Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonalcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease in the United States. It describes several clinicopathologic entities from simple hepatic steatosis to nonalcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma. This article describes the epidemiology, clinical features, natural history, and pathogenesis of NAFLD.
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PMID:Approach to the diagnosis and treatment of nonalcoholic fatty liver disease. 1620 67

The incidence of hepatocellular carcinoma is increasing, but the temporal changes of risk factors remain unclear. A significant proportion of hepatocellular carcinoma (7-30%) develops in cryptogenic cirrhosis, and may represent the most worrisome complication of non-alcoholic steatohepatitis. Non-alcoholic steatohepatitis is tightly related to insulin resistance and several features of the metabolic syndrome, i.e obesity, type 2 diabetes and dyslipidaemia. Nearly two-thirds of adults in the United States and an increasing percentage of the population worldwide are overweight or obese. Diabetes prevalence is increasing as well. The rising prevalence of risk factors associated with non-alcoholic steatohepatitis can partially account for the increasing incidence of cryptogenic cirrhosis and subsequent hepatocellular carcinoma. Moreover, recent evidence demonstrates that both obesity and diabetes are per se associated with an increased cancer risk. Large prospective studies show a significant association with obesity for several cancers, including cancers of the colon, female breast, endometrium, kidney, oesophagus and liver (hepatocellular carcinoma). Type 2 diabetes is also related with increased risks of colon, endometrial, kidney, pancreatic cancer and hepatocellular carcinoma. In western countries, the insulin resistance syndrome is emerging as a risk factor for a wide variety of cancers, including hepatocellular carcinoma.
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PMID:Review article: steatosis, the metabolic syndrome and cancer. 1622 71

Nonalcoholic fatty liver disease (NAFLD) is a condition of increasing incidence in western Countries seldom associated to other diseases of high prevalence in general population (i.e. diabetes and obesity). NAFLD ranges from simple fatty liver to steatohepatitis (NASH), which may lead to cryptogenic cirrhosis and in some cases hepatocellular carcinoma (HCC). Natural history of NAFLD in humans is poorly understood and progression of liver disease seems to be due to interaction between hosting (i.e. genetic, gut flora, insulin resistance) and environmental factors (social and eating behaviours) that should be responsible of increased oxidative stress within hepatocytes. Even if we need non-invasive markers able to describe the progression of liver disease, only meaning of liver biopsy is useful to characterize the stigmata of worsening such as inflammation and fibrosis.
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PMID:The natural history and risk factors for progression of non-alcoholic fatty liver disease and steatohepatitis. 1623 89

Nonalcoholic fatty liver disease (NAFLD) is increasingly recognized as one of the most common causes of chronic liver damage in the western world. It is strongly associated with insulin resistance, obesity and other features of the metabolic syndrome. The entity NAFLD embraces a clinical spectrum from benign steatosis over steatohepatitis to hepatic cirrhosis with its complications liver failure and hepatocellular carcinoma. Treatment is currently based on prescriptive diet and physical exercise. A well-defined pharmacotherapy of NAFLD still remains to be established due to the lack of randomized, controlled trials. Yet, for several drugs such as Metformin and Thiazolidinediones, smaller trials report promising results.
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PMID:[Therapeutic options for nonalcoholic fatty liver disease and steatohepatitis]. 1624 33

Nonalcoholic fatty liver disease (NAFLD) is an increasingly recognized health problem. Increased fat accumulation in the liver is observed in 20-30% of the population in the Western world, and in approximately 10% of this cohort it is associated with nonalcoholic steatohepatitis, which is characterized by inflammation and fibrosis. Disease presentation of NAFLD ranges from asymptomatic disease to cirrhosis with the complication of liver failure and hepatocellular carcinoma. NAFLD is suspected on the basis of various clinical aspects (an elevated alanine aminotransferase concentration, presence of obesity and diabetes) that alone are not sufficient to establish diagnosis or prognosis. The major diagnostic procedure is liver biopsy, which allows assessment of liver injury. In most cases, NAFLD is associated with insulin resistance, which is therefore the target of most current NAFLD treatment modalities. Various treatment strategies such as weight loss and/or exercise, thiazolidinediones, metformin, lipid-lowering agents and antioxidants have been studied. So far, no single intervention has convincingly improved liver histology. It is recommended that patients at high risk of developing advanced liver disease, and who are not part of controlled studies, should receive nutritional counseling and take physical exercise to achieve moderate weight loss and improve insulin sensitivity.
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PMID:Treatment strategies in nonalcoholic fatty liver disease. 1626 56

