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)

Immigration, cheap air travel, and globalization are all factors contributing to a worldwide spread of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection. End-stage chronic liver disease (ESLD) as a result of co-infection with HBV/HCV is now the major cause of death for individuals who have been infected with the HIV virus. The high incidence of HCV infection in Egypt--the legacy left from the mass use of tartar emetic to eradicate schistosomiasis, as in other high prevalence areas--will take years to reduce. Steatohepatitis due to non-alcoholic fatty liver disease is developing into a new and major health problem as a result of rising levels of obesity in populations worldwide. Hepatic steatosis also has an adverse influence on the progression of other liver diseases including chronic HCV infection and alcoholic liver disease. In many countries, considerable public concern is on the rise due to increased levels of alcohol consumption adversely affecting younger and affluent age groups. With the rising prevalence of cirrhosis, primary hepatocellular carcinoma (HCC) is increasing in frequency as is that of primary intrahepatic cholangiocarcinoma. Finally, despite the successes of liver transplantation, many deserving patients are not getting transplants due to low levels of cadaver organ donation in many countries, thereby increasing pressures on the use of living donor liver transplantation. Only through a concerted effort from governments, health agencies, healthcare professionals at all levels, and the pharmaceutical industry can this grim outlook for liver disease worldwide be reversed.
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PMID:Global challenges in liver disease. 1694 87

Cirrhosis and chronic liver failure are leading causes of morbidity and mortality in the United States, with the majority of preventable cases attributed to excessive alcohol consumption, viral hepatitis, or nonalcoholic fatty liver disease. Cirrhosis often is an indolent disease; most patients remain asymptomatic until the occurrence of decompensation, characterized by ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, or variceal bleeding from portal hypertension. Physical examination of patients with cirrhosis may reveal a variety of findings that necessitate a hepatic- or gastrointestinal-based work-up to determine the etiology. Some patients already may have had laboratory or radiographic tests that incidentally uncovered signs of cirrhosis and its comorbidities. No serologic or radiographic test can accurately diagnose cirrhosis. A significant correlation has been demonstrated between persistently elevated liver function tests and biopsy-proven underlying hepatic disease; thus, a more targeted serologic work-up is indicated in patients whose liver function test results are persistently abnormal. Unnecessary medications and surgical procedures should be avoided in patients with cirrhosis. Referral for liver biopsy should be considered only after a thorough, non-invasive serologic and radiographic evaluation has failed to confirm a diagnosis of cirrhosis; the benefit of biopsy outweighs the risk; and it is postulated that biopsy will have a favorable impact on the treatment of chronic liver disease.
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PMID:Cirrhosis and chronic liver failure: part I. Diagnosis and evaluation. 1739 87

As persons with HIV live longer, chronic liver disease is increasingly important. Nonalcoholic fatty liver disease (NAFLD) is characterized by excess fat in hepatocytes in patients without significant alcohol use. It can progress from steatosis to nonalcoholic steatohepatitis (NASH) to cirrhosis. Visceral obesity and insulin resistance are integral to the pathogenesis of NAFLD. Patients with HIV are at greater risk of NAFLD due to antiretroviral therapy and viral hepatitis coinfection. Antiretroviral therapy can lead to patterns of injury that include steatosis and NASH. Coinfection with hepatitis C virus increases the risk of insulin resistance and hepatic steatosis, and co-existent features of NASH have also been reported. Histological-based, longitudinal studies are needed that address the interactions of NAFLD and HIV infection, the effects of antiretroviral therapy and hepatotropic virus coinfection, and inform better management strategies.
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PMID:Nonalcoholic fatty liver disease and HIV infection. 1697 Aug 37

The aim of this investigation was to evaluate the efficacy of Alisma orientalis methanolic extract (AOME) on the experimental nonalcoholic fatty liver disease (NAFLD) induced by high-fat diet. Rats were fed with high-fat diet for six weeks and then gavaged the AOME for another six weeks. Typical pathological symptoms of NAFLD occurred in the high-fat diet rats. Administration with the AOME (150,300 and 600 mg kg (-1)) markedly decreased the serum and liver lipids; the high level of fasting serum glucose was reduced and insulin resistance was improved. The AOME treatment was also helpful in preventing the oxidative stress by lessening lipid peroxidation and activating antioxidant enzymes. Markers of the liver injury, aminotransferase abnormalities and hepatomegaly were improved and morphological changes, such as liver steatosis, mixed inflammation and collagen deposition, were lessened in rats treated with the AOME. These results suggested that the AOME showed hepatoprotective effects on NAFLD and may be a potential clinical application for treatment of this chronic liver disease.
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PMID:Protective effects of the Alisma orientalis extract on the experimental nonalcoholic fatty liver disease. 1703 63

