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)

Thus, the pathologic consequences of feeding a CD diet are fatty liver, liver cell death, liver cell proliferation, and liver cell cancer. The fatty liver with CD is similar to that with other types of fatty liver in that the most attractive current hypothesis is based on some interference with the production and output of VLDL by the liver. The induction of cell death appears to be consistent with quite a different hypothesis, genesis and/or increase in liver free radicals leading to both acute necrosis and initiation of carcinogenesis. Especially noteworthy is the low incidence of liver cirrhosis, even after 2 years of exposure to the CD diet. The feeding of the CD diet reproducibly induces severe and persistent fatty liver coupled with extensive cell death, a combination that is frequently considered to be appropriate for the induction of "micronodular" (fatty) cirrhosis in humans. The findings with the LD diet, the high incidence of cirrhosis, with severe persistent fatty liver without significant cell death, together with the low incidence of cirrhosis with the CD diet, stand out as unpredictable and strange, according to current concepts of the pathogenesis of human cirrhosis. The CD model offers an unusual opportunity to explore in increasing detail the possible roles of free radicals in two important problems in pathology and medicine-acute cell injury and neoplasia. The challenges include mechanistic studies on how the free radicals are generated and how they relate to the biological consequences. The relatively slow sequential changes in the induction of cell injury and neoplasia makes the CD model one of the best for mechanistic studies relating to free radicals.
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PMID:Choline deficiency, lipotrope deficiency and the development of liver disease including liver cancer: a new perspective. 768 Jul 28

Liver fatty acid binding protein (L-FABP), a cytoplasmic 14 kDa protein previously termed Z protein, is conventionally considered to be an intracellular carrier of fatty acids in rat hepatocytes. The following evidence now indicates that L-FABP is also a specific mediator of mitogenesis of rat hepatocytes: a. the synergy between the action of L-FABP and unsaturated fatty acids, especially linoleic acid, in the promotion of cell proliferation; b. the specific requirement for L-FABP in induction of mitogenesis by two classes of nongenotoxic hepatocarcinogenic peroxisome proliferators (amphipathic carboxylates and tetrazole-substituted acetophenones); c. the direct correlation between the binding avidities of different prostaglandins for L-FABP and their relative growth inhibitory activities toward cultured rat hepatocytes; d. the temporal coincidences between the covalent binding to L-FABP by chemically reactive metabolites of the genotoxic carcinogens, 2-acetylaminofluorene and aminoazo dyes, and their growth inhibitions of hepatocytes during liver carcinogenesis in rats; e. and f. the marked elevations of L-FABP in rat liver during mitosis in normal and regenerating hepatocytes, and during the entire cell cycle in the hyperplastic and malignant hepatocytes that are produced by the genotoxic carcinogens, 2-acetylaminofluorene and aminoazo dyes. These actions of L-FABP are consistent with those of a protein involved in regulation of hepatocyte multiplication. Discovery that L-FABP, the target protein of the two types of genotoxic carcinogens, is required for the mitogenesis induced by two classes of nongenotoxic carcinogens points to a common process by which both groups of carcinogens promote hepatocyte multiplication. The implication is that during tumor promotion of liver carcinogenesis, these genotoxic and nongenotoxic carcinogens modify the normal process by which L-FABP, functioning as a specific receptor of unsaturated fatty acids or their metabolites, promotes the multiplication of hepatocytes.
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PMID:Modulation of mitogenesis by liver fatty acid binding protein. 771 94

