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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report presents results of studies using the spectral-shift zero-crossing method to measure frequency-dependent attenuation (FDA) in normal liver and spleen and in diseased liver. We developed a new system for attenuation analysis that calculated FDA in dB/cm/MHz according to the following equation: (formula: see text). Data are collected from the region of interest on the scan image. Graphite-gel phantoms of known attenuation value are used to create a high degree of accuracy in this new system. Mean attenuation of normal livers was 0.55 +/- 0.05 dB/cm/MHz, while that of normal spleen was 0.37 +/- 0.06 dB/cm/MHz. No correlation between FDA and age could be seen. FDA was 0.81 +/- 0.17 dB/cm/MHz in fatty liver, 0.63 +/- 0.13 dB/cm/MHz in liver cirrhosis, and 0.64 +/- 0.12 dB/cm/MHz in chronic hepatitis. These values are higher than those obtained from normal liver, while tumor masses in the liver (hepatocellular carcinoma, hepatoblastoma, hemangioma) and diffuse infiltration by malignant lymphoma produced lower than normal values, averaging 0.38 +/- 0.08 dB/cm/MHz.
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PMID:Studies on frequency-dependent attenuation in the normal liver and spleen and in liver diseases, using the spectral-shift zero-crossing method. 315 99

The usefulness of ultrasound and echo-guided fine-needle biopsy (FNB) in the diagnosis of focal fatty liver change (FFLC) is stressed, on the basis of a retrospective series of 21 patients (8 of whom with a past history of primary cancer), followed-up for a mean period of 13.7 months. FFLC presented with various echographic patterns, shapes, dimensions and localizations. In 17 patients the diagnosis of FFLC was made by FNB, yielding cytologic and/or histological samples with steatotic, but also normal, hepatocytes. In another 4 patients the diagnosis was made by echographic follow-up. In all patients, clinical, hematological and echographic follow-up excluded the onset of neoplastic disease, confirming the high specificity of FNB in diagnosing FFLC. The possibility of changing appearance over time, and the inconstant correlation of FFLC with known causes of hepatic steatosis are discussed, as well as the hypothesis that the focal defect seen with ultrasound, could be an area of normal hepatic tissue in a fatty liver. The authors affirm the necessity to perform FNB on each doubtful lesion, but certainly when the patient has a history of malignancy.
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PMID:Ultrasonography and echo-guided fine-needle biopsy in the diagnosis of focal fatty liver change. 331 51

Resectability was studied in relation to both the functional reserve of the liver or pancreas and radicality in 112 cases of primary liver cancer and 34 cases of pancreatic head cancer resected in our department over an 11-year period. 1. Primary liver cancer: In extended hepatectomy including one segment beyond the tumor-bearing area, recurrence rate was low with a high long-term survival rate of more than 3 years, although hepatic insufficiency occurred frequently. In limited resection of the segment of the tumor or enucleation, many patients died due to recurrence within 2 years, except for those with small liver cancers. 2. Pancreatic head cancer: Extended surgery especially total pancreatectomy, had higher radicality with a higher 3-year survival rate than for the standard operation, even in case of advanced stage III or IV cancer. However, extended surgery produced a high incidence of postoperative fatty liver due to disturbance of pancreatic exo- and endocrine function, and severe diarrhea following dissection of the nerve plexus. Therefore, it is necessary to select a suitable operative method upon consideration of both radicality and functional reserve of the liver or the pancreas.
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PMID:[Resectability of primary carcinoma of the liver and pancreas, with special reference to radicality and functional reserve]. 338 89

A study of FAM (5-FU, ADM, MMC) hepatic infusion chemotherapy via the left subclavian artery was performed in 40 patients with liver metastasis from colorectal carcinoma. The response rate was 61.1% (1 CR and 21 PR among 36 evaluable cases), and the 50% survival period was 11.6 months. CT imaging in the 22 responders was discussed. The CT scan images showed no remarkable changes except for tumor size in 10 cases (45.5%), a decrease of marginal density in 4 cases (18.2%), an increase of calcification in 2 cases (9.1%), dimpling sign in 3 cases (13.6%) and fatty liver degeneration and abscess formation in the hepatic duct in 1 case (4.5%). These findings on CT scan were important for evaluating the effects and side effects in patients receiving hepatic infusion chemotherapy, and provided useful information for follow-up.
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PMID:[The effect and CT imaging of FAM hepatic infusion chemotherapy in patients with liver metastasis from colorectal carcinoma]. 363 74

