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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological studies have shown that obesity is a risk factor for hepatocellular carcinoma. Similar studies further indicate that diabetes is also a major risk factor. Both obesity and diabetes are frequently associated with nonalcoholic fatty liver disease, and case reports have shown progression of nonalcoholic fatty liver disease to cirrhosis and hepatocellular carcinoma. Although no study has clearly tied all of these variables together, it is likely that the association of hepatocellular carcinoma with obesity represents the progression of underlying nonalcoholic fatty liver disease to cirrhosis. The mechanism most likely involves replicative senescence of steatotic mature hepatocytes and compensatory hyperplasia of progenitor (oval) cells as a reaction to chronic injury due to ongoing nonalcoholic steatohepatitis and resultant hepatic fibrosis. Growth factors associated with chronic inflammation, type 2 diabetes, and DNA mutations as a result of lipid peroxidation probably play significant roles in clonal expansion and hepatocellular carcinoma progression. It remains unclear whether cirrhosis is a prerequisite for the development of hepatocellular carcinoma or whether hepatocellular carcinoma can develop in fatty liver in the absence of cirrhosis. However, well-documented case reports suggest that most cases of hepatocellular carcinoma arise in the setting of nonalcoholic steatohepatitis with cirrhosis. Whether therapy aimed at nonalcoholic fatty liver disease reduces the risk of hepatocellular carcinoma remains to be shown. Prophylactic measures and the role of cancer surveillance have not been adequately investigated, but current evidence suggests a risk for hepatocellular carcinoma in nonalcoholic steatohepatitis-related cirrhosis that rivals that of hepatocellular carcinoma in hepatitis C virus-related cirrhosis, particularly in older male patients.
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PMID:Obesity and hepatocellular carcinoma. 1550 9

Non-alcoholic fatty liver disease (NAFLD) is a frequent syndrome encompassing fatty liver alone and steatohepatitis (NASH). Often asymptomatic, the suspicion arises because of abnormal aminotransferases or a bright liver on abdominal ultrasound. It should be suspected during evaluation of associated conditions as obesity, diabetes or dyslipidaemia. The diagnostic evaluation must exclude other potential causes of liver disease and may include a liver biopsy, the only method able to confirm features of necroinflammation and fibrosis that define NASH and its prognostic implications. Indeed, the presence of necroinflammation has been associated with a significant risk of progression to cirrhosis and eventually hepatocellular carcinoma. Age >45 years, obesity and diabetes have also been associated with an increased risk of liver fibrosis and progression to cirrhosis. Given the high prevalence of NAFLD, general measures of life-style changes, focusing on exercise, diet, and total alcohol abstinence, should be implemented before a liver biopsy is considered.
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PMID:Non-alcoholic fatty liver disease/non-alcoholic steatohepatitis (NAFLD/NASH): diagnosis and clinical course. 1556 40

There is good evidence from in vitro studies that green tea catechins have a role in protection against degenerative diseases. However, the concentrations used in vitro are often higher than those found in animal or human plasma, and so in vivo evidence is required to demonstrate any protective effect of catechins. This article summarizes the most interesting in vivo animal studies on the protective effects of green tea catechins against biomarkers for cancer, cardiovascular disease, and other degenerative diseases. Generally, most studies using animal models show that consumption of green tea (catechins) provides some protection, although most studies have not examined dose response. Tea catechins could act as antitumorigenic agents and as immune modulators in immunodysfunction caused by transplanted tumors or by carcinogen treatment. Green tea has antiproliferative activity in hepatoma cells and hypolipidemic activity in hepatoma-treated rats, and some studies report that it prevents hepatoxicity. It could act as a preventive agent against mammary cancer postinitiation. Nevertheless, the implications of green tea catechins in preventing metastasis have not been clearly established. Long-term feeding of tea catechins could be beneficial for the suppression of high-fat diet-induced obesity by modulating lipid metabolism, could have a beneficial effect against lipid and glucose metabolism disorders implicated in type 2 diabetes, and could also reduce the risk of coronary disease. Further investigations on mechanisms, the nature of the active compounds, and appropriate dose levels are needed.
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PMID:A review of the health effects of green tea catechins in in vivo animal models. 1557 50

