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)

Liver protocallagen proline hydroxylase activity (PPH activity) was determined in patients with various liver diseases, CCl4-induced liver fibrosis rats and cholin deficiency (tcd) fatty liver rats. The following results were obtained: Liver PPH activity in patients with chronic hepatitis was higher than that in patients with acute hepatitis, while the activity in patients with liver cirrhosis was much higher than that in patients with chronic hepatitis. The activity was higher in patients with chronic active hepatitis than in those with chronic inactive hepatitis. Patients with active and progressive liver cirrhosis were found to have an especially high PPH activity, in whom the activity reflected well the degree of liver fibrosis. Even though fibrosis in persistent hepatitis was almost negligible or slight, the degree of liver PPH activity in persistent hepatitis was similar to that in liver cirrhosis. Liver PPH activities in CCl4-induced liver fibrosis rats and CD fatty liver rats elevated proportionally to the lapse of time. Whilst liver PPH activity in rats of CD fatty liver without fibrosis in 23 to 31 weeks after the start of the experiment was slightly lower than that in rats of CD fatty liver with fibrosis. But liver PPH activity of the former was considerably higher than that of control rats.
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PMID:Liver protocollagen proline hydroxylase in human liver diseases and experimental liver fibrosis. 19 57

Chronic hepatitis is one of liver diseases with arguments from the clinical and histopathological aspects. Histopathological examinations were made on 687 biopsy cases clinically diagnosed as chronic hepatitis. Histopathological classification was based on our own criteria by referring to discussions in the series of Inuyama symposia on hepattis and others. The correlation between histological diagnosis and clinical data was also examined. Histopathological diagnoses made of the 687 cases were classified as follows; normal liver or liver with no pathognomonic changes of 77 cases (11.2%), non-specific reactive hepatitis of 56 cases (8.0%), viral hepatitis of 488 cases (71.0%), alcoholic hepatitis of 25 cases (3.6%), fatty liver of 23 cases (3.3%), massive liver necrosis of 3 cases, liver fibrosis of 2 cases, congestive liver of 1 case, and unclassified 12 cases due to inadequate specimens or other reasons. Among 488 viral hepatitis cases, histological stages were as follows; acute hepatitis (38 cases, 7.8%), persistent hepatitis (23 cases, 4.7%), chronic inactive hepatitis (142 cases, 29.1%), chronic active hepatitis (165 cases, 33.8%), chronic hepatitis with subloblar necrosis (33 cases, 6.8%), precirrhosis (51 cases, 10.5%), cirrhosis (27 cases, 5.5%). The relationship between histological aspects and clinical features was discussed by sex, age, and others. Of 41 follow up cases, significant values of histological type, presence of HB ag., or alcoholic were discussed as for the causative factors evolving liver cirrhosis.
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PMID:[Chronic hepatitis--clinicopathological studies of 687 cases (author's transl)]. 46 98

We present pathologic findings for 52 livers (51 autopsy specimens and one wedge biopsy specimen) from patients with systemic lupus erythematosus (SLE). Hepatic congestion was the most common disease (40 livers), followed by fatty liver (38), arteritis (11), cholestasis (nine), peliosis hepatis (six), chronic persistent hepatitis (six), nonspecific reactive hepatitis (five), cholangiolitis (four), nodular regenerative hyperplasia of the liver (three), and hemangioma (three). The data obtained here suggest that arteritis of the SLE liver is more common than has been recognized previously. One patient had hepatic infarction complications induced by arteritis. On the basis of the findings in the present study and a review of the literature, we suggest that hepatic infarction resulting from arteritis is rare in SLE. On the other hand, while occurrence of nodular regenerative hyperplasia of the liver in SLE patients has been considered to be rare, our findings suggest that it may be more common than has been recognized previously. Although congestion and cholestasis may be acute terminal illnesses, fatty change is considered to be specific to the SLE liver. Statistical analysis indicates that exposure to a large dosage of glucocorticoids is a significant factor in the etiology of severe fatty liver. In addition, our review of Japanese autopsy registry data for 1,468 patients with SLE indicates that the incidence of chronic liver diseases in SLE autopsy cases is as follows: chronic hepatitis, 2.4%; cirrhosis, 1.1%; and liver fibrosis, 0.8%.
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PMID:The liver in systemic lupus erythematosus: pathologic analysis of 52 cases and review of Japanese Autopsy Registry Data. 139 43

To clarify the effect of the pathological state of the liver on ultrasonic attenuation, we produced two experimental rabbit models. The influence of fat on ultrasonic attenuation was examined using a fatty liver model without liver fibrosis, and that of fibrosis on attenuation using a liver fibrosis model without fatty infiltration. Ultrasonic data were obtained in vivo directly from the liver, and an acoustic attenuation coefficient slope was obtained by the spectral difference method. Tissue components of the liver, namely the total lipid, hydroxyproline and water contents, were measured precisely by quantitative methods. We revealed that ultrasonic attenuation depends mainly on fatty infiltration of the liver and to a lesser extent on fibrosis, but not on the water content.
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PMID:Dependence of ultrasonic attenuation of liver on pathologic fat and fibrosis: examination with experimental fatty liver and liver fibrosis models. 144 Sep 87

