitis]. 5 74

Intracytoplasmic hyaline globules (IHG) were found in 16 out of 105 hepatocellular carcinomas (15.2%). In all cases, there was a male preponderance, most of the patients were Black, and the mean age was in the fifth decade. IHG were mostly noted in the better-differentiated tumors. Bile production was present in 12% of all tumors. Over 80% of tumors with globules showed necrosis as compared with 40% of the tumors without globules. Cirrhosis was present in almost half the cases, with liver cell dysplasia in 15%. These globules are possibly alpha-fetoprotein. Some of them may be giant lysosomes. Their role in carcinogenesis and prognosis is uncertain.
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PMID:Intracytoplasmic hyaline globules in hepatocellular carconomas. 5 81

Certain characteristics of 328 Mozambican male Shangaans with primary hepatocellular cancer (PHC) have been compared with those of 163 Shangaan men with hepatomegaly from causes other than PHC and with those of 122 Black Southern African men with the same tumour but who belonged to tribes other than the Shangaan. Shangaans with PHC were significantly younger than non-Shangaans with the tumour (mean age 33,4 cf. 40,0 years; Pless than 0,001). They also had a significantly higher positivity rate of alpha-fetoprotein by immunodiffusion (71,4%) than the non-Shangaans (16%), although in other respects the tumours appeared to be similar. Cirrhosis of the non-tumorous part of the liver was present at necropsy in 62% of the Shangaans and in 66% of the non-Shangaans. The hepatitis B (surface) antigen (HBsAg) was detected in the serum of 60% of the Shangaans with PHC compared with only 9% of the controls. The antigen was present in 53,4% of the non-Shangaans with PHC (the difference between this fifure and that in the Shangaans was not significant). HBsAg was detected in the serum of 64% of the Shangaans with PHC and cirrhosis, but also in 74% of those with the tumour without associated cirrhosis. The possible role of the hepatitis B verus in the aetiology of PHC is considered in the light both of these findings and of the possibility that the frequency with which the tumour is associated with cirrhosis may be decreasing in Shangaans. Some of the dietary habits of the Shangaans with PHC were compared with those of the controls. Virtually all the patients with PHC, but also almost all the controls, ate groundnuts in large quantities from an early age, as well as cashew nuts in smaller amounts. Cycad pips, mopani leaves and pods, mopani worms and locusts were not eaten by significantly more of the Shangaans with PHC than the controls. The limitations of this type of dietary analysis are discussed.
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PMID:Some characteristics of Mozambican Shangaans with primary hepatocellular cancer. 6 57

19 Indian children with liver disease were studied. 5 in whom a clinical and histological diagnosis of Indian Childhood Cirrhosis was made had massive orcein-staining deposits in liver cells. The hepatic copper content in these 5 cases was strikingly high (1389 microgram/g dry tissue, range 1045--2303) the normal range being 15--55 microgram/g. Of the other 14 cases, only 2 had hepatic copper levels above normal (170 and 262 microgram/g.) This high hepatic copper concentration may be caused by excessive copper ingestion or an abnormality of copper metabolism.
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PMID:Increased hepatic copper concentration in Indian childhood cirrhosis. 8 75

Morphological, histochemical, and chemical study of three necropsy specimens of liver in the terminal stage of Indian Childhood Cirrhosis revealed a strikingly high copper content. it is proposed that excess accumulation of copper in the cytoplasm of hepatocytes disturbs the microtubular system, causing hydropic swelling and the formation of Mallory's hyalin. Copper and copper-binding protein showed topographical association with Mallory's hyalin. Diffuse cytoplasmic staining and the lysosomal copper distribution also suggested that copper had a cytotoxic effect. The pattern of copper distribution in Indian Childhood Cirrhosis differs from that in Wilson's disease and in prolonged cholestasis with excessive hepatic copper deposition, indicating a different mechanism of the copper accumulation.
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PMID:Cytoplasmic copper and its toxic effects. Studies in Indian childhood cirrhosis. 8 76