Obesity-related liver disease, particularly nonalcoholic fatty liver disease and its more severe form nonalcoholic steatohepatitis, is being increasingly recognized as a common liver disease in developed countries and represents hepatic manifestation of the metabolic syndrome. Nonalcoholic steatohepatitis results in progressive fibrosis, cirrhosis, and end-stage liver disease, with its increased incidence of hepatocellular carcinoma. Liver biopsy remains the gold standard in detection, evaluation, staging, and grading of nonalcoholic steatohepatitis. Liver biopsy also provides an important tool to detect concomitant liver disease that may accelerate the progression of steatohepatitis in these patients. Surgical or drug-induced weight loss has been documented to reduce the amount of inflammation, to induce regression of fibrosis, and, in some cases, to cause a reversal of cirrhosis in obese patients with steatohepatitis. Pretreatment or intraoperative liver biopsy should be performed to assess the presence of steatohepatitis, and stage and grade of steatohepatitis. This article will discuss obesity-related liver diseases, focusing on pathologic features in liver biopsies from obese patients, obesity-related hepatocellular carcinoma, and the effect of weight loss treatment on histopathology.
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PMID:Liver pathology in obesity. 1560 4

Nonalcoholic steatohepatitis (NASH) is a liver disease characterized by the histological features of steatohepatitis in the absence of significant alcohol consumption. The natural history of NASH is poorly defined. Here we report our experience with a patient to illustrate the clinical course of cirrhotic NASH. A 67-year-old woman was admitted with hematemesis due to the rupture of esophageal varices. Her varices were treated by endoscopic ligation and endoscopic sclerotherapy. Her medical history was unremarkable. Both the patient and her family members were asked about alcohol intake several times during her illness, but all of them denied a history of alcohol intake. She had insulin resistance, as determined by homeostasis model assessment. Serological tests for viral hepatitis were all negative. Viral hepatitis, autoimmune liver disease, iron overload, and metabolic liver disorders were all excluded. Imaging tests failed to reveal any steatosis, because of the presence of severe fibrosis. Liver biopsy showed moderate steatosis, moderate inflammation, ballooning degeneration, and Mallory bodies. We diagnosed NASH associated with cirrhosis based on the clinicopathological features. Almost 2 years later, she developed hepatocellular carcinoma (HCC) and she died of multiple HCCs. At autopsy, tumor invasion was seen throughout liver segment 8. The noncancerous liver showed burnt-out NASH; the steatosis, necroinflammation, ballooning degeneration, and Mallory bodies had all disappeared. In Japan, the prevalence of nonalcoholic fatty liver disease will increase as obesity has been increasing, so it is important to understand how to diagnose NASH. When a patient has NASH, careful follow-up should be performed.
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PMID:Nonalcoholic steatohepatitis: cirrhosis, hepatocellular carcinoma, and burnt-out NASH. 1562 89

Obesity is a rapidly growing health issue in Mexico and throughout the world because it is perceived as an alarming threat directly related with lifestyle in both children and adults, although cardiovascular, metabolic, neoplasic, and sleep-disorder complications of obesity are being investigated. However, overweight is a risk factor for chronic liver disease because liver fibrosis can develop in overweight patients free of any other known causes of liver disease. Obesity has been associated with development of hepatocellular carcinoma.
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PMID:[Obesity and its association with cryptogenic cirrhosis and hepatocarcinoma]. 1564 76

The number of papers published in the topic of hepatocellular carcinoma (HCC) increased remarkably from last year. The prevalence of chronic hepatitis C infection has increased the incidence of HCC. However, studies confirm that obesity and nonalcoholic fatty liver disease are important factors for the development of HCC in the United States. Alpha-fetoprotein is the most widely used tumor marker, but has poor diagnostic accuracy and ethnic variability. Using proteonomic genome analysis, new candidate tumor markers have been identified but await validation. Dynamic gadolinium magnetic resonance imaging seems to be more sensitive than spiral computed tomography scan for the identification of HCC, and seems to be modality of choice in most centers. Transplantation offers the best long-term option for patients with HCC, but in a certain group of patients without portal hypertension and well-preserved liver function, surgical resection is an acceptable option. A large study from Europe confirms the utility of resection in some patients with early HCC. However, most patients are not candidates for curative intervention. A meta-analysis and a randomized, controlled trial showed that chemoembolization offers a survival advantage in selected patients (Child class A and B) with nonresectable HCC. Finally, chemoprevention in patients with chronic hepatitis C infection with interferon is a promising strategy to prevent HCC.
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PMID:Hepatocellular carcinoma. 1570 64

