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)

We studied Gm typing of serum samples from 838 donors; 177 had chronic hepatitis, 166 liver cirrhosis, 113 primary hepatocellular carcinoma, 21 alcoholic hepatitis, 18 fatty liver and 343 were unrelated normal blood donors. The distribution of Gm phenotypes and haplotypes in sera from patients with primary hepatocellular carcinoma differed from that in the normal controls; the Gm phenotype (1,2,21,13,15,16) and the haplotype Gm1,2,21 were significantly more common in this patient group (X2 = 18.56, corrected P less than 0.01, relative risk = 3.12; X2 = 25.52, corrected P less than 0.005, respectively). Overall, in the other liver diseases, we observed no significant Gm phenotype or haplotype association. The commitment to progression to primary liver carcinoma seems to be ascribable to a gene or polygenes close to the IgG heavy chain loci.
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PMID:Primary hepatocellular carcinoma and IgG heavy chain allotypes. 630 57

This study was carried out in order to assess the value of ultrasonography in the diagnosis of cirrhosis. One hundred patients were studied within 2 weeks of the histological diagnosis of the liver disease (cirrhosis 49, acute or chronic hepatitis: 23, fatty liver: 16, normal liver: 12). Ultrasonic patterns were classified by a second examiner according to 5 hepatic criteria (volume, outline, echogenicity, attenuation of the ultrasound beam, enlargement of caudate lobe) and 3 extrahepatic criteria (dilatation of the portal vein, ascites, splenomegaly), leading to a ultrasonic diagnosis. Cirrhosis was diagnosed in 36 out of 49 patients (73 p. 100) by the echographist whereas clinical and biological data lead to diagnosis in only 27 out of these 49 patients (P = 0.057). Hepatocellular carcinoma was diagnosed only in 2 out of 5 patients. Splenomegaly (0.60) and caudate lobe enlargement (0.59) were the signs whose predictive value was the best for this group of patients. The ratio thickness of caudate lobe/global hepatic thickness (as measured on a sagittal cut through the inferior vena cava) allowed for easy assessment of caudate lobe size. The mean value of this ratio was significantly different (P less than 0.001) in the cirrhotic group (0.38 +/- 0.07) when compared to the non-cirrhotic one (0.28 +/- 0.06). Ratios greater than 0.35 were not seen in subjects with normal livers, nor were ratios greater than 0.40 seen in non-cirrhotic patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Evaluation of ultrasonography in the diagnosis of cirrhosis. Retrospective studies of 100 consecutive tests]. 661 77

Lipids of HDL (high density lipoproteins) and their subfractions (HDL2 and HDL3), and LCAT activity (lecithin: cholesterol acyltransferase) were determined in hepatobiliary diseases without severe hyperbilirubinemia (less than 10 mg/dl). The decrease in major lipid constituents (cholesterol and phospholipids) of HDL was mainly attributable to the decrease in those of HDL3, except in some liver diseases of acute or severe stage (acute hepatitis in an acute stage and hepatoma) which were accompanied with a simultaneous moderate decrease in those of HDL2 and in fatty liver which showed a preferential decrease in those of HDL2. The LCAT activity also decreased in several diseases. Some of the hepatobiliary diseases, on the contrary, showed an increase in HDL-triglycerides (mostly in HDL3 and in some diseases also in HDL2) which might participate to some extent in secondary hyperlipidemia in the liver parenchymal diseases, although they were the minor lipid constituents of HDL. From results that HDL3- but not HDL2-cholesterol levels significantly correlated with serum total protein, albumin and choline esterase, it was suggested that the decrease in large constituents of HDL, particularly of HDL3, is caused by hepatocellular dysfunction which causes inhibition of protein and lipid syntheses in the liver in most of the hepatobiliary diseases except for fatty liver which has a preferential decrease in HDL2 lipids.
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PMID:Changes in high density lipoproteins in patients with hepatobiliary diseases. Levels and lipid composition of HDL2 and HDL3 and LCAT reaction. 685 43

