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 present a rare case of posterior mediastinal ganglioneuroma with fat tissue. A 50-year-old man visited our Department of Internal Medicine because of hypertension and fatty liver. On screening with abdominal CT a soft tissue tumor was found in the posterior mediastinum. CT and MRI revealed that the tumor appeared to have an abundant fatty component. To obtain a definitive diagnosis, the tumor was resected thoracoscopically. The histological diagnosis was ganglioneuroma. A ganglioneuroma containing a fat component has rarely been reported after cross-sectional imaging. We infer that the tumor may have resulted from spontaneous regression, with subsequent infiltration of adipose tissue from the posterior mediastinum.
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PMID:[A case of posterior mediastinal ganglioneuroma with fat tissue]. 1182 37

Development of hepatocellular carcinomas in rats caused by a choline-deficient, L-amino acid-defined (CDAA) diet, usually associated with fatty liver, fibrosis, cirrhosis and oxidative DNA damage, has been recognized as a useful model of hepatocarcinogenesis caused by endogenous factors. In the present study, in order to further explore involved factors and genes, we established an equivalent model in spontaneous liver tumor-resistant C57BL/6J mice. Six-week-old males and females were continuously fed the CDAA diet and histological liver lesions and oxidative DNA damage due to 8-hydroxydeoxyguanosine (8-OHdG) were examined after 22, 65 and 84 weeks. In male mice, fatty change and fibrosis were evident at 22 weeks, and preneoplastic foci of altered hepatocytes were seen at an incidence of 8/8 (100%) and a multiplicity of 6.6 +/- 4.0 per mouse at 65 weeks. Hepatocellular adenomas and carcinomas developed at incidences of 16/24 (66.7%) and 5/24 (20.8%), and multiplicities of 1.42 +/- 1.32 and 0.29 +/- 0.62, respectively, at 84 weeks. The female mice exhibited resistance to development of these lesions. The CDAA diet also increased 8-OHdG levels in male but not female mice. These results indicate that a CDAA diet causes hepatocellular preneoplastic foci, adenomas and carcinomas associated with fibrosis and oxidative DNA damage in mice, as in rats, providing a hepatocarcinogenesis model caused by endogenous factors in mice.
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PMID:Development of hepatocellular adenomas and carcinomas associated with fibrosis in C57BL/6J male mice given a choline-deficient, L-amino acid-defined diet. 1185 75

Localized, abnormal attenuation/intensity areas on unenhanced and/or enhanced study of CT/MR imaging do not necessarily correspond to tumors themselves or real tumor size. Pitfalls in the diagnosis of liver tumor are described dividing into enhanced study (vascular variants, vascular abnormalities, hyperplastic nodules, around the tumor, and miscellaneous) and unenhanced study (fatty change, focal spared area of diffuse fatty liver, and miscellaneous).
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PMID:Pitfalls in liver imaging. 1197 63

Diffuse fatty degeneration often occurs after pancreaticoduodenectomy due to altered lipid metabolism and nutritional malabsorption. Focal fatty change of the liver is characterized by a well-demarcated region, and the pathogenesis remains unclear. A 60-year-old woman underwent pancreaticoduodenectomy for bile duct cancer 10 years before. During follow-up, an intrahepatic tumor was detected in the lateral segment in the liver. The differential diagnosis included cholangiocarcinoma and metastatic tumor on images of plain computed tomography, ultrasonography, and magnetic resonance angiography. The patient underwent lateral segmentectomy of the liver. The tumor was a soft yellow mass, and histological examination indicated focal fatty liver. It was thought that the fatty liver was caused by localized low blood supply and dysabsorption of lipoprotein after pancreaticoduodenectomy.
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PMID:Focal fatty liver after pancreaticoduodenectomy: a case report of a rare entity of intrahepatic tumor. 1214 8

The role of imaging in screening and evaluation of cirrhotic patients is to assess the extent of cirrhosis and portal hypertension (liver morphology, varices, ascites, vessel patency) and to detect hepatocellular carcinoma (HCC). Ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI) have valuable roles, with catheter angiography usually reserved for specific problem solving. Ultrasonography is highly operator-dependent, and detection of focal masses is often difficult or impossible because of large patient body habitus and hepatic steatosis and fibrosis, which attenuate the ultrasound beam. For sonography, as well as CT and MRI, the use of intravenous contrast material with multiphasic imaging (arterial, portal venous, and delayed) is essential to accurately depict the morphology and hemodynamics of focal hepatic lesions. Computed tomography and MRI are highly accurate in diagnosis of large HCC but are much less accurate for lesions less than 2 cm in diameter. Many factors influence the choice and timing of imaging tests, including the etiology of the chronic liver disease, the elevation of serum tumor markers, and the availability and excellence of equipment and personnel. In our practice, helical multiphasic CT is obtained at least every 12 months, more frequently in patients judged to be at high risk for HCC.
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PMID:Use of radiologic techniques to screen for hepatocellular carcinoma. 1239 12

