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

Hepato-biliary disorders are rare complications of pregnancy, but they may be severe, with high fetal and maternal morbidity and mortality. Imaging is, therefore, essential in the rapid diagnosis of some of these conditions so that appropriate, life-saving treatment can be administered. This pictorial essay illustrates the multimodality imaging features of pregnancy-induced hepato-biliary disorders, such as acute fatty liver of pregnancy, preeclamsia and eclampsia, and HELLP syndrome, as well as those conditions which occur in pregnancy but are not unique to it, such as viral hepatitis, Budd-Chiari syndrome, focal hepatic lesions, biliary sludge, cholecystolithiasis, and choledocholithiasis.
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PMID:Multimodality imaging of hepato-biliary disorders in pregnancy: a pictorial essay. 1922 16

Liver diseases in pregnancy may be categorized into liver disorders that occur only in the setting of pregnancy and liver diseases that occur coincidentally with pregnancy. Hyperemesis gravidarum, preeclampsia/eclampsia, syndrome of hemolysis, elevated liver tests and low platelets (HELLP), acute fatty liver of pregnancy, and intrahepatic cholestasis of pregnancy are pregnancy-specific disorders that may cause elevations in liver tests and hepatic dysfunction. Chronic liver diseases, including cholestatic liver disease, autoimmune hepatitis, Wilson disease, and viral hepatitis may also be seen in pregnancy. Management of liver disease in pregnancy requires collaboration between obstetricians and gastroenterologists/hepatologists. Treatment of pregnancy-specific liver disorders usually involves delivery of the fetus and supportive care, whereas management of chronic liver disease in pregnancy is directed toward optimizing control of the liver disorder. Cirrhosis in the setting of pregnancy is less commonly observed but offers unique challenges for patients and practitioners. This article reviews the epidemiology, pathophysiology, diagnosis, and management of liver diseases seen in pregnancy.
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PMID:Liver disease in pregnancy. 1924 87

The economic burden of end stage liver disease is set to increase due to the rising prevalence of cirrhosis secondary to alcohol, viral hepatitis and fatty liver disease. Screening for liver disease has been advocated, as most cases of cirrhosis are preventable with early interventions. Liver function tests (LFTs) are routinely used as a first line investigation to screen for liver diseases but can be normal despite significant underlying liver fibrosis, hepatitis, steatohepatitis or even cirrhosis. Their relationships are far from linear and with little predictive value in some cases. Newer non-invasive modalities are emerging but currently their roles are largely experimental. This review will discuss the role of serum biomarkers and imaging techniques as new modalities to screen for liver disease.
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PMID:Screening for liver disease - are LFTs old hat? 1935 98

Liver progenitor (oval) cells have enormous potential in the treatment of patients with liver disease using a cell therapy approach, but their use is limited by their scarcity and the number of donor livers from which they can be derived. Bone marrow may be a suitable source. Previously the derivation of oval cells from bone marrow was examined in rodents using hepatotoxins and partial hepatectomy to create liver damage. These protocols induce oval cell proliferation; however, they do not produce the disease conditions that occur in humans. In this study we have used the choline-deficient, ethionine-supplemented (CDE) diet (which causes fatty liver) and viral hepatitis as models of chronic injury to evaluate the contribution of bone marrow cells to oval cells under conditions that closely mimic human liver disease pathophysiology. Following transplantation of lacZ-transgenic bone marrow cells into congenic mice, liver injury was induced and the movement of bone marrow cells to the liver monitored. Bone marrow-derived oval cells were observed in response to the CDE diet and viral injury but represented a minor fraction (0-1.6%) of the oval cell compartment, regardless of injury severity. In all situations only rare, individual bone marrow-derived oval cells were observed. We hypothesized that the bone marrow cells may replenish oval cells that are expended by protracted liver injury and regeneration; however, experiments involving a subsequent episode of chronic liver injury failed to induce proliferation of the bone marrow-derived oval cells that appeared as a result of the first episode. Bone marrow-derived hepatocytes were also observed in all injury models and controls at a frequency unrelated to that of oval cells. We conclude that during viral-and steatosis-induced liver disease the contribution of bone marrow cells to hepatocytes, either via oval cells or by independent mechanisms, is minimal and that the majority of oval cells responding to this injury are sourced from the liver.
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PMID:Bone marrow cells play only a very minor role in chronic liver regeneration induced by a choline-deficient, ethionine-supplemented diet. 1938

Known risk factors for hepatocellular carcinoma (HCC) include hepatitis C, hepatitis B, and alcoholic liver disease. Several studies have examined diabetes as a risk factor for HCC because of its association with fatty liver disease and non-alcoholic steatohepatitis. The current study by Tung et al. found that neither diabetes nor overweight was a risk factor for HCC. Results were consistent using both a cross-sectional and a case-control study approach. Findings from this study suggest that diabetes and overweight alone are not adequate to increase the risk of HCC in the absence of concomitant viral hepatitis or liver disease.
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PMID:Diabetes and hepatocellular carcinoma: what role does diabetes have in the presence of other known risk factors? 2005 44

The finding of lipid accumulation in the liver, so-called hepatic steatosis or non-alcoholic fatty liver disease, is a common condition frequently found in healthy subjects. Its prevalence, in fact, has been estimated by magnetic resonance studies to be about 35% in the general population and 75% in obese persons. Nevertheless, its presence generates liver damage only in a small percentage of subjects not affected by other liver diseases. It should be defined as a "co-factor" capable of affecting severity and progression, and also therapeutic perspectives, of liver diseases to which it is associated. Herein we will evaluate the impact of hepatic steatosis and obesity on the most common liver diseases: chronic viral hepatitis C and B, and alcoholic liver disease.
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PMID:Steatosis as a co-factor in chronic liver diseases. 2022 59