Non-alcoholic fatty liver disease (NAFLD) is an important complication of the metabolic syndrome, which is becoming an increasingly common cause of chronic liver disease. Histological changes typically mainly affect perivenular regions of the liver parenchyma and include an overlapping spectrum of steatosis, steatohepatitis and persinusoidal or pericellular fibrosis, in some cases leading to cirrhosis. Once cirrhosis has developed, typical hepatocellular changes are often no longer conspicuous, leading to such cases being mistakenly diagnosed as 'cryptogenic'. Portal inflammation, ductular reaction and periportal fibrosis can also be seen as part of the morphological spectrum of NAFLD, particularly in the paediatric population. Hepatocellular carcinoma has also been described as a complication of NAFLD-associated cirrhosis. NAFLD is also an important cofactor in other chronic liver diseases, especially hepatitis C. Histological assessments have an important role to play in the diagnosis and management of NAFLD. These include making the potentially important distinction between simple steatosis and steatohepatitis and providing pointers to the aetiology, including cases where a dual pathology exists. A number of systems have been devised for grading and staging the severity of fatty liver disease. These require further evaluation, but have a potentially important role to play in determining prognosis and monitoring therapeutic responses.
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PMID:Histological assessment of non-alcoholic fatty liver disease. 1706 91

Nonalcoholic fatty liver disease (NAFLD) is a frequent and potentially progressive chronic liver disease that occurs in subjects who do not abuse alcohol. NAFLD is often associated with obesity, metabolic syndrome and insulin resistance and its more aggressive form, nonalcoholic steatohepatitis (NASH) is a major cause of cryptogenic cirrhosis. NAFLD/NASH are commonly detected because of elevated serum aminotransferase levels, ultrasonographic fatty liver and, at liver histology, steatosis, inflammation, and occasionally fibrosis that may progress to cirrhosis. No established treatment exists for this potentially serious disorder. Current management of NAFLD/NASH is largely conservative and includes diet regimen, aerobic exercise, and interventions towards the associated metabolic abnormalities. The main concern is therefore to decrease liver steatosis and its progression toward steatohepatitis and fibrosis, and the risk of "cryptogenic" cirrhosis. Among the most promising medications, weight reducing drugs, insulin sensitizers and lipid-lowering agents, antioxidants, bile salts, co-factors increasing the mitochondrial transport of fatty acids are being considered. Among them, thiazolidinediones are the most promising drug family that act by activating PPARgamma nuclear receptors and by regulating both microsomal and peroxisomal lipid oxidative pathways. Pharmacological treatment of obesity and probiotics should be considered as potential therapeutic options. In this review, after summarizing the general background on fatty liver, the most current and attractive pharmacological approaches to the problem of NAFLD/NASH are discussed.
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PMID:Current pharmacological treatment of nonalcoholic fatty liver. 1707 35

This study examined whether the standard deviation (SD) values on the histogram measured in the picture archiving and communication system (PACS) views of an ultrasound (US) can be used as an index to determine the homogeneity or heterogeneity of a hepatic parenchymal echo. Patients (n = 202) underwent an abdominal US examination. One US unit was used with a convex (3 to 5 MHz) transducer. The echogenicity of the hepatic parenchyma was measured in four different regions-of-interest (ROIs) of the liver with all vessels, bile ducts and calcification being avoided. The SDs were calculated automatically on the histogram of the ROI in the PACS views. The echo patterns of the liver were classified into normal, fatty liver (FL) and chronic liver disease (CLD). The distribution of the SD calculated from the ROI histogram of these three groups was examined, and statistical analysis for multiple comparisons of the average SD of the three groups was carried out using one-way analysis of variance. Among the 202 patients, there were 72 normal patients (mean SD: 11.10 +/- 0.91), 66 with a FL (mean SD: 11.09 +/- 1.04) and 64 with CLD (mean SD: 14.21 +/- 2.32). The SD values of the normal and FL groups were similar (p > 0.05), but there were significant differences (p < 0.0001) between the CLD and normal groups, and between the CLD and FL groups. The SD values of the abdominal US examination, which had been calculated on the ROI histogram of the PACS view, are believed to reflect the homogeneity or heterogeneity of the hepatic parenchyma. Smaller SD values are thought to represent normal or FL conditions, and larger SD values reflect the possibility of CLD that shows coarse echo. Therefore, it is concluded that the SD can be used as a useful quantitative value that can determine the coarseness of CLD.
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PMID:Usefulness of standard deviation on the histogram of ultrasound as a quantitative value for hepatic parenchymal echo texture; preliminary study. 1716 93