Five alcoholics with chronic liver disease showed focal low density areas of the liver that varied in distribution on computed tomography (CT) but no corresponding lesions on ultrasonography. The densities of these areas on CT were much lower than that of spleen. All the areas disappeared 2 days to 4 weeks after patients entered the hospital, suggesting that they were focal areas of fatty liver. Four patients had liver cirrhosis and one liver fibrosis. These observations may add further evidence to our previous finding that increased echogenecity of the liver produced by fatty infiltration is attenuated by complicating fibrosis.
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PMID:Loss of echogenic lesion of focal fatty infiltration in fibrotic liver. 192 46

Liver fibrosis was observed in non-alcoholic, non-diabetic obese patients with fatty liver. The extent of fibrosis was more severe in patients who were obese for a long time and had severe fatty deposition in the liver. Laboratory data were not useful for differentiating between fatty livers with and without liver fibrosis. The results suggested that fatty liver in obese patients should be treated by weight reduction in order to prevent the progression of liver fibrosis.
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PMID:Liver fibrosis in obese patients with fatty livers. 262 18

Techniques are reviewed for the experimental feeding of alcohol, including a liquid diet procedure invented 25 years ago. This technique results in much higher ethanol intake than with other approaches. As a consequence, various complications observed in alcoholics can be reproduced in animal models. These include fatty liver, hyperlipemia, various metabolic and endocrine disorders, tolerance to ethanol and other drugs, physical dependence and withdrawal and, in the baboon, liver fibrosis and cirrhosis. Variations of the liquid diet formulation are compared, and adequacy of nutrition in terms of minerals, vitamins, lipotropes, carbohydrates and proteins is discussed. The importance of selecting proper controls is emphasized. The respective advantages of three standardized basic rat formulas are reviewed: (i) an all-purpose (35% fat) diet, comparable to the diet previously referred to as the "Lieber-DeCarli formula" and suitable for most experimental applications, particularly those intended to mimic the clinical situation in which the various effects of alcohol occur in the setting of hepatic changes characterized by a fatty liver; (ii) a low-fat diet comparable in all respects to the preceding diet but with a lower fat content, intended to minimize the hepatic changes, and (iii) a high-protein formula particularly useful in those circumstances in which an oversupply of dietary protein might be recommended (i.e. pregnancy). Variations of this technique, including continuous intragastric infusion, are also discussed. It is concluded that, for most experimental studies of chronic alcohol consumption, the liquid diet technique provides one of the most efficient tools to study the effects of ethanol under controlled nutritional conditions because it allows for alcohol consumption of clinical relevance and offers flexibility to adjust to special experimental or physiologic needs by allowing for various substitutions required for a particular experimental design, including changes in lipids, proteins or other dietary constituents. The technique also facilitates the comparison with controls by simplifying the pair feeding and is the best procedure available for the study of the toxic effects of alcohol and their interactions with deficiency or excess of various nutrients.
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PMID:Experimental methods of ethanol administration. 267 71

Histopathological analysis for 94 Japanese alcoholic patients revealed alcoholic hepatitis 11%, chronic hepatitis 14%, fatty liver 16%, alcoholic liver fibrosis 22% and liver cirrhosis 31%. Alcoholic hyaline was found in only 30% of the cases of alcoholic hepatitis. Alcoholic liver fibrosis (without any findings except fibrosis and steatosis) was distinct from other type of diseases. Chronic hepatitis in alcoholics was mostly chronic active hepatitis (77%), whereas only 35% was chronic active hepatitis in nonalcoholics. Histologically typical alcoholic liver cirrhosis was uncommon.
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PMID:Characteristic features of liver disease in Japanese alcoholics. 407 6

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

Microsomal UDP-glucuronosyltransferase activity toward the bile acids (chenodeoxycholic, deoxycholic, ursodeoxycholic, lithocholic, and glycolithocholic) has been detected in human specimens of liver, kidney, and intestinal mucosa. The characteristics of hepatic and extrahepatic UDP-glucuronosyltransferase activities toward these bile acids were compared with respect to kinetic parameters and other catalytic properties. Whereas no organ-specific differences in the affinities of individual bile acids to hepatic and extrahepatic UDP-glucuronosyltransferases were observed, the individual bile acids showed reaction rates in liver that were about twice the rates estimated in kidney and about twice to three times the rates observed in duodenal mucosa. In intestinal mucosa the rate of chenodeoxycholic acid glucuronidation exhibited a progressive decrease from duodenum to colon, where it was 30% of the duodenal level. Comparison of the glucuronidation rates that were estimated with different bile acids in hepatic or extrahepatic tissues showed that for each organ a bile acid structure-activity relationship existed, with highest activity observed for lithocholic and ursodeoxycholic acids, which was about twofold higher compared with chenodeoxycholic or deoxycholic acids. Lowest activity was estimated for glycolithocholic acid. UDP-glucuronosyltransferase activity toward chenodeoxycholic acid was studied in biopsy specimens of liver that were obtained from a large group of patients with the following liver diseases: liver cirrhosis, liver fibrosis, granulomatous hepatitis, fatty liver hepatitis, and fatty liver. A significant decrease in enzyme activity was observed in patients with liver cirrhosis and in patients with granulomatous hepatitis compared with patients without liver disease.
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PMID:Hepatic and extrahepatic glucuronidation of bile acids in man. Characterization of bile acid uridine 5'-diphosphate-glucuronosyltransferase in hepatic, renal, and intestinal microsomes. 643 Sep 60


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