Six main types of histopathological changes were found in 463 patients with chronic alcoholism admitted during the 10-year period from 1966 to 1975: group I, normal liver in 2.6%; group II, fatty liver in 8.4%; group III, acute alcoholic hepatitis (AAH) in 7.6%; group IV, cirrhosis with or without steatosis in 68.7%; group V, cirrhosis with AAH in 12.8%; group VI, liver cell carcinoma (LCC) in 1.9% (all of the latter patients were also included in group IV). Seventy-three % were males and 27% were females. Females tended to be older than males. Cirrhosis was found in 68% of the group between 21 and 30 yr and in 85% between 51 and 60 yr. Normal histology or steatosis was less frequent after the age of 50 yr. Ascites and jaundice were more frequent in patients with AAH than in patients with steatosis. The majority of patients had SGOT under 100 karmen units/ml; SGPT was normal in 80% of patients with cirrhosis and higher than 100 karmen units/ml in 10%. SGPT was higher than SGOT in only 11.9% of the patients. Mortality was 46.7% according to the followup until 1978. Survival was 38.4% at the end of the first year and decreased very slowly afterwards to 32.8% in males and 11.5% in females after a 5-yr period.
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PMID:Alcoholic liver diseases in Portugal. Clinical and laboratory picture, mortality, and survival. 704 74

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

Rats fed a choline deficient diet develop foci of enzyme-altered hepatocytes with subsequent formation of hepatic tumors. This is the only nutritional deficiency that, in itself, causes cancer. We suggested that carcinogenesis is triggered, in part, because of abnormalities in cell signals which regulate cell proliferation and cell death. Because choline deficient rats develop fatty liver (choline is needed for hepatic secretion of certain lipoproteins), we examined whether an important lipid second messenger involved in proliferative signaling, 1,2-sn-diacylglycerol, accumulated in liver and resulted in the prolonged activation of protein kinase C. We observed that 1,2-sn-diacylglycerol accumulated in the plasma membrane from the non-tumor portion of livers of rats fed a choline deficient diet, and that unsaturated free fatty acids, another activator of protein kinase C, also accumulated in deficient livers. Protein kinase C in the hepatic plasma membrane and nucleus of choline deficient rats was elevated for months; this is the only model system which exhibits such prolonged activation of protein kinase C. Premalignant, abnormal hepatic foci were detected only in the deficient rats, and 15% of deficient rats (none of the controls) had hepatocellular carcinoma at 1 year on the diet. In rats, an early event in choline deficiency is an increase in the rate of cell death. In liver from choline deficient rats, we observed an increase in the numbers of liver cells with fragmented DNA (characteristic of programmed cell death; apoptosis). We used a cell culture model (immortalized rat hepatocytes) to study the effects of choline deficiency on apoptosis. Liver cells grown in a choline deficient medium became depleted of choline, accumulated triacylglycerol and 1,2-sn-diacylglycerol, and had increased DNA fragmentation and other morphologic and biochemical changes associated with apoptosis. This model has great potential as a tool for studying the underlying link between choline deficiency and the regulation of the balance between cell proliferation and cell death. We suggest that choline deficiency altered the cell proliferation signals mediated by protein kinase C within liver, and altered cell apoptosis. These changes in cell signaling may be the triggering events which result in hepatic carcinogenesis.
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PMID:Choline and hepatocarcinogenesis in the rat. 764 29

Recently, the multicentric origin of hepatocellular carcinoma (HCC) has been recognized, but its clinical importance has still not yet been clarified. The histological characteristics of small hyperechoic HCCs coexisting in 44 consecutively resected Japanese patients whose main HCCs were < 5.0 cm in size were studied. Twelve small hyperechoic HCCs were found and classified into the following two groups: eight nodules in seven patients (15.9%) were early-stage HCC, and four nodules in four patients (9.1%) were more advanced HCC. Thus, early-stage HCC comprised 66.7% of the small echogenic HCCs. Eight HCCs detected as small hyperechoic lesions (found in 15.9% of the patients) showed varying degrees of fatty change yet proved to be well differentiated and retained the preexisting liver structure of either associated liver cirrhosis or chronic hepatitis. Moreover, the histologic characteristics of the eight early-stage HCCs were different from those of the main HCCs. In conclusion, approximately 15% of HCCs in Japanese patients may have a synchronous multicentric origin, and small hyperechoic lesions should be carefully evaluated. However, in the United States or other areas where the occurrence of fatty liver is common, that advice for small hyperechoic lesions may be overly cautious.
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PMID:Synchronous multicentric development of hepatocellular carcinoma. 766 19