Nonalcoholic steatohepatitis and chronic viral hepatitis C are the two dominant liver diseases in the Netherlands. Hepatic steatosis is usually innocuous but in twenty percent of patients it develops into steatohepatitis. One-fifth of these patients develop liver cirrhosis and hepatocellular carcinoma can also be a consequence of the disease. Nonalcoholic steatohepatitis is characterized by macrovesicular steatosis, necroinflammation, loss ofhepatocytes and fibrosis. Nonalcoholic steatohepatitis often is associated with type 2 diabetes mellitus, hypertension, dyslipoproteinemia and obesity. Insulin resistance plays a major role in the pathogenesis of this disease. Drugs against insulin resistance can ameliorate nonalcoholic steatohepatitis. Gradual weight loss, a diet including polyunsaturated fatty acids and exercise are other important treatment components of this condition.
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PMID:[Nonalcoholic steatohepatitis: diagnosis, pathogenesis, treatment and prognosis]. 1583 33

Non-alcoholic steatohepatitis is a chronic disease that occurs in persons without significative consumption of alcohol, characterized by macrovesicular steatosis, mixed inflammatory infiltrate, and diverse degrees of fibrosis. It can progress to cirrhosis and its evolution to hepatocellular carcinoma has been described. It principally occurs in patients with obesity, diabetes mellitus, and hyperlipidemia, and is at present considered a manifestation of metabolic syndrome with insulin resistance. In pathogenesis, diverse factors, fundamentally insulin resistance as a mechanism that determines hepatic steatosis, have been described. Later, alteration of signalling cascades, oxidative stress, and other mechanisms occur that lead to inflammation, necrosis, and finally to hepatic fibrosis, the details of which will be described in this review.
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PMID:[Pathogenic molecular mechanisms in non-alcoholic steatohepatitis]. 1575 91

Hepatic steatosis is the hallmark of nonalcoholic fatty liver disease (NAFLD), which is the consequence of multiple metabolic derangements among which insulin resistance plays a pivotal role. Steatosis is, also, a feature of hepatitis C virus (HCV) infection. However, in chronic hepatitis C, the prevalence of steatosis is 2.5-fold more elevated than that expected by a chance concurrence with NAFLD, suggesting that HCV may be implied in the development of steatosis. As observed in NAFLD, in patients infected with HCV genotype 1 steatosis is associated with an increased body mass index. On the other hand, in patients infected with genotype 3 the extent of steatosis strictly correlates with the viral load indicating that steatosis is mainly "virus-related". Regardless of the "metabolic" or "viral" etiology, hepatic steatosis in HCV contributes to the progression of liver fibrosis, to the development of hepatocellular carcinoma and to an impaired response to interferon treatment. Features such as obesity, insulin resistance and type 2 diabetes mellitus are shared by NAFLD and HCV-associated steatosis. In addition, HCV infection, directly or through steatosis, favors the development of type 2 diabetes mellitus. Hyperlipidemia is an independent predictor of the development of NAFLD, but not of HCV-associated steatosis. Arterial hypertension is common in nonalcoholic steatohepatitis patients, and HCV infection has recently been acknowledged as an independent risk factor for atherosclerosis. The role of iron in the progression of both NAFLD and HCV-associated steatosis remains controversial while lipoperoxidation and oxidative stress are pathogenic mechanisms shared by both. Some metabolic risk factors may be shared by both HCV-associated steatosis and NAFLD although the disease progression and pathophysiological background may be different. Preliminary data suggest that the therapeutic options for NAFLD may also be useful to improve HCV-associated steatosis.
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PMID:[Hepatitis C virus-associated and metabolic steatosis. Different or overlapping diseases?]. 1585 90


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