Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Procollagen type I carboxyterminal and type III aminoterminal peptide concentrations were measured in sera of 60 patients with alcoholic and 14 with nonalcoholic liver disease to study whether these assays are useful as clinical tests to differentiate various stages of alcoholic liver injury. Both propeptides were markedly elevated in alcoholic hepatitis and cirrhosis: procollagen type III peptide in 90% and type I peptide in 60-80% of these patients. Moderately increased values were found less frequently in patients with fatty liver. These tests did not differentiate patients with simple fatty liver from those with fatty liver and early fibrosis. There was a significant difference in serum procollagen type III peptide between fatty liver and both alcoholic hepatitis and cirrhosis (p less than 0.001), and in type I peptide between fatty liver and alcoholic hepatitis (p less than 0.005). Although serum peptide values correlated with the degree of liver fibrosis, appreciable overlap of values was found between the various groups. The peptide concentrations also seemed to be related to the degree of hepatic inflammation, and the highest values were observed in a subgroup of patients with alcoholic hepatitis in whom numerous Mallory bodies were found. The data suggest that in alcoholic liver diseases, serum collagen propeptide determination may be useful in diagnosing severe alcoholic hepatitis.
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PMID:Diagnostic value of serum procollagen peptide measurements in alcoholic liver disease. 638 61

To evaluate the diagnostic significance of the collagen Type III (Col 1-3) N-terminal propeptide of procollagen Type III, with respect to activity and degree of liver fibrosis, Col 1-3 serum concentrations were measured in 111 patients with chronic liver diseases and in 60 patients were correlated with liver histology and morphometry. Col 1-3 was measured by a specific radioimmunoassay. Biopsies were read without knowledge of diagnosis. Periportal and intralobular lesions were assessed semiquantitatively by allocating 1 of 4 severity grades to each parameter. All portal areas were measured morphometrically. Compared to 27 normal controls, Col 1-3 concentrations were significantly elevated in patients with untreated chronic active hepatitis, cirrhosis and primary biliary cirrhosis, but not in chronic persistent hepatitis or fatty liver. Morphometrically measured portal tract area significantly correlated with Col 1-3 plasma levels. Among the semiquantitatively measured periportal lesions, the number of fibroblasts exhibited the closest relationship with Col 1-3 levels; there was no relationship between Col 1-3 levels and intralobular lesions. These data suggest that Col 1-3 serum levels reliably reflect the activity and degree of liver fibrosis and are useful along with liver biopsy in follow-up of patients with chronic liver disease.
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PMID:The N-terminal propeptide of collagen type III in serum reflects activity and degree of fibrosis in patients with chronic liver disease. 647 51

A morphological, endoscopic and bioptic (histologic and electron microscopic) study carried out in 86 patients with acute persisting hepatitis (APH) and 240 patients with noncirrhogenous alcoholic hepatitis (AH) allowed the observation of some aspects with predictive-evolutive value in liver diseases. In APH the endoscopic observation of a change of colour from bright red to variegated and the appearance on histologic examination of portal infiltrate with invasive tendency as well as of collagen spurs penetrating in the portal spaces, suggest the onset of the chronicity. In AH the changes with predictive value present in both AH and hepatic steatosis are, the alterations of the liver surface, and especially perivenular and perisynusoidal fibrosis.
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PMID:Morphological markers with predictive-evolutive value in liver diseases. 651 94

Disturbances of intravenously administered indocyanin green (ICG) elimination are related to the effective circulating blood volume and the amount of binding protein for transportation in blood plasma through the liver because of the narrowed sinusoidal space due to the enlarged liver cells with fullness of confluent fat droplets in the cytoplasma. However, morphologic changes of the liver resulting in disturbances of ICG elimination could not be actually clarified until the present. Therefore, morphologic changes of the liver resulting in delayed ICG elimination in fatty liver, occurring in diabetes mellitus were investigated in contrast with those in fatty liver in non-diabetic, non-alcoholic diseases of the liver. An electron microscopic study of the liver with delayed ICG elimination revealed thickening and amorphous growth of the sinusoidal wall with obscure pores followed by membraneous formation, narrowness of Disse's space, rarefaction of sinusoidal microvilli and proliferation of collagen fibers, in fatty livers derived from both diabetes mellitus and other diseases. The term "intrasinusoidal block" in fatty liver should be utilized on the basis of these electron microscopic features of the liver.
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PMID:Light microscopic and electron microscopic study on morphologic features resulting in the delay of ICG elimination in diabetic and non-diabetic fatty liver. 653 68

