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

Collagen in bulk was isolated in about 30% yield from the livers of normal human beings and from livers of persons with alcholic cirrhosis. Analyzed chemically and examined by electron microscopy, the collagen in each case was shown to consist of two types identical with, or resembling closely, type I and type III collagens of skin. The collagen from normal liver was predominantly type I, whereas, that from cirrhotic livers consisted or approximately equal amounts of the two types. By chromatography on carboxymethyl-cellulose, the type I collagen from the cirrhotic livers showed one alpha2chain and two alpha1 chains. The alpha1 chains were separable from one another, but gel electrophoretic patterns of peptides obtained from them after treatment with CNBr were almost identical, and resembled the pattern obtained with CNBr peptides of the alpha1 chain of rat skin type I collagen. The increased collagen of both types was responsible in part for the observed distortion of the architecture of the cirrhotic livers associated with increased rigidity of the stroma. The predominance of type III collagen in the areas of collapse of architecture where, as shown by others, few fibroblasts are present, suggests that hepatocytes might have an important function in fibrogenesis during the course of liver cirrhosis.
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PMID:Increase in type I and type III collagens in human alcoholic liver cirrhosis. 106 Nov 56

Development and regression of liver fibrosis and cirrhosis induced by CCl4 in male F-344 rats were strictly followed during and after an 8-week treatment. The relative amount of collagen was measured by morphometry and the number of glycosaminoglycan (GAG) containing fat storing cells was counted at each time point. The expression of proteoglycan genes (decorin, versican and BPG-5 HSPG) was studied in parallel with the development of cirrhosis. Collagen content of the liver as well as the number of GAG-containing mesenchymal (fat storing) cells increased in parallel until two weeks after the cessation of CCl4 treatment. Later, both the collagen content and the number of GAG-containing cells decreased in parallel and significantly. Proteoglycan gene expression in the nonparenchymal fraction of liver cells indicated an active proteoglycan synthesis in the course of the development of cirrhosis. It is concluded that modified Ito (fat storing) cells synthesize proteoglycans and play an important role in the formation of connective tissue fibers in liver fibrosis.
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PMID:Role of the modified (glycosaminoglycan producing) perisinusoidal fibroblasts in the CCl4-induced fibrosis of the rat liver. 138 23

Liver biopsy specimens (178 percutaneous and 39 transjugular) were assessed from 217 consecutive patients with alcoholic liver disease, 77 noncirrhotics and 140 cirrhotics, whose cases were followed for 5 yr. Cirrhotic patients were categorized into two groups, with and without "hepatitis" using a criteria to define "hepatitis" that included only degrees of inflammation, necrosis, and Mallory bodies that had a prognostic weight in terms of mortality in 1 yr. This classification resulted in a sharp separation between a group of 42 patients with cirrhosis without "hepatitis" and with low mortality, both at 1 yr (7.1% +/- 4.0%) and at 5 yr (31% +/- 7%), and another group of 98 patients with cirrhosis and "hepatitis" and a high mortality both at 1 yr (26.5% +/- 4.5%, p less than 0.01), and at 5 yr (47% +/- 5%, p less than 0.02). Importantly, the 1-yr mortality in patients with cirrhosis and no "hepatitis" was not statistically different from that of patients with no cirrhosis or "hepatitis" (most of whom had only fatty liver) both at 1 yr (6.9% +/- 3.3%) and at 5 yr (24% +/- 6%). There were marked differences in several variables between cirrhosis with and without "hepatitis" [combined clinical and laboratory index: no "hepatitis": 4.9 +/- 0.7, with "hepatitis": 7.8 +/- 0.5, p less than 0.01; score of collagen in space of Disse: no "hepatitis": 2.1 +/- 0.4, with "hepatitis": 3.7 +/- 0.3, p less than 0.01; hepatocyte cross-sectional surface area: no "hepatitis": 682 +/- 51 micron 2, with "hepatitis": 841 +/- 31 micron 2, p less than 0.01]. These findings were more severe in the transjugular group than in the percutaneous group. Collagen in the space of Disse and hepatocyte surface area were not statistically different when cirrhosis without "hepatitis" was compared with a similar no "hepatitis" group of patients having noncirrhotic alcoholic liver disease. In this patient sample the presence of parenchymal nodules and fibrous septa, per se, did not result in an increase in mortality with respect to alcoholic patients without cirrhosis and with no "hepatitis."
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PMID:Prognosis of alcoholic cirrhosis in the presence and absence of alcoholic hepatitis. 378 Nov 89

To determine how choline supplementation affects the liver and whether it can protect against ethanol-induced liver injury, baboons were fed either normal or choline-supplemented diets, each with or without ethanol. Eighteen baboons were pair-fed for 3 to 4 years liquid diets with 50% of total energy as ethanol or isocaloric carbohydrate; ten animals were given our regular diets, whereas in eight the choline content was increased 5-fold. Six additional animals were fed individually with the control diets (with or without additional choline). With both ethanol-containing diets, ethanol intake was comparable and resulted in hepatic steatosis and striking mitochondrial lesions, with increases in serum bilirubin and SGOT, SGPT and glutamate dehydrogenase activities. In addition, of the five animals fed alcohol with the regular diet, one progressed to incomplete cirrhosis and two others developed perivenular and associated perisinusoidal fibrosis. Similarly, in the four baboons fed alcohol with choline supplementation, incomplete cirrhosis developed in one and perivenular fibrosis in two. Collagen deposition was demonstrated by immunoperoxidase with a specific antibody against procollagen Type III. These animals also displayed proliferation of myofibroblasts in the perivenular area and transformation of fat-storing cells to transitional cells in the perisinusoidal space, with associated enhanced collagen fiber deposition. Thus, in baboons, choline supplementation failed to prevent alcohol-induced steatosis and fibrosis. All parameters remained normal in the eight baboons fed the regular control diet. However, in the choline-supplemented controls, serum bilirubin, SGOT and glutamate dehydrogenase activities increased moderately and serum albumin decreased. Occasional fat droplets appeared in hepatocytes with mitochondrial changes (enlargement and alterations of the cristae) and an abundance of "myelin" figures in the cytoplasm, indicating that choline supplementation exerts moderate hepatotoxicity.
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PMID:Choline fails to prevent liver fibrosis in ethanol-fed baboons but causes toxicity. 401 29