A radioimmunoassay for the accurate measurement of T.B.G., developed by Crouzat-Reynes, was used to perform T.B.G. concentration in sera of euthyroid subjects in different clinical situations, in hypothyroid and hyperthyroid patients. In normal control, the T.B.G. concentration was not different from men and women, from young and old subjects (m = 21,1; sigma = 3,9). On the other hand, in women either pregnant (m = 51,2; sigma = 18,1) or receiving oral contraception (m = 30,1; sigma = 5,7), the T.B.G. levels were significantly higher than euthyro subjects. Cirrhosis of the liver and liver carcinoma were without apparent effect on T.B.G. levels because it was a too few number of patients and the group was too heterogeneous. In the group of hypothyroid (m = 25,9; sigma = 6,5) and hyperthyroid (m = 21,1; sigma = 5,5) patients, the T.B.G. serum concentrations were not significantly different from normal. The ratio T4/T.B.G., as I.T.L. (T4 X T3 uptake) permit to bring back in normal range T4 levels changed by extrathyroidal process; however, this ratio seems to us to be less interesting than standard I.T.L. The T.B.G. assay has not to be considered only as a substitution of T3 uptake because they do not study the same parameters.
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PMID:[Preliminary results of a new radioimmunoassay for thyroxine binding globulin (T.B.G.) (author's transl)]. 10 71

A 29 year old patient with Crohn's disease and posthepatitic HBsAg-positive cirrhosis developed zinc deficiency in the course of complete parenteral nutrition. Zinc deficiency was proven by a low plasma zinc level of 12 microgram/dl. The daily input of zinc was 0.5 mg as calculated from the zinc concentration of infusion solutions used in parenteral nutrition during 3 1/2 months of treatment. The clinical picutre was that of acrodermatitis enteropathica. Cirrhosis of the liver and Crohn's disease were contributory causes of zinc deficiency. 6 bolus injections of 12-36 mg of zinc (total amount 144 mg) were given during 13 days. The plasma zinc level increased to 60-80 microgram/dl. 52% of the total amount of zinc injected were excreted by urine. The plasma half-life times of zinc were independent from basic zinc concentrations and averaged 1.55 +/- 0.22 h. It is concluded that severe signs of zinc deficiency will develop during parenteral nutrition in the presence of conditions leading to a negative zinc balance. In the case of long-term complete parenteral nutrition zinc should be substituted from the beginning of the treatment on.
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PMID:[Zinc deficiency syndrome during long-term parenteral nutrition in a patient with Crohn's disease and cirrhosis of the liver. Casuistry and zinc-pharmacokinetic (author's transl)]. 11 3

Hepatic collagen synthesis was studied during progressive fibrosis induced by carbon tetrachloride in male Sprague-Dawley rats by determination of prolyl hydroxylase activity and hydrocyproline levels along with morphological assessment of fibrosis. Cirrhosis was present after approximately 4 weeks treatment. Prolyl hydroxylase activity was increased significantly before fibrosis was apparent histologically or by hydroxyproline levels. The significance of this finding is discussed.
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PMID:Hepatic prolyl hydroxylase activity in experimental cirrhosis. 17 70

Cirrhosis of the liver was induced in rats weighing 120--140 g by CCl4 administration for a period of 2 months. Iodated oil, which caused emboly of the portal vein branches and foci of necrosis in the heptic tissue, was administered through the spleen to experimental and intact animals. The volume of necrotic foci, and also the mitotic actinity of hepatites were determined. Necrotic foci resolved more rapidly in cirrhosis of the liver. An increase of mitotic index of the second day after the administration of iodated oil was more significant in control rats.
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PMID:[Change in the mitotic activity of hepatocytes and resorption of necrotic areas in the formation of liver cirrhosis]. 18 Nov 2

To assess the role of hepatic function and alcohol on vitamin D metabolism, serum 25-hydroxyvitamin D (25-OHD) levels were measured in 20 healthy nonalcoholic control subjects, 31 "inactive" cirrhotics whose alcoholism was in remission, 8 alcoholic cirrhotics, and 15 alcoholics with normal liver function. Cirrhosis but not alcoholism, was assoicated with low serum 25-OHD levels. The aminopyrine breath test (ABT) was performed because aminopyrine, like vitamin D3, is metabolized by hepatic microsomes; the ABT correlated highly (r = 0.74, rho less than 0.01) with serum 25-OHD in the inactive cirrhotics. After an intravenous injection of 120 mug vitamin D3, serum 25-OHD rose significantly within 24 hr in 6 healthy controls and 2 patients with celiac disease but not in 6 inactive cirrhotics. The data suggest impaired 25-hydroxylation of vitamin-D impaired in patients with cirrhosis, related predominantly to the degree of hepatic dysfunction.
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PMID:Abnormal vitamin D metabolism in patients with cirrhosis. 18 83


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