Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-alcoholic fatty liver disease (NAFLD), comprising a spectrum of conditions ranging from pure steatosis to steatohepatitis and cirrhosis, has reached epidemic proportions and represents the most common cause of chronic liver disease in the community. The prevalence of NAFLD has been estimated to be between 20% and 30% in the general population, but this value is much higher ( approximately 70-80%) in type 2 diabetic patients, who are also at higher risk of developing advanced fibrosis and cirrhosis. Increasing recognition of the importance of NAFLD and its strong relationship with the metabolic syndrome has stimulated an interest in the possible role of NAFLD in the development of cardiovascular disease (CVD). Several epidemiological studies indicate that NAFLD, especially in its more severe forms, is linked to an increased risk of CVD, independently of underlying cardiometabolic risk factors. This suggests that NAFLD is not merely a marker of CVD, but may also be actively involved in its pathogenesis. The possible molecular mediators linking NAFLD and CVD include the release of pro-atherogenic factors from the liver (C-reactive protein, fibrinogen, plasminogen activator inhibitor-1 and other inflammatory cytokines) as well as the contribution of NAFLD per se to whole-body insulin resistance and atherogenic dyslipidemia, in turn favouring CVD progression. The clinical impact of NAFLD on CVD risk deserves particular attention in view of the implications for screening and surveillance strategies in the growing number of patients with NAFLD.
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PMID:Increased risk of cardiovascular disease in non-alcoholic fatty liver disease: causal effect or epiphenomenon? 1876 7

Non-alcoholic fatty liver disease (NAFLD) is a major complication linked with the metabolic syndrome associated with dyslipidemia, inflammation, and oxidative stress. Impact of type 2 diabetes with hyperlipidemia in NAFLD has to be established, as well as the utility of commonly prescribed anti-diabetic and lipid-lowering agents in improving liver injury markers. Genetic type 2 diabetic Goto-Kakizaki rats were fed with a high-fat diet to test hepatic effects of type 2 diabetes with hyperlipidemia and the effect of atorvastatin and insulin, individually and in combination, in systemic and hepatic inflammatory and oxidative stress markers. High-fat diet aggravated fasting glycemia, systemic and liver lipids, and inflammatory and oxidative stress markers. Individual treatments improved glycemic and lipid profiles, but failed to improve inflammatory markers, whereas insulin was able to reduce liver oxidative stress parameters. Combination of insulin and atorvastatin further improved glycemic and lipid profiles and decreased circulating C-reactive protein levels and liver inflammatory and oxidative stress markers. Insulin and atorvastatin combination leads to better glycaemic and lipid profiles and to better protection against liver inflammation and oxidative stress, giving a superior level of liver protection in type 2 diabetic with hyperlipidemia.
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PMID:A role for atorvastatin and insulin combination in protecting from liver injury in a model of type 2 diabetes with hyperlipidemia. 1893 12

Nonalcoholic fatty liver disease (NAFLD) is a very common cause of chronic liver disease in the United States. A large proportion of patients with NAFLD have coexisting metabolic syndrome, a major risk factor for cardiovascular disease. A strong association between NAFLD and cardiovascular disease has been long suspected, and recent studies have confirmed that cardiovascular disease is the single most important cause of mortality in this patient population. NAFLD may pose cardiovascular risk beyond the risk conferred by traditional factors such as dyslipidemia, diabetes, and smoking. Health care providers managing patients with NAFLD should recognize this increased cardiovascular risk and should undertake early, aggressive risk factor modification.
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PMID:Nonalcoholic fatty liver disease and cardiovascular risk. 1916 59

Non-alcoholic fatty liver disease (NAFLD), defined as excessive fat accumulation into the hepatocytes, has a prevalence of approximately 15 to 25%. Frequently associated risk factors for NAFLD are obesity, type 2 diabetes and dyslipidemia. It has been proponed that a mitochondrial dysfunction would play a crucial role in the disease development.On the other hand, focus is on insulin resistance syndrome, the only metabolic alteration strongly associated with this malady. The disease is suspected in individuals with insulina resistance characteristics such as metabolic syndrome and also in those with augmented serum aminotransferases levels. Different tests with biochemical markers have been proposed to predict the development of fibrosis or steatohepatitis. Therapeutic options in NAFLD patients are limited and weight lost remains as the most recommended one.
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PMID:[Non alcoholic fatty liver. A frequent entity with an unknown outcome]. 1942 8