Collagen content was measured in 38 needle liver biopsies (8 steatosis, 8 chronic hepatitis, 7 fibrosis and 15 cirrhosis) by a new colorimetric method based on the selective capacity of Sirius red and Fast green to bind to collagen and noncollagenous proteins, respectively. The values were compared with those obtained after determination of the degree of fibrosis by morphometry in the same tissue. In biopsies with cirrhosis and fibrosis, there was a higher amount of collagen than in biopsies with chronic hepatitis and steatosis. Furthermore, there was a highly significant direct correlation between the collagen content measured colorimetrically and the degree of fibrosis determined morphometrically (r = 0.77, p less than 0.001), suggesting that this new colorimetric method is useful in measuring the degree of fibrosis in needle liver biopsies.
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PMID:Measurement of fibrosis in needle liver biopsies: evaluation of a colorimetric method. 402 93

Five patients with maturity-onset diabetes mellitus and hepatomegaly were studied. This group in cluded moderately obese females in whom hepatomegaly and abnormal liver studies were associated with a marked elevation in the erythrocyte sedimentation rate. Liver biopsies from all 5 showed fatty steatosis and pericentral fibrosis. In 3 of the 5, fibrous bridging between central veins and portal tracts was present. Collagen surrounded swollen hepatocytes, some of which contained intracellular hyalin indistinguishable from Mallory's hyalin. Polymorphonuclear neutrophils and regenerating nodules were not present. None of the patients had a history of alcohol use, and in 2 followed closely for 2 yr, alcohol was never detected in random blood samples. The recognition of this morphologic lesion may help to clarify the significance of this finding as an intermediate lesion between fatty steatosis and cirrhosis in diabetics.
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PMID:Pericentral hepatic fibrosis and intracellular hyalin in diabetes mellitus. 615 66

Four factors which stimulate collagen synthesis and prolyl hydroxylase activity in cultures of human and mouse fibroblasts have been isolated by molecular sieve chromatography from animal and human fibrotic and cirrhotic livers. These factors do not stimulate protein or DNA synthesis or total DNA in these cultures. It has also been shown that these factors, designated collagen stimulating factors F1-F4, do not owe their activity to ascorbate or glutamine. Collagen stimulating factors are heat stable, and F1 and F2 have apparent molecular weights of about 4000 and 1000 respectively. Since these factors are not present in normal animal or human liver it is suggested that they may be responsible for increased collagen production in vivo in hepatic fibrosis and cirrhosis.
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PMID:Collagen stimulating factors in hepatic fibrogenesis. 632 76

Collagen types and their levels were compared between bile ducts from Fasciola infected rats and bile ducts from uninfected animals. Both collagen types I and III were shown to be increased in infected animals but, levels of type I increased less than type III. These results indicate that fascioliasis produces changes in the collagen composition of the bile duct that are similar to those produced in cirrhosis of the liver and other pathologic conditions including wound healing. Such observations suggest that a study of the chronology of collagen deposition in fascioliasis might provide information on the sequence of molecular events which result in bile duct hyperplasia.
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PMID:Levels of type I and type III collagen in the bile duct of rats infected with Fasciola hepatica. 662 19

Rats were treated for 3-4 months with ethanol or carbon tetrachloride or kept on a high fat-low protein diet. The cell distribution of the liver was investigated with special emphasis on the Kupffer cells with reference to lipids and collagen. Lipids were increased both histologically and chemically in all groups treated. All three treatments caused an increase of Kupffer cells, especially in the high fat-low protein group. The number of Kupffer cells and the content of liver lipids were strongly correlated. Collagen rose in the CCl4- and high fat-low protein groups. Cirrhosis was observed in CCl4--treated rats only.
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PMID:Effects of long-term treatment of rats with ethanol, carbon tetrachloride and high fat-low protein diet on the Kupffer cell distribution with reference to chemical composition of the liver. 688 Jul 53

The hepatotoxin, CCl4, was used to develop cirrhosis in rats in an attempt to compare fibrosis of this experimental disease with the alcoholic liver disease in humans. Several observations noted were as follows: (1) Collagen synthesis was increased by as much as 5-fold during the experimental period. Removal of the hepatotoxin led to a dramatic reduction of collagen synthesis within 2 weeks. The increased collagen synthesis was more marked after 21 and 80 days of CCl4 administration as compared with the rate after 200 days of administration. (2) Type III collagen from liver from rats with fibrosis was purified and eight CNBr-derived peptides characterized by molecular weight and amino acid composition. (3) After CNBr digestion of whole livers, quantitation of alpha 1(I)-CB8 and alpha 1-(III)-CB8 revealed that both type I and type III interstitial collagens, were increased by the same amount when measured in terms of either net synthesis or total collagen in the liver. At all stages, rat liver contained 35--40% type III collagen when compared with the total quantity of type I and type III interstitial collagens.
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PMID:Interstitial collagen polymorphism in rat liver with CCl4-induced cirrhosis. 741 7


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