It is generally accepted that non-alcoholic fatty liver disease will be the most frequent liver disease in the near future and that the management of patients with non-alcoholic fatty liver disease will be a challenge for hepatologists in the next decades. Non-alcoholic fatty liver disease is considered the hepatic manifestation of the metabolic syndrome, in which insulin resistance plays a crucial role. Although steatosis will often not progress to severe liver disease, in some patients, it results in cirrhosis and even hepatocellular carcinoma. Therefore, it is important to identify those patients at risk for developing fibrosis. Age, diabetes, obesity and hypertriglyceridaemia are independent risk factors for fibrosis in patients with elevated serum alanine aminotransferase levels and steatosis on ultrasound. The presence of multiple metabolic disorders increases the risk. Apart from diet, exercise and correction of underlying metabolic abnormalities, no specific treatment is available at the moment. Theoretically, thiazolidinediones are an attractive way to treat non-alcoholic fatty liver disease, because they improve insulin resistance. Some preliminary studies with thiazolidinediones were encouraging, as steatosis, inflammation and fibrosis improved in a substantial number of patients. Although no serious side effects occurred in the pilot studies, we should look vigilantly for hepatotoxicity, as the first generation thiazolidinediones proved to be toxic for the liver.
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PMID:Review article: the treatment of non-alcoholic steatohepatitis with thiazolidinediones. 1626 63

Nonalcoholic fatty liver disease (NAFLD) is an increasingly recognized form of chronic liver injury. Nonalcoholic steatohepatitis (NASH) is the term applied to the microscopically-defined subset of NAFLD with known progression to cirrhosis and the complications that may be associated, including metabolic imbalances, liver failure and hepatocellular carcinoma. NASH is also being considered as a significant precursor of end-stage liver disease, ''cryptogenic cirrhosis'', in which the histologic features of the initial liver disease can no longer be appreciated. Because of the increasing prevalence and the known significance of this form of liver disease, current investigations are focused on discerning the clinical features of susceptible patients, the histopathologic findings that characterize the entity and serve as markers of progression, pathogenetic mechanisms that result in triglyceride accumulation, liver injury and fibrosis, and ultimately, treatment options.
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PMID:The pathology of nonalcoholic steatohepatitis. 1649 Oct 48

Non-alcoholic fatty liver disease (NAFLD), the liver manifestation of the metabolic syndrome, is now considered to be the commonest liver problem in the western world. This apparent 'epidemic', coupled with an accumulating body of evidence that a significant proportion of patients with NAFLD can progress to cirrhosis, liver failure and hepatocellular carcinoma (HCC), has--perhaps not surprisingly--led to an exponential growth in clinical and basic studies investigating all aspects of this hitherto largely ignored disease. The result is a vast increase in understanding of the natural history, clinical features and pathophysiology of NAFLD over the last five years which has now begun to inform the development of rational management strategies.
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PMID:Non-alcoholic fatty liver disease: current concepts and management strategies. 1652 51

Nonalcoholic fatty liver disease (NAFLD) is being increasingly recognized as one of the most common chronic liver diseases. The natural history of this liver disease remains unclear due to its indolent nature, the paucity of prospective studies, and the lack of consensus regarding the various forms of this disorder. Based on retrospective studies, it appears that the histologic features of NAFLD may be important determinants of the clinical course of this disease; patients with nonalcoholic steatohepatitis (NASH) appear to have a higher likelihood of progression to cirrhosis. There is an increased risk of hepatocellular carcinoma and end-stage liver disease among patients with NASH-related cirrhosis and those with cryptogenic cirrhosis, which likely represents a late stage of NAFLD. Recurrence of NASH has been described among patients who have undergone liver transplantation for NASH-related end-stage liver disease.
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PMID:Natural history of nonalcoholic steatohepatitis. 1654 Jul 61

Nonalcoholic fatty liver disease (NAFLD) is a metabolic liver disease with widely variable phenotypes extending from simple steatosis, through nonalcoholic steatohepatitis (NASH) to cirrhosis and hepatocellular carcinoma. Inevitably, this reflects the interplay of well-recognized environmental factors and disease associations such as obesity and insulin resistance with host genetic factors, which are polygenic or complex in nature. Most of the observed phenotypic variability will probably be explained by variations in single nucleotide polymorphism frequency, although knowledge of the effect of most polymorphisms on biologic function is currently limited. Several observational studies of kindred with NASH suggest a genetic contribution. Most data characterizing genetic variation in different NAFLD phenotypes is derived from case-control association studies involving putative candidate genes. These candidate genes have been selected largely based upon the "two-hit hypothesis" of the pathogenesis of NAFLD, although other hypothesis-independent approaches can also be informative in gene selection. Thus far, candidate gene association studies have had significant limitations such as small cohort sizes and poor reproducibility. Rapid technologic developments are increasing the capability of detecting genetic variation. Identification of the genetic contribution to NAFLD will inform theories of disease pathogenesis and progression and ultimately improve management.
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PMID:Genetic influences in nonalcoholic fatty liver disease. 1654 Jul 64


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