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)

Portal hypertension, widely recognized as a complication of cirrhosis, may also develop as an intrahepatic consequence of numerous hepatic disorders in the absence of cirrhosis. When gastrointestinal bleeding occurs in such cases, ruptured esophageal varices must be considered. Among chronic liver diseases, some, such as schistosomiasis, are commonly associated with portal hypertension and its complications. In others, including tuberculosis, amyloidosis, and polycystic disease, well-documented portal hypertension has been reported in only a small minority of cases. Nevertheless, because of the ever-present possibility of variceal hemorrhage whenever portal hypertension occurs, clinicians should be aware of these disorders. Acute conditions associated with noncirrhotic intrahepatic portal hypertension include acute (and particularly fulminant) viral or drug-induced hepatitis, acute alcoholic hepatitis, acute veno-occlusive disease, and acute fatty liver of pregnancy. Portal hypertension may be reversible following recovery in these settings. Particular attention is called to the increasing frequency of acute veno-occlusive disease on bone marrow transplant units, presumably as a complication of high-dose chemo- and radiotherapy.
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PMID:Noncirrhotic intrahepatic portal hypertension. 354 26

Advances in imaging technology and development of liver-specific contrast agents have significantly increased the role of radiology in the detection and characterization of processes diffusely involving the liver. Tailored magnetic resonance imaging (MRI) sequences allow an accurate detection of many storage and metabolic diseases, such as iron overload disorders and steatosis (fatty liver). Faster scanning techniques available with both computed tomography (CT) and MRI provide, by assessing contrast dynamics, sufficient information for the characterization of diffuse neoplastic and vascular disorders. Characteristic changes in attenuation on CT, signal intensity on MRI, and enhancing features can be used to diagnose specific diffuse diseases such as candidiasis, diffuse/multifocal hepatocellular carcinoma, and schistosomiasis. Although an overlap in imaging findings still exists, familiarity with the imaging features of uncommon disorders such as Wilson's disease, amyloidosis, and sarcoidosis may be diagnostic in the proper clinical setting. This review focuses on the current role of imaging in the detection and characterization of diffuse liver disorders. Recent developments that have amplified the role of noninvasive diagnostic evaluation of these conditions are especially highlighted.
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PMID:Imaging of diffuse liver disease. 1143 72

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

This study investigated whether long-term feeding a high-fat diet (HFC) has an effect on schistosomiasis mansoni outcome compared to standard chow diet (SC). Swiss Webster female mice (3 wk old) fed each diet over 5 months, and then were infected with 50 Schistosoma mansoni cercariae. Their nutritional status was assessed by monitoring growth rates twice a week and measuring serum levels of lipoproteins. Mice were euthanised 63 days after infection. Parasitological and liver histological analyses were performed. The levels of TC, HDL-C and LDL-C, fecal and tissue schistosome eggs were statistically different (p<0.05) between groups. Livers from HFC mice showed exudative, exudative/exudative-productive, exudative-productive and productive granulomas, some degree of hepatic steatosis and focal necrosis. Mice fed normal-chow did not present productive granulomas and hepatic steatosis. The morphometric evaluation of hepatic granulomas did not reach statistical significance (p>0.05) between diets assayed. The high-fat diet for long-term produces effects on schistosomiasis mansoni outcome.
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PMID:Long-term feeding a high-fat diet causes histological and parasitological effects on murine schistosomiasis mansoni outcome. 1711 19

High-fat diets induce weight gain and fatty liver in wild-type mice. Schistosomiasis mansoni infection also promotes hepatic injury. This study was designed to quantify hepatic alterations in schistosomiasis mansoni-infected mice fed a high fat-rich chow compared to mice fed a standard rodent chow, using stereology. Female SW mice fed each either high-fat diet (29% lipids) or standard chow (12% lipids) over 8 months, and then were infected with Schistosoma mansoni cercariae. Four experimental groups were studied: infected mice fed a high-fat diet (IHFC) or standard chow (ISC), uninfected mice fed a high-fat diet (HFC) or standard chow (SC). Mice were sacrificed during early infection (9 weeks from exposure). The following hepatic biometry and the stereology parameters were determined: volume density (hepatocytes [h], sinusoids [s], steatosis [st] and hepatic fibrosis [hf]); numerical density (hepatocyte nuclei - Nv[h]); absolute number of total hepatocyte N[h], normal hepatocyte N[nh], and binucleated hepatocyte N[bh], percentage of normal hepatocyte P[nh] and binucleated hepatocyte P[bh]. IHFC and HFC groups exhibited TC, HDL-C, LDL-C, and body mass significantly greater (p < 0.05) than control group. No significant differences were found regards liver volume (p = 0.07). Significant differences were observed regards P[nh] (p = 0.0045), P[bh] (p = 0.0045), Nv[h] (p = 0.0006), N[h] (p = 0.0125), N[bh] (p = 0.0164) and N[nh] (p = 0.0078). IHFC mice group presented 29% of binucleated hepatocytes compared to HFC group (19%), ISC group (17%) and SC (6%). Volume density was significantly different between groups: Vv[h] (p = 0.0052), Vv[s] (p = 0.0025), Vv[st] (p = 0.0004), and Vv[hf] (p = 0.0007). In conclusion, schistosomiasis mansoni infection with concurrent high-fat diet promotes intensive quantitative changes in hepatic structure, contributing to an increasing on hepatic regeneration.
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PMID:Hepatic stereology of Schistosomiasis mansoni infected-mice fed a high-fat diet. 1730 78