In this investigation, the ultrastructural features of the nutritional cardiomyopathy of protein-calorie-malnourished rats were examined. Protein-calorie malnutrition was induced in young rats by feeding them a low-protein diet (4% protein) for 6 weeks. Control animals were fed a high-protein diet (16% protein). The deficient rats showed severe restriction of body-weight gain, fatty liver and hypoproteinaemia. The results of the present study clearly demonstrated that the experimentally induced protein-calorie malnutrition brings about striking morphological changes in the heart of the rat. On light microscopy hyalinization an vacuolization of muscle fibres, loss of cross striations and myofibrils, small foci of necrosis, interstitial fibrosis and mononuclear-cell infiltration could be detected. The ultrastructural lesions were characterized by myofibrillar degeneration, contraction-band formation, dilatation of sarcoplasmic reticulum, mitochondrial swelling, dehiscence of intercalated discs, and widened interstitial spaces, especially around vessels, due to oedema fluid and cellular infiltration by mononuclear cells an activated fibroblasts with collagen fibres and microfibrils. In addition, an increase in relative heart weight was also observed. The potential role of catecholamines in the pathogenesis of this cardiomyopathy is discussed.
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PMID:Ultrastructural changes in nutritional cardiomyopathy of protein-calorie malnourished rats. 680 35

Specific antibodies to collagen type IV, laminin, and fibronectin were used to localise these proteins by indirect immunofluorescence in frozen sections of normal and fibrotic liver. In normal livers distinct staining was found in basement membranes of blood and lymph vessels, of bile ducts and ductules and around nerve axons. Positive reactions for type IV collagen and fibronectin were also observed in the perisinusoidal space, while hepatocytes and most of the interstitial matrix of portal fields remained unstained. Liver specimens obtained from patients with alcoholic liver disease (fatty liver, hepatitis or cirrhosis) and chronic active hepatitis showed a more intense reaction with the antibodies in the perisnusoidal space including now distinct staining for laminin. These patterns were particularly prominent at borders between fibrotic septa and remnants of parenchyma or pseudolobules. Strong reactions were also found for type IV collagen and fibronectin in the periportal interstitium and in large fibrotic areas. The findings support previous electron-microscopical and chemical evidence for increased basement membrane production in human liver fibrosis and demonstrate that this may involve different proteins and occur at different anatomical sites.
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PMID:Distribution of basement membrane proteins in normal and fibrotic human liver: collagen type IV, laminin, and fibronectin. 698 3

Regression of the main components of atherosclerotic leseions is compared with regression of other related pathological masses in the body, notably the fatty liver, the large abscess, the large thrombus, the tuberculous granuloma, the lipid implantation granuloma, an the at first reversible but later irreversible proliferation of tissues in response to certain hydrocarbons. The unique obstacles to the regression of advanced artheromata -- as compared to regression of pathological masses elsewhere -- are identified as a lack of early capillarisation, a dependence on evacuation by a very slow unidirectional filtration across an extremely dense and contracted tissue, a lack of an unending imigration of leucocytes for the phagocytic or lysosomal removal of large extracellular lipid pools, and the massive deposits of collagen, an insulating material of extremely long half-life that seems, in addition, to promote wall fragility and supra-plaque thrombosis. The origin and the fate of the myocyte proliferation in hyperlipemia-induced plaques is scrutinized; arguments are presented in favor of its regenerative rather than platelet-induced origin and in favor of the possibility that protracted hyperlipemia may induce the development of some regression-resistsant myocytic mutants. The special difficulties and pitfalls of regression research are analysed. The current conclusions from the most critical experimental studies to date indicate that incipient or young lesions are capable of significant regression, but there is as yet no evidence that advanced or complicated plaques will regress in any species.
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PMID:Overview of studies on regression of atherosclerosis. 701 65