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

Liver metastasis located at the confluence of the major hepatic veins developed after an operation for sigmoid colon carcinoma in a 63-year-old patient. Curative resection of the tumor was performed by in situ hypothermic perfusion of the liver and extracorporeal circulation. Intra-abdominal bleeding occurred on the first postoperative day, and ligation of the right inferior phrenic artery was performed via an emergency laparotomy. Only mild elevation of ALT and recovery of the arterial ketone body ratio to the "safety zone" was noted on the second postoperative day. Hepatic function gradually deteriorated after the 4th postoperative day with no distinct cause. Diffuse fatty liver was suspected as a cause of liver failure. The patient died on the 31st postoperative day. The problems encountered in this case are discussed in this paper.
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PMID:Hepatectomy with extracorporeal circulation for liver metastasis from colon carcinoma located at the confluence of the major hepatic vein: a case report. 805 3

It is assumed that hepatobiliary, cell-specific contrast agents will be adversely affected by the presence of diffuse liver disease. The diagnostic efficacy for tumor detection in the presence of fatty liver disease was experimentally studied at contrast-enhanced magnetic resonance (MR) imaging with manganese-DPDP (N,N'-dipyridoxylethylenediamine-N,N'-diacetate 5,5'-bis[phosphate]) and gadobenate dimeglumine (Gd-BOPTA/dimeg) and compared with conventional and chemical shift imaging. Carcinosarcoma was implanted into the liver of rats, and fatty liver was induced with L-ethionine. Without contrast agents, the tumor-fatty liver contrast-to-noise ratio (C/N) was increased on T1-weighted and decreased on T2-weighted MR images relative to tumor-bearing control rats without fatty liver. Chemical shift imaging (phase-contrast method) increased the tumor-fatty liver C/N from 2.3 +/- 1.0 to 6.1 +/- 1.7 (P < .001). Mn-DPDP and Gd-BOPTA/dimeg increased the tumor-fatty liver C/N from -5.4 +/- 1.6 to -11.0 +/- 1.9 and -9.8 +/- 3.4, respectively (P < .001). The hepatobiliary, cell-specific contrast agents were equally effective in both fatty and non-fatty liver and outperformed both chemical shift and conventional MR imaging in detecting liver tumors.
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PMID:Enhanced tumor detection in the presence of fatty liver disease: cell-specific contrast agents. 806 31

Two cases of hepatic metastatic tumor occurring in irregular fatty liver are reported. These metastatic tumors appeared as irregularly shaped hyperdense areas and were difficult to distinguish from focally spared areas of irregular fatty liver. Even if areas of focal sparing are irregular in shape, hepatic tumors should be carefully ruled out in patients at high risk for liver tumors.
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PMID:Metastatic tumors in irregular fatty liver mimicking focal sparing. 807 6

A prospective study of computed tomographically guided core needle biopsy samples was done to determine whether diagnostic accuracy could be improved in these specimens. Eighteen specimens from 16 patients were analyzed by routine and immunohistochemical stains on paraffin-embedded tissue and DNA probe hybridization on frozen tissue. Pathologic diagnoses based on light microscopy and immunostaining were malignant lymphoma (8), lymphoid tissue (1), malignant tumor (3), fibrous tissue (2), fatty liver and hepatic adenoma (2), giant cell tumor (1), and necrotic tissue (1). Analyzable DNA was obtained from nine specimens (50%); 67% of those yielding insufficient DNA (six of nine) were samples of benign liver, connective tissue, and necrotic tissue. Extracted DNA was hybridized with probes for JH, JK, CT beta, and bc/II. In 67% of analyzable cases (six of nine) the diagnosis of lymphoma was confirmed; in 33% the diagnosis of lymphoma or nonlymphoma was aided or resolved when the pathologic diagnosis was uncertain. Of the eight cases of lymphoma diagnosed by light microscopy, six were confirmed by genotyping and two yielded insufficient DNA for analysis. In all nine cases with sufficient DNA, hybridization identified B-cell monoclonality and confirmed or excluded follicular center cell origin, data not uniformly obtained with other studies. Molecular analysis can be a useful adjunct to routine methods of diagnosis of needle specimens, improving diagnostic accuracy in at least one-third of cases.
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PMID:Improved diagnostic accuracy in needle biopsy interpretation using molecular probes. 815 41