A 92-year-old Japanese woman with moderate liver fibrosis, schistosomiasis and steatohepatitis-like lesion, was diagnosed with hepatocellular carcinoma (HCC) by dynamic CT and elevated serum levels of alpha-fetoprotein and des-gamma-carboxyprothrombin. During follow up, the levels of tumor markers became normal without any treatment, and dynamic CT showed disappearance of the tumor and progression of hepatic steatosis. The mechanism of this spontaneous regression of HCC is unclear although massive necrosis due to rapid tumor growth or cancer immunity may have played a role.
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PMID:Spontaneous regression of hepatocellular carcinoma. 2289 Jul 82

Schistosomiasis is a neglected tropical disease of a significant public health impact. The water rat Nectomys squamipes is one of the most important non-human hosts in the schistosomiasis mansoni transmission in Brazil, being considered a wild reservoir. Cellular mechanisms that contribute to the physiological adaptation of this rodent to the Schistosoma mansoni parasite are poorly understood. Here we identified, for the first time, that a hepatic steatosis, a condition characterized by excessive lipid accumulation with formation of lipid droplets (LDs) within hepatocytes, occurs in response to the natural S. mansoni infection of N. squamipes, captured in an endemic region. Significant increases of LD area in the hepatic tissue and LD numbers/hepatocyte, detected by quantitative histopathological and ultrastructural analyses, were paralleled by increased serum profile (total cholesterol and triglycerides) in infected compared to uninfected animals. Raman spectroscopy showed high content of polyunsaturated fatty acids (PUFAs) in the liver of both groups. MALDI-TOFF mass spectroscopy revealed an amplified pool of omega-6 PUFA arachidonic acid in the liver of infected animals. Assessment of liver functional activity by the levels of hepatic transaminases (ALT and AST) did not detect any alteration during the natural infection. In summary, this work demonstrates that the natural infection of the wild reservoir N. squamipes with S. mansoni elicits hepatic steatosis in the absence of liver functional harm and that accumulation of lipids, markedly PUFAs, coexists with low occurrence of inflammatory granulomatous processes, suggesting that lipid stores may be acting as a protective mechanism for dealing with the infection.
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PMID:Natural Schistosoma mansoni Infection in the Wild Reservoir Nectomys squamipes Leads to Excessive Lipid Droplet Accumulation in Hepatocytes in the Absence of Liver Functional Impairment. 2788 Aug 8

Human and experimental studies have shown that chronic schistosomiasis mansoni protects against metabolic disorders through direct and indirect pathways. This study aims to investigate the co-morbidity between the acute schistosomiasis and nonalcoholic fatty liver. To address this, male C57BL/6 mice fed a high-fat chow (60% fat) or standard chow (10% fat) for 13 weeks and later infected with 80 Schistosoma mansoni cercariae. Mice were assigned into four groups: uninfected fed standard (USC), uninfected fed high-fat chow (UHFC), infected fed standard (ISC), and infected fed high-fat chow (IHFC). Blood sample and tissues were obtained at nine weeks post-infection (acute schistosomiasis) by necropsy. UHFC mice showed higher body mass, visceral adiposity, impaired glucose tolerance, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), triglyceride (TG), and liver steatosis compared to USC mice. IHFC mice showed lower blood lipid levels, blood glucose, improved glucose tolerance, body mass, and liver steatosis (macro and microvesicular) compared to UHFC mice. IHFC showed more massive histopathological changes (sinusoidal fibrosis, hepatocellular ballooning, and inflammatory infiltrates) compared to ISC. In conclusion, the co-morbidity results in both beneficial (friend) and detrimental (foe) for the host. While the acute schistosomiasis improves some metabolic features of metabolic syndrome, comorbidity worsens the liver injury.
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PMID:The acute schistosomiasis mansoni ameliorates metabolic syndrome in the C57BL/6 mouse model. 3222 27