Hepatitis C virus (HCV) is a major cause of chronic liver disease that frequently leads to steatosis, cirrhosis, and eventually hepatocellular carcinoma (HCC). HCV core protein is not only a component of viral particles but also a multifunctional protein because liver steatosis and HCC are developed in HCV core gene-transgenic (CoreTg) mice. Proteasome activator PA28gamma/REGgamma regulates host and viral proteins such as nuclear hormone receptors and HCV core protein. Here we show that a knockout of the PA28gamma gene induces the accumulation of HCV core protein in the nucleus of hepatocytes of CoreTg mice and disrupts development of both hepatic steatosis and HCC. Furthermore, the genes related to fatty acid biosynthesis and srebp-1c promoter activity were up-regulated by HCV core protein in the cell line and the mouse liver in a PA28gamma-dependent manner. Heterodimer composed of liver X receptor alpha (LXRalpha) and retinoid X receptor alpha (RXRalpha) is known to up-regulate srebp-1c promoter activity. Our data also show that HCV core protein enhances the binding of LXRalpha/RXRalpha to LXR-response element in the presence but not the absence of PA28gamma. These findings suggest that PA28gamma plays a crucial role in the development of liver pathology induced by HCV infection.
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PMID:Critical role of PA28gamma in hepatitis C virus-associated steatogenesis and hepatocarcinogenesis. 1723 12

Nonalcoholic fatty liver disease is increasingly recognized as a condition that may progress to chronic liver disease. Most cases of fatty liver are asymptomatic and often are detected during routine medical or laboratory examinations. There also are some rare genetic diseases such as abetalipoproteinemia and familial hypobetalipoproteinemia that may cause fatty liver disease. Both are inherited disorders of lipoprotein metabolism. Although abetalipoproteinemia and homozygous familial hypobetalipoproteinemia patients present with severe manifestations, heterozygotes are usually asymptomatic. In the last several years, case reports or studies indicating a relationship between hepatosteatosis and familial heterozygote hypobetalipoproteinemia (FHBL) have been reported. Here, we report three cases of FHBL with characteristic lipid profile, mildly elevated liver enzymes and hepatosteatosis confirmed by ultrasonography.
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PMID:Hepatosteatosis with hypobetalipoproteinemia. 1739 54

Hepatitis C virus infections are recognized as a major causative factor of chronic liver disease. A characteristic feature of chronic hepatitis C, alcoholic liver disease and non-alcoholic fatty liver disease is hepatic steatosis. Hepatic steatosis leads to an increase in lipid peroxidation in hepatocytes, which, in turn, activates hepatic stellate cells (HSCs). HSCs are also thought to be the primary target cells for inflammatory and oxidative stimuli, and to produce extracellular matrix components. Based on available clinical information, chronic hepatitis C appears to progress more rapidly in men than in women, and cirrhosis is predominately a disease of men and postmenopausal women. Estradiol is a potent endogenous antioxidant. Hepatic steatosis was reported to become evident in an aromatase-deficient mouse and was diminished in animals after treatment with estradiol. Our previous studies showed that estradiol suppressed hepatic fibrosis in animal models, and attenuated HSC activation by suppressing the generation of reactive oxygen species in primary cultures. Variant estrogen receptors were found to be expressed to a greater extent in male patients with chronic liver disease than in female subjects. A better understanding of the basic mechanisms underlying the gender-associated differences observed in the progression of chronic liver disease would provide valuable information relative to the search for effective antifibrogenic therapies.
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PMID:Protection of estrogens against the progression of chronic liver disease. 1739 11


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