Tissue characterization of different pathologies of the liver can be achieved by differences of relaxation time on changing of pulse sequences in magnetic resonance imaging (MRI). The usefulness of MRI for detection of liver disease is limited when the pathological change is subtle. Chemical shift is a fundamental characteristics in nuclear magnetic resonance (NMR). Chemical shift imaging (CSI) in MRI is based on the different Larmor frequency of proton in water and fat; and therefore it was able to enhance the effectiveness of pathology. For this study, Dixon's method was used to detect liver pathologies and compare its detectability with conventional pulse sequences. Forty cases were enrolled for study; they included 5 health volunteers, 15 hepatomas, 1 cholangiocarcinoma, 5 metastatic hepatic tumors and 14 fatty livers. In hepatic tumors, the lesion number, tumor margination and lesion-to-liver contrast in images were read and analyzed. Signal intensities, signal-to-noise ratio and contrast-to-noise ratio were compared, after measurement, from stored data. In fatty livers, the relative change of signal intensities in different areas of the liver in in-phase and out-phase images were compared with the back muscle and spleen to find where the fatty metamorphosis happened. CSI in spin echo or gradient echo pulse sequences was found to be adequate and valuable for detecting fatty liver, when compared with conventional MRI. CSI not only identified the extension of disease itself but also characterized the fatty change in liver parenchyma. Though CSI affords no further advantages than conventional pulse sequences for detection of hepatic tumors, occasionally, when the image quality of the conventional pulse sequences is not satisfactory or equivocal in lesion detection, the use of CSI might be attempted.
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PMID:[The chemical shift imaging of liver]. 825 59

Asymptomatic patients with abnormal results on liver function test pose a diagnostic challenge. In general, determinations of routinely ordered tests of liver function are neither sensitive nor specific for liver disease. Fatty liver, alcohol-related liver damage and chronic viral hepatitis are the most common causes of abnormal liver function test results in asymptomatic patients. Causes of asymptomatic liver disease include hemochromatosis, Wilson's disease, drug toxicity, chronic autoimmune hepatitis, biliary cirrhosis, sclerosing cholangitis, alpha1-antitrypsin deficiency and sarcoidosis. The most efficient screening tests for liver damage are alanine transaminase, alkaline phosphatase and bilirubin. Repeat testing when results are abnormal, and use of ancillary tests, such as creatine phosphokinase or gamma-glutamyl-transferase, may confirm liver damage. Imaging studies help exclude biliary obstruction or neoplasm. Treatable illnesses should be ruled out. Three to six months of observation for progressive symptoms and liver dysfunction may follow. After the period of observation, further laboratory tests, a diagnostic liver biopsy and/or referral to gastroenterologist may be needed.
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PMID:Evaluating asymptomatic patients with abnormal liver function test results. 862 23

Valine-depleted amino acid imbalance solution markedly inhibits tumor growth but causes fatty liver as a side effect. However, much remains unknown about the mechanism of the development of fatty liver. Valine-depleted amino acid imbalance solution containing various concentrations of calories was administered to tumor-bearing rats for four days by means of total parenteral nutritional methods to investigate the interaction of caloric intake and the development of fatty liver. Compared with the total parenteral nutrition control group the triglyceride content of the liver rose significantly in the group given valine-depleted amino acid imbalance solution with an increase in caloric intake. Plasma total protein and albumin significantly decreased. The very-low-density lipoprotein concentration in serum was also significantly lower than that in the control group. Valine-depleted amino acid imbalance caused hypoproteinemia, suggesting a fall in synthesis of apolipoproteins in the liver indispensable for lipid release. Along with the increase in the total caloric intake, triglyceride synthesis in the liver increased, resulting in augmentation of fatty content of the liver, probably because of the decreased lipid release.
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PMID:Effects of caloric intake on anticancer therapy in rats with valine-depleted amino acid imbalance. 920 Jan 58


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