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)

Non-alcoholic steatohepatitis (NASH) is a part of the spectrum of non-alcoholic fatty liver disease (NAFLD), which can progress to hepatic cirrhosis and end-stage liver disease or hepatocellular carcinoma (HCC). Its pathogenesis is associated with insulin resistance (IR) and the metabolic syndrome. Hepatic steatosis has also been considered an early marker of IR. It is now accepted that NASH is a multistep process with a prominent role for IR, where oxidative stress and cytokines retain a central role. Markers for predicting NAFLD with advanced fibrosis are needed. Once considered irreversible, liver fibrosis is now recognized a dynamic process with significant prospects for remission. The liver biopsy is still a gold standard in assessment of liver fibro-inflammatory activity in the injured liver, but has its own limitations: invasiveness, small tissue sample and inter- and intra-observer error. The lack of non-invasive tests limits the ability of monitoring progression of hepatic fibrosis and response to treatment. Therefore, clinical trials focused on finding of new non-invasive diagnostic tools giving possibilities of frequent, more accurate and reproducible assessment of hepatic fibrosis are constantly conducted.
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PMID:[Non invasive markers of non-alcoholic steatohepatitis]. 1894 40

Non-alcoholic fatty liver disease includes a broad spectrum of liver abnormalities ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), which can progress to cirrhosis and hepatocellular carcinoma. Patients with primary NASH have the metabolic (or insulin resistance) syndrome, condition typically associated with obesity, diabetes, hyperlipidemia and hypertension. To understand the mechanisms implicated in development of NASH, animal models of non-alcoholic fatty liver disease have been generated. These have greatly improved our understanding of some of the aspects of this disease. The challenge now is to identify the common mechanisms between the animal models and humans, which could eventually lead to a better prognosis and development of novel therapeutic strategies.
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PMID:Non-alcoholic steatohepatitis and animal models: understanding the human disease. 1902 69

Nonalcoholic fatty liver disease (NAFLD) is fast becoming the most common chronic liver condition in many parts of the world. It is a heterogeneous disease encompassing a broad spectrum of histologic states characterized universally by macrovesicular hepatic steatosis. NAFLD is now recognized as the hepatic manifestation of the metabolic syndrome and is a major cause of liver-related morbidity and mortality. The prevalence of the disease is increasing, tied closely to the increased prevalence of insulin resistance in industrialized countries. Risk factors for NAFLD include obesity, diabetes, insulin resistance, and hypertriglyceridemia. The clinical course of NAFLD depends upon the histologic subtype. Patients with simple hepatic steatosis generally are thought to have a benign long-term prognosis. However, nonalcoholic steatohepatitis can progress to cirrhosis and may have a similar prognosis as cirrhosis from other liver disease with progression to end stage liver disease and hepatocellular carcinoma. The decision to obtain a biopsy is determined by weighing the risks of the biopsy against the information obtained from the biopsy. No standardized therapeutic approach exists although many promising modalities are under investigation. This paper presents an overview of the incidence and prevalence of disease, diagnosis, histologic spectrum, natural history, pathogenesis, clinical course, and current treatment of nonalcoholic fatty liver disease.
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PMID:Nonalcoholic fatty liver disease. 1903 56

Nonalcoholic fatty liver disease (NAFLD) is probably the most common spectrum of metabolic liver disease in the world, encompassing simple steatosis to steatohepatitis, advanced fibrosis, cirrhosis and hepatocellular carcinoma. NAFLD affects a significant part of the general population worldwide. The existing correlation between obesity and NAFLD in combination with the increase in the frequency of obesity in the developed world implies that the incidence and severity of NAFLD will increase in the near future. Newer data support the idea that NAFLD constitutes the more important cause of cryptogenic cirrhosis of the liver and a ground for the development of hepatocellular carcinoma. Liver biopsy remains the most specific and sensitive method to differentiate NAFLD, providing important information on the long-term prognosis of the patients. The 'two hit' hypothesis constitutes the currently prevailing theory for the development of NAFLD and nonalcoholic steatohepatitis. The first 'hit' is purported to be the increase of free fatty acids in hepatocytes, which results in a decrease of beta-oxidation. The second step includes all mechanisms contributing to the development of necroinflammation and fibrosis. Currently, an effective treatment for patients with NAFLD does not exist. Improvement in liver histology remains the primary goal of any therapeutic approach in patients with NAFLD. Viewing NAFLD in the frame of the metabolic syndrome opens the possibility that both the onset of the disease and disease progression could be prevented by changes in lifestyle. Physical exercise and a low calorie diet in combination with the gradual loss of body weight represent the cornerstone for the management of NAFLD patients.
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PMID:Nonalcoholic fatty liver disease: from clinical recognition to treatment. 1907 71

About 30% of patients with cirrhosis have diabetes mellitus (DM). Nowadays, it is a matter for debate whether type 2 DM in the absence of obesity and hypertriglyceridemia may be a risk factor for chronic liver disease. DM, which develops as a complication of cirrhosis, is known as "hepatogenous diabetes". Insulin resistance in muscular and adipose tissues and hyperinsulinemia seem to be the pathophysiologic bases of diabetes in liver disease. An impaired response of the islet beta-cells of the pancreas and hepatic insulin resistance are also contributory factors. Non-alcoholic fatty liver disease, alcoholic cirrhosis, chronic hepatitis C (CHC) and hemochromatosis are more frequently associated with DM. Insulin resistance increases the failure of the response to treatment in patients with CHC and enhances progression of fibrosis. DM in cirrhotic patients may be subclinical. Hepatogenous diabetes is clinically different from that of type 2 DM, since it is less frequently associated with microangiopathy and patients more frequently suffer complications of cirrhosis. DM increases the mortality of cirrhotic patients. Treatment of the diabetes is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs. This manuscript will review evidence that exists in relation to: type 2 DM alone or as part of the metabolic syndrome in the development of liver disease; factors involved in the genesis of hepatogenous diabetes; the impact of DM on the clinical outcome of liver disease; the management of DM in cirrhotic patients and the role of DM as a risk factor for the occurrence and exacerbation of hepatocellular carcinoma.
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PMID:Liver cirrhosis and diabetes: risk factors, pathophysiology, clinical implications and management. 1914 Feb 27