Twenty alcoholic patients underwent sequential biopsy of the liver as part of their medical evaluation. Of the 10 patients with simple fatty liver, 9 showed no progression of the histologic lesion after 1-2 yr. By contrast, of 10 patients with perivenular fibrosis, of the 9 who continued to drink all showed progression. Laboratory parameters did not distinguish between these two groups at the time of initial biopsy. The ultrastructure of the perivenular lesion was evaluated in 11 patients. The thickness of the perivenular rim was variable, but there was a good correlation between the thickness of the perivenular rim and the number of mesenchymal cells surrounding the venules (correlation coefficient r = 0.7634, p less than 0.001). Myofibroblasts represented the most common cell type but there was also infiltration with other mononuclear cells. Collagen fibers surrounding myofibroblasts were observed in the perivenular fibrotic area. Thus, in the group of alcoholics who were investigated in this study, myofibroblast proliferation and collagen deposition around the terminal hepatic venule represent the first apparent lesions in the sequence of events leading to alcoholic cirrhosis.
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PMID:Perivenular fibrosis in alcoholic liver injury: ultrastructure and histologic progression. 710 8

Examination of 51 human liver specimens with the modified Kupffer's gold impregnation method confirmed the presence and distribution of fat-storing cells in various kinds of diseased livers such as fatty liver, acute centrolobular necrosis, subacute massive necrosis and cirrhosis as well as in liver cell carcinoma. In normal liver, gold-reactive fat-storing cells were distributed in the central area or diffusely in lobules. In the liver with marked fatty change and obstructive jaundice, presence of fat-storing cells was able to be clarified by this method. In cases of acute hepatocellular necrosis, the necrotic areas contained a large number of fat-storing cells in contrast to adjacent areas. In cases of subacute massive hepatic necrosis and cirrhosis, the areas with abundant newly formed collagen fibers (type III collagen) contained many gold-reactive fat-storing cells. In the septa consisting of dense type I collagen fibers, by contraries, fat-storing cells were hardly visible. The features suggested that fat-storing cells are closely related to intralobular fibrogenesis. In one case of liver cell carcinoma, there were many gold-reactive fat-storing cells in tumour tissue.
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PMID:Pathological study on gold impregnation of fat-storing cells in human liver. 723 21

Following the pioneer report of Di Luzio (Physiologist 6, 169-173, 1963) concerning the prevention of the acute ethanol-induced fatty liver by antioxidants, many observations have shown that ethanol-induced liver injury may be linked, at least partly, to an oxidative stress resulting from increased free radical production and/or decreased antioxidant defence. The disturbances induced in the major hepatic enzymatic and non-enzymatic antioxidant systems following experimental acute and chronic ethanol administration are reviewed, emphasizing the important role of dietary alpha-tocopherol in modifying the induction of oxidative stress and its usual expression as increased lipid peroxidation. Adaptative increases in some elements of the hepatic antioxidant defence partly counteract the enhanced generation of prooxidant free radicals following chronic ethanol intake. By contrast, lipid peroxidation is favoured when ethanol is administered together with a fat-rich diet and/or various xenobiotics. Chronic ethanol feeding has also been reported to potentiate the oxidative stress resulting from an acute ethanol load. By generating potent chemoattractants for human neutrophils and/or by stimulating the expression of genes involved in collagen biosynthesis, liver lipid peroxidation may play an important role in the progression of steatosis to hepatitis and cirrhosis. Oxidative stress has been shown not to be restricted to the liver, but also to affect, under some experimental conditions of ethanol administration, extrahepatic tissues, such as the central nervous system, the heart and the testes. This stress can be partly prevented by vitamin E supplementation. Ethanol-induced antioxidant disturbances have also been reported in clinical studies in blood and liver biopsies. Pharmacological antioxidants could have beneficial effects in reducing the incidence of ethanol-induced changes in cellular lipids, proteins and nucleic acids. The antioxidants considered could act by reducing free radical production (e.g. chelators of redox-active iron derivatives), trapping free radicals themselves, interrupting the peroxidation process or reinforcing the natural antioxidant defence.
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PMID:Alcohol and antioxidant systems. 781 35


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