The B6C3F1 strain of mice is prone to develop liver nodules as animals grow older. This spontaneous tumor development is enhanced by dietary lipotrope deficiency. The present studies were performed to evaluate the liver of the B6C3F1 mice in early periods of lipotrope deficiency and before the nodules appear. Mice were fed high levels of dietary fat (cotton seed oil or beef fat) without choline or vitamin B12. The livers of these mice were compared with those of mice subjected to partial hepatectomy or dietary phenobarbital both of which enhance liver nodule formation. The ability of putative preneoplastic hepatocytes to exclude parenteral-administered iron was used to detect this eventual phenotype. A lipotrope-deficient condition was established which typically exhibited fatty liver and increased cell proliferation, the latter measured by autoradiography. In the time periods evaluated the lipotrope-devoid diets were not sufficient to induce nodular or putative preneoplastic lesions. An excessively high activity of p-nitroanisole-O-demethylase and a single small fatty nodule were obtained when phenobarbital was added to the lipotrope-deficient diet. Scattered eosinophilic hepatocytes were seen in every experimental group when the histologic slides were stained for iron pigments, but their biologic significance in the present experiments could not be established. Under the conditions of this study, the liver of the B6C3F1 strain of mouse exhibited only minor indications of future tumor development.
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PMID:Early stages of nodular transformation of the B6C3F1 mouse liver induced by choline deficiency. 403 60

Focal fatty infiltration of the liver is an entity that may be confused with liver metastasis on computed tomography (CT). The imaging results and medical records of 16 patients with CT appearance suggestive of focal fatty liver were reviewed, three of whom had the simultaneous presence of metastatic liver disease. Focal fatty liver often has a distinctive appearance with CT, usually with a nonspherical shape, absence of mass effect, and a density close to water. Liver metastases are usually round or oval, and unless cystic or necrotic, they have CT attenuation values closer to normal liver parenchyma than water. A radionuclide liver scan almost always resolves any confusion about the differential diagnosis of focal fatty liver: a well defined focus of photon deficiency is due to neoplasm rather than focal fatty infiltration. Sonography sometimes helps to confirm the CT impression, but may be misleading if the diagnosis of focal or diffuse fatty infiltration is not suspected before the examination.
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PMID:CT appearance of focal fatty infiltration of the liver. 697 79

Ten patients with fatty liver, distinct from the well known diffuse alcoholic variety, comprise this report. All patients had an initial ultrasound examination followed by 99mTc-sulfur colloid liver and computed tomography (CT) body scans. Six patients had focal fatty infiltration producing a space-occupying mass within the liver. Four had ultrasound evidence of diffuse fat occurring in association with focal masses. These masses were all echo poor relative to the adjacent fat, and were subsequently found to represent nodules of normal uninvolved liver in two patients, and metastatic neoplasm and multiple liver cysts in single patients respectively. The clinical picture associated with fatty liver is variable and may include, in addition to alcohol abuse, obesity, malnutrition, exogenous glucocorticoids, diabetes mellitus, and other less well defined factors. Dramatic improvement in fatty liver occurred in two patients following appropriate therapy. The spectrum of changes produced by fatty infiltration of the liver on ultrasonic, radionuclide, and CT scans is extremely varied depending on the amount of fat deposition, its focal or generalized nature, and the presence of associated liver disease.
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PMID:Fatty infiltration of the liver--an imaging challenge. 716

The case report on an acute intrahepatic cholestasis caused by alcoholic intoxication in a 52-year-old medical laboratory assistant is given. In addition to extreme pathologic cholestasis parameters the increase of the tumor marker CA 19-9 was remarkable. By means of laparoscopy and histology, chronic fatty liver hepatitis due to alcoholic intoxication was found. The tumor marker CA 19-9 returned to normal following abstinence from alcohol parallel to the deline of the cholestasis parameters, which means the diagnostic importance of tumor markers in diseases with intrahepatic cholestasis is to be seen in relative terms.
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PMID:[Toxic alcohol-induced, acute intrahepatic cholestasis with reversible increase of the CA 19-9 tumor marker in chronic alcoholic hepatitis]. 748 17

Attenuation differences bordered by straight lines within the liver (the straight border sign) are sometimes seen at computed tomography (CT). This phenomenon, which was demonstrated with unenhanced CT over a dozen years ago, does not represent a hepatic mass and is often associated with vascular compromise. Major causes of the straight border sign include fatty liver, confluent fibrosis, radiation hepatitis, and vascular abnormalities such as tumor thrombus, thromboembolus, compression, and arterioportal shunt. The frequency of this finding increases when intense contrast enhancement is used, especially when contrast material is administered via the superior mesenteric artery (CT during arterial portography) or hepatic artery (CT arteriography). The use of spiral CT is apparently increasing the chances of encountering this sign in daily practice. To correctly interpret the straight border sign, one should consider the distribution (anatomic vs nonanatomic), the attenuation (low vs high), and the use and technique of contrast enhancement.
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PMID:Straight border sign of the liver: spectrum of CT appearances and causes. 750 52

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


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