The prognosis and management of liver disease greatly depends on the amount of liver fibrosis. Non-alcoholic fatty liver disease (NAFLD), ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), is emerging as a major cause of liver disease in Western countries because of the increasing prevalence of obesity and type 2 diabetes. A key issue in patients with NAFLD is the differentiation of NASH from simple steatosis. It is particularly important to identify NASH patients as they are at greatest risk of developing complications such as cirrhosis, liver failure and hepatocellular carcinoma. The limitations of liver biopsy (invasive procedure, sampling errors, interobserver variability and non-dynamic fibrosis evaluation) have stimulated the search for non-invasive approaches for the assessment of steatosis and liver fibrosis in patients with NAFLD. A variety of methods, including serum markers, imaging techniques such as ultrasound, CT, MRI and measurement of liver stiffness by transient elastography, have been proposed for the non-invasive assessment of steatosis and hepatic fibrosis. This review discusses the advantages and limitations of these different methods in clinical practice.
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PMID:Non-invasive diagnosis of steatosis and fibrosis. 1919 29

Diabetes developed as a complication of cirrhosis is known as hepatogenous diabetes>> (HD). Around 30% to 60% of cirrhotic patients suffer from this metabolic disorder. Insulin resistance in muscular, hepatic and adipose tissues as well as hyperinsulinemia, seem to be pathophysiologic bases for HD. An impaired response of the islet ss-cells of the pancreas and the hepatic insulin resistance are also contributing factors. Diabetes develops when defective oxidative and nonoxidative muscle glucose metabolism develops. Non-alcoholic fatty liver disease (NAFLD), alcoholic cirrhosis, chronic hepatitis C (CHC), and hemochromatosis are more frequently associated with HD. HD in early cirrhosis stages may be sub clinical. Only insulin resistance and glucose intolerance may be observed. As liver disease advances, diabetes becomes clinically manifest, therefore HD may be considered as a marker for liver function deterioration. HD is clinically different from that of type 2 DM since it is less frequently associated with microangiopathy and patients suffer complications of cirrhosis more frequently as well as increased mortality. Insulin resistance and HD associate to a decrease in the sustained response to antiviral therapy and an increased progression of fibrosis in patients with CHC. Diabetes treatment is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs that are frequently prescribed to these patients. This paper will review current concepts in relation to the pathopysiology, the impact on the clinical outcome of cirrhosis, and the therapy of HD. Finally, the role of HD as a risk factor for the occurrence and exacerbation of hepatocellular carcinoma (HCC) will also be reviewed.
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PMID:Hepatogenous diabetes. Current views of an ancient problem. 1922 28

Non-alcoholic fatty liver disease (NAFLD) includes a spectrum of clinical entities ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) with possible evolution to cirrhosis and hepatocellular carcinoma. Iron is considered a putative element that interacts with oxygen radicals in inducing liver damage and fibrosis. The role of hepatic iron in the progression of NASH remains controversial, but in some patients, iron may have a role in the pathogenesis of NASH. Though genetic factors, insulin resistance, dysregulation of iron-regulatory molecules, erythrophagocytosis by Kupffer cells may be responsible for hepatic iron accumulation in NASH, exact mechanisms involved in iron overload remain to be clarified. Iron reduction therapy such as phlebotomy or dietary iron restriction may be promising in patients with NASH/NAFLD to reduce insulin resistance as well as serum transaminase activities.
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PMID:Role of hepatic iron in non-alcoholic steatohepatitis. 1926 Oct 2

Obesity and related disorders are a common cause of morbidity worldwide. Nonalcoholic fatty liver disease is the most important hepatic consequence of adipose accumulation. There is strong evidence of obesity-related disorders as risk factors for hepatocellular carcinoma and of nonalcoholic fatty liver disease as a cause of hepatocellular carcinoma, but it is apparently less important than other chronic liver diseases. Unfortunately, preventive measures are not well validated in the population of patients with NAFLD. In this review, we analyze the available information supporting the increased risk of hepatocellular carcinoma in obese patients and patients with nonalcoholic fatty liver disease, considering the epidemiological and basic research-derived evidence.
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PMID:Role of nonalcoholic fatty liver disease in hepatocellular carcinoma. 1938 Nov 22

Nonalcoholic fatty liver disease (NAFLD) is recognized as the most common cause of chronic liver disease in western countries. NAFLD is etiologically associated with systemic and hepatic insulin resistance and is considered by many as the hepatic manifestation of the metabolic syndrome. NAFLD has a wide histological spectrum ranging from 'simple' steatosis to nonalcoholic steatohepatitis (NASH), which may progress to cirrhosis. Hepatocellular carcinoma may occur in NASH-related cirrhosis. The diagnosis of NAFLD/NASH is based on clinico-pathological criteria. Currently available noninvasive tests for the diagnosis of NASH lack specificity and sensitivity, so liver biopsy, despite its limitations, still remains the 'golden standard' for confirming or excluding NASH in a patient with chronically-elevated liver enzymes and image-detected steatosis. This review examines the currently used criteria for the histopathological diagnosis of NAFLD/NASH in adults and children and the relevant histological scoring systems.
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PMID:Nonalcoholic fatty liver disease/nonalcoholic steatohepatitis: histological diagnostic criteria and scoring systems. 1947 76


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