Hepatitis, a common human disease, may be followed by severe liver injury, eventually leading to fatty liver, liver fibrosis and hepatocellular carcinoma. CD8 T cells are a double-edged sword in the response to infection with the hepatitis virus. On one hand, rapid activation of CD8 T cells is critically important for the elimination of the virus. On the other hand, in persistent viral infection, the activation of CD8 T cells substantially contributes to liver injury. The clinical course of hepatitis, thus, critically depends on mechanisms regulating the activity of CD8 T cells. In observations in human hepatitis and in mice infected with the lymphocytic choriomeningitis virus, the clinical course of hepatitis is modified by several immunological factors including neutralizing antibodies: RIG-I, TLRs, MyD88, interferon type I, TNF-alpha, MHC I, Tap, TCR, CD8, IL-2, IL-7, PD-1, IFN-I, IL-10, IFN-gamma, perforins, serotonin and iNOS (table 1) . Additional experimental effort is needed to understand the concerted interplay of those molecules in viral hepatitis of man and mice.
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PMID:Host mechanisms in viral hepatitis. 2046 Aug 87

Hepatic encephalopathy is a reversible neuro-psychiatric syndrome that complicates liver insufficiency. The changes are complex and disorders are detected in digestive and neural systems. Disturbed consciousness and intellectual deterioration, particularly communicative difficulties are observed: speech is slurred, voice monotonous, writing disturbances, amimic face and rigid posture. Difficulties of socialization and tendency to self-isolation are observed. Memory, attention and perception are decreased. We suppose that disorders of cognitive functions are determined by impairment of speech and other communicative abilities. According to the theories of linguistic determinism and linguistic relativity thought categories move through the mould of native language. That means, speech impairment causes misperception of the real world. To confirm this hypothesis we investigated 106 patients with following diseases: peptic ulcer - 46, fatty liver - 30, liver cirrhosis - 19, viral hepatitis - 11 and 19 controls. Brain magnetic resonance tomography was carried out and psychometric tests were performed to patients with symptoms of hepatic encephalopathy. Atrophic changes in frontal, temporal and insular area of brain cortex were revealed in most cases. Those regions are responsible for actor observation, imitation and emotion, i.e. for empathy and sociability. They are very sensitive to the increased levels of ammonia and glutamine. In case of early treatment only slight atrophic changes are presented but without treatment atrophic processes become stable and expressed by impairments of speech and entire communicative ability. Human beings are very much at the mercy of the particular language which has become the medium of expression for their society. They do not live in the objective world alone, or in the world of social activity alone. Accordingly, damage of speech in hepatic encephalopathy is primary and predisposes to cognitive dysfunction.
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PMID:[Speech impairment predisposes to cognitive deterioration in hepatic encephalopathy]. 2049 25

Cirrhosis of the liver is a rising epidemic in the United States, affecting 2 out of every 1,000 adults. It is responsible for the deaths of more than 27,000 people each year. The primary diseases that underlie cirrhosis include viral hepatitis, alcoholic liver disease, and nonalcoholic fatty liver disease. Monitoring the extent of fibrosis and aggressively treating the underlying disease is essential for maintaining quality of life and preventing the complications of cirrhosis. As patients progress toward end-stage liver disease, the most common complications include portal hypertension, the development of esophageal varices, and hepatic encephalopathy. Esophageal varices can lead to hemorrhaging, a dangerous complication that is fatal in 30-50% of patients during the first occurrence. Hepatic encephalopathy is another serious complication of end-stage liver disease, as it significantly reduces patient quality of life and places heavy economic and caregiving burdens upon the patient's family. In this clinical roundtable monograph, the latest advances in the monitoring of liver disease and the management of portal hypertension and hepatic encephalopathy are discussed.
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PMID:The treatment of hepatic encephalopathy in the cirrhotic patient. 2056 82

Lipid metabolism disorders related to viral etiology are described in chronic viral hepatitis, independent of age, gender and liver synthetic function. Steatosis is present, especially in chronic hepatitis C but also in chronic hepatitis B. Although liver biopsy is the gold standard in determining presence of steatosis, its presence can be determined by ultrasonographic examination as an initial screening test. Our aim in this study was to evaluate the presence of steatosis in chronic hepatitis B and C, to determine its frequency in both hepatitis type, and to explore possible relationships between presence of steatosis, lipid metabolism disorders and viral etiology. Our study lot included 66 patients, 36 subjects with chronic hepatitis C, and 30 with chronic hepatitis B. We only encountered significant levels of steatosis in the chronic hepatitis B sub-group. We found the average age, cholesterol, triglyceride, HDL-C, VLDL-C levels in the group with steatosis to be significantly higher than those in the group without steatosis (p < 0.05). Ultrasound reports of hepatic steatosis were particularly associated with histological inflammation, as well as fibrosis; however, the sensitivity and specificity of steatosis on ultrasound was poor when compared to steatosis on biopsy. Hepatic steatosis was significantly more frequent in chronic hepatitis C than in chronic hepatitis B. Severe inflammation and advanced fibrosis were more frequently found in HCV-infected patients with steatosis than in patients without steatosis.
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PMID:Steatosis and serum lipid patterns in patients with chronic viral hepatitis: differences related to viral etiology. 2080 28


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