The authors investigated the epidemiology of hepatitis C virus (HCV) related to liver diseases in Korea. Anti-HCV was studied by EIA in sera from patients with chronic liver diseases (CLD), individuals at high risk, healthy individuals, and family members of patients with CLD. We also evaluated the efficacy of a new anti-HCV assay kit, HCD EIA, consisting of 3 recombinant peptides derived from CORE, NS3 and NS5 regions of the HCV genome, for screening HCV infection. The prevalence of anti-HCV in HCD EIA was 15.4% of 1055 cases studied, while that in the anti-C100-3 EIA was 11.1%. The incidence of anti-HCV in HCD EIA was 5.9% of 17 cases with acute hepatitis, 18.1% of 293 cases with chronic hepatitis, 24.1% of 79 cases with liver cirrhosis, 28.0% of 100 cases with hepatocellular carcinoma, 19.8% of 81 cases maintained with hemodialysis, 31.3% of 16 cases with blood dyscrasias, 4.4% of 114 cases with fatty liver, 1% of 100 healthy persons, 1.3% of 150 blood donors, and 6.2% of 97 family members from 26 patients with type C CLD. Familial HCV clustering was detected in 3 (11.5%) of 26 patients with anti-HCV(+) CLD. The prevalence of anti-HCV in 190 HBsAg positive CLD was 8.4%. The relative proportions of positive anti-HCV, HBsAg, both positive 17.4%, 40.7%, and 3.7%, respectively, while 38.2% of the cases were negative for both anti-HCV and HBsAg. The prevalence of anti-HCV among CLD increased significantly in relation to age (p < 0.05), and it became higher than that of HBsAg after age 60.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence of hepatitis C virus related to liver diseases in Korea. 768 3

Family history of hepatocellular carcinoma (HCC) has been identified as a risk factor of HCC. The pathogenesis is still uncertain. In order to evaluate the risk factors and to detect the small HCC. 721 asymptomatic family members (419 males and 302 females with a mean age of 40.21 years) of the index cases of HCC received a series of examinations including: serum GOT, GPT, alpha-fetoprotein (AFP). HBsAg, Anti-HCV, and abdominal ultrasonography (US). Of the 18 patients with liver tumor detected by US. 6 were proved to be HCC, 8 were hemangioma, and the nature of the rest was undetermined. The US found 22 with cirrhosis, 24 with chronic liver disease, 133 with fatty liver, and 14 with a liver cyst. The incidence of HCC in our study was 0.96% in males (4 of 419 cases), and 0.66% in females (2 of 302 cases) which was much higher than that in the general population of Taiwan (0.025% in males and 0.01% in females). The positive rate of HBsAg in the participants, including all the newly detected HCC patients, was 46.5% (335 cases) which was also higher than the prevalence in Taiwan (15-20%). Male, sibling and liver cirrhosis seemed to have higher risk. These results suggest that family members of patients with HCC have a high risk of developing HCC. The hepatitis B virus may be the most important link. Early diagnosis is possible by screening the family members by means of AFP and abdominal US.
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PMID:Risk factors of hepatocellular carcinoma with familial tendency. 776 61

We developed a sensitive enzyme-linked immunosorbent assay (ELISA) for serum ornithine carbamoyltransferase (OCT) protein, and examined serum OCT concentrations in patients with various liver diseases. OCT concentrations were markedly elevated in cases of hepatic encephalopathy, 'acute on chronic', and those with the acute phase of acute hepatitis, moderately in chronic hepatitis, liver cirrhosis, hepatocellular carcinoma, primary biliary cirrhosis, and slightly in those with a fatty liver. High percentages (92-98%) of patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma had higher than normal concentrations of serum OCT protein. There was a close correlation with aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and moderate correlations with those of mitochondrial AST, glutamate dehydrogenase and gamma-glutamyltranspeptidase. The OCT/ALT ratio was higher in patients with liver cirrhosis than in those with chronic hepatitis (p < 0.001), and was still higher in cases of hepatocellular carcinoma (p < 0.05). In 2 patients with 'acute on chronic' disease, OCT concentrations decreased similarly with or more rapidly than AST or ALT activities after admission. In 2 patients with hepatic encephalopathy, the OCT concentrations changed similarly with AST and ALT activities. This OCT ELISA system will aid in diagnosing various liver diseases and in the follow-up of the patients, and the OCT/ALT ratio may serve for a differential diagnosis of liver diseases.
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PMID:Clinical evaluation of serum ornithine carbamoyltransferase by enzyme-linked immunosorbent assay in patients with liver diseases. 778 67


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