The fatty liver Shionogi (FLS) mouse is an inbred strain that develops spontaneous fatty liver (hepatic steatosis) chronically without obesity. Here, we reported that the mice develop spontaneous hepatocellular tumors with high incidences. The mice with age of over 1 year frequently developed whitish protuberant nodules in the livers, which were histologically diagnosed as hepatocellular adenoma and/or carcinoma (HCC). An incidence of HCC was 12/30 (40%) in males at 15-16 months of age, while in females that was 0/36 at 13-16 months and 4/42 (9.5%) at 20-24 months. Furthermore, histological examinations showed that after 2-4 months of age mononuclear cell infiltration and clusters of foamy cells appear in the fatty liver with elevated serum alanine aminotransferase, suggesting presence of inflammatory responses and liver injury. These observations show that the FLS mice develop hepatocellular tumors following steatohepatitis. The mouse might be a good animal model for investigating liver tumor and non-alcoholic steatohepatitis.
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PMID:Spontaneous development of hepatocellular carcinomas in the FLS mice with hereditary fatty liver. 1286 Feb 88

Although hepatitis C virus (HCV) is a well-known causative agent of hepatocellular carcinoma (HCC), the mechanism by which HCV induces HCC remains obscure. To elucidate the role of HCV in hepatocarcinogenesis, a model of hepatocyte injury was established using HCV core transgenic mice, which were developed using C57BL/6 mice transfected with the HCV core gene under control of the serum amyloid P component promoter. After 18-24 months, neither steatosis nor hepatic tumors were found in transgenic mice. The extent of hepatocyte injury and tumorigenesis were then examined in transgenic mice following repeated administration of carbon tetrachloride (CCl(4)) using various protocols (20%, 1/week; 10%, 2/week and 20%, 2/week). Serum alanine aminotransferase (ALT) levels did not differ among HCV core transgenic mice and non-transgenic littermates; however, after 40 weeks, hepatic adenomas preferentially developed in transgenic mice receiving 20% CCl(4) once weekly. Moreover, HCC was observed in transgenic mice receiving 2 weekly injections of a 20% solution of CCl(4), and was not observed in the non-transgenic control mice. In conclusion, the HCV core protein did not promote hepatic steatosis or tumor development in the absence of hepatotoxicity. However, the HCV core protein promoted adenoma and HCC development in transgenic mice following repeated CCl(4) administration. These results suggest that hepatotoxicity resulting in an increased rate of hepatocyte regeneration enhances hepatocarcinogenesis in HCV-infected livers. Furthermore, this experimental mouse model provides a valuable method with which to investigate hepatocarcinogenesis.
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PMID:Repeated hepatocyte injury promotes hepatic tumorigenesis in hepatitis C virus transgenic mice. 1290 92

MeCP2 is a member of a family of proteins [methyl- (cytosine-guanine)CpG-binding proteins] that bind specifically to methylated DNA and induce chromatin remodeling and gene silencing. Dietary deficiency of folate, choline and methionine causes decreased tissue S-adenosylmethionine concentrations (methyl deficiency), global DNA hypomethylation, hepatic steatosis, cirrhosis and ultimately hepatic tumorigenesis in rodents. We investigated the effects of this diet on expression of MeCP2 during pre-neoplastic transformation of liver tissue. After 9 weeks, MeCP2 mRNA level was slightly higher in methyl-deficient rats compared with replete controls, while after 36 weeks, a difference in MeCP2 mRNA level was no longer observed. In contrast, MeCP2 protein level was reduced almost 2-fold in the deficient rats compared with replete controls at both 9 and 36 weeks. Conversely, a second methyl-CpG-binding protein, MBD2, showed increased levels of both message and protein at the two time points. Low MeCP2 protein in the deficient rats was associated with a low level of the co-repressor protein, Sin3a, at 36 weeks. Moreover, a known gene target of MeCP2, the tumor suppressor gene metallothionein-I, was over-expressed in the deficient rat livers at both 9 and 36 weeks, suggesting that reduction in MeCP2 may have functional consequences. Methyl deficiency also caused an increase in the ratio of long to short variants of MeCP2 transcripts. This finding suggests that reduced MeCP2 protein level is the result of a reduced rate of translation. Reduction of MeCP2 protein expression may influence the initiation and/or progression of hepatic cancer induced by methyl deficiency and may provide a useful marker of pre-neoplastic change.
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PMID:Methyl deficiency causes reduction of the methyl-CpG-binding protein, MeCP2, in rat liver. 1294 43

We report a case of 19-year-old male with an underlying case of chronic hepatitis C infection who suffered from two types of benign liver tumor: focal nodular hyperplasia (FNH) and pseudotumor due to focal fatty spared area in a fatty liver. These two kinds of lesions rarely occur simultaneously. The spectral Doppler ultrasound (US) images of these lesions were also provided. We suggest that spectral Doppler US provides an alternative diagnostic tool for the differentiation of liver tumors regarding their vascular pattern, which might help ensure a correct diagnosis.
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PMID:Coexistence of focal nodular hyperplasia and pseudotumor caused by focal spared lesion in the liver of a young man. 1453 93

A primary or metastatic liver tumor sometimes blocks portal venous flow and causes a focal sparing in the fatty liver. We herein report a case of segmental sparing due to the portal tumor thrombus extending from the metastatic liver tumor. The present case demonstrates characteristic computer-associated tomographic findings, a distal oval hypodense tumor with proximal "crescent-shaped sparing", which may indicate underlying portal tumor thrombus at the apex of the sparing.
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PMID:A crescent-shaped sparing proximal to a liver tumor may indicate underlying portal tumor thrombus. 1457 2


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