Non-alcoholic steatohepatitis (NASH) has been associated with hepatocellular carcinoma (HCC) often arising in histologically advanced disease when steatohepatitis is not active (cryptogenic cirrhosis). Our objective was to characterize patients with HCC and active, histologically defined steatohepatitis. Among 394 patients with HCC detected by ultrasound imaging over 8 years and staged by the Barcelona Clinic Liver Cancer (BCLC) criteria, we identified 7 cases (1.7%) with HCC occurring in the setting of active biopsy-proven NASH. All were negative for other liver diseases such as hepatitis C, hepatitis B, autoimmune hepatitis, Wilson disease, and hemochromatosis. The patients (4 males and 3 females, age 63 +/- 13 years) were either overweight (4) or obese (3); 57% were diabetic and 28.5% had dyslipidemia. Cirrhosis was present in 6 of 7 patients, but 1 patient had well-differentiated HCC in the setting of NASH without cirrhosis (fibrosis stage 1) based on repeated liver biopsies, the absence of portal hypertension by clinical and radiographic evaluations and by direct surgical inspection. Among the cirrhotic patients, 71.4% were clinically staged as Child A and 14.2% as Child B. Tumor size ranged from 1.0 to 5.2 cm and 5 of 7 patients were classified as early stage; 46% of all nodules were hyper-echoic and 57% were <3 cm. HCC was well differentiated in 1/6 and moderately differentiated in 5/6. Alpha-fetoprotein was <100 ng/mL in all patients. HCC in patients with active steatohepatitis is often multifocal, may precede clinically advanced disease and occurs without diagnostic levels of alpha-fetoprotein. Importantly, HCC may occur in NASH in the absence of cirrhosis. More aggressive screening of NASH patients may be warranted.
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PMID:Does hepatocellular carcinoma in non-alcoholic steatohepatitis exist in cirrhotic and non-cirrhotic patients? 1978 50

Non-alcoholic fatty liver disease (NAFLD) is a condition associated with metabolic disturbances. The aim of the present study was to investigate the biochemical characteristics and risk factors for NAFLD. The study was carried out in a total of 881 subjects diagnosed by ultrasonography. NAFLD occurred mainly in middle-aged individuals, with a prevalence of 63.1 per cent. Multiple logistic regression analysis showed that male gender, presence of obesity, hypertension, dyslipidemia, or Type 2 diabetes and elevated serum alanine transaminase activities were independent risk factors for the development of NAFLD. Subjects with NAFLD were obese, hypertensive and often had signs of disturbances in lipid and glucose metabolism and abnormalities in hepatic functions. These findings show risk factors in the development and offer opportunities for prevention of NAFLD.
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PMID:Biochemical characteristics and risk factors in non-alcoholic fatty liver. 2003 59

Non-alcoholic fatty liver represents one of the most prevalent conditions affecting about one third of the general population in the Western world, and its prevalence is continuously increasing parallel to the epidemics of obesity. Non-alcoholic fatty liver is a strong predictor of non-alcoholic steatohepatitis, but also of cirrhosis, end-stage liver disease and hepatocellular carcinoma. In recent years, non-alcoholic fatty liver (in addition to overall and visceral obesity) has emerged as a risk factor for insulin resistance, hypertension, dyslipidemia, cardiovascular events and type 2 diabetes. This review summarizes the information currently available about the mechanisms involved in liver fat accumulation (e.g. hepatic lipid supply, de novo lipogenesis, lipid oxidation and the packaging and secretion of triglycerides in the form of very-low-density lipoproteins). New aspects concerning mechanisms potentially leading to a 'dissociation' of fatty liver and insulin resistance are also discussed. Understanding the pathogenesis of fatty liver and its complications, including the identification of new factors secreted from the liver under excess fat accumulation that are involved in the regulation of metabolism ('hepatokines'), is crucial in order to develop and implement efficient prevention and treatment strategies.
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PMID:Environmental and genetic determinants of fatty liver in humans. 2046 Sep 7

Non-alcoholic fatty liver disease (NAFLD) includes a spectrum of diseases that have insulin resistance in common and are associated with metabolic conditions such as obesity, type 2 diabetes mellitus, and dyslipidemia. NAFLD ranges from simple liver steatosis, which follows a benign course, to nonalcoholic steatohepatitis (NASH), a more severe entity, with necroinflammation and fibrosis, which can progress to cryptogenic cirrhosis and end-stage liver disease. Liver biopsy remains the gold standard for evaluating the degree of hepatic necroinflammation and fibrosis; however, several noninvasive investigations, such as serum biomarkers, have been developed to establish the diagnosis and also to evaluate treatment response. These markers are currently neither available in all centers nor validated in extensive studies. Examples include high-sensitivity C reactive protein and plasma pentraxin 3, which are associated with extensive liver fibrosis in NASH. Interleukin-6 correlates with inflammation, and cytokeratin-18 represents a marker of hepatocyte apoptosis (prominent in NASH and absent in simple steatosis). Tissue polypeptide specific antigen seems to have a clinical utility in the follow-up of obese patients with NASH.
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PMID:Noninvasive investigations for non alcoholic fatty liver disease and liver fibrosis. 2093 6

Non-alcoholic fatty liver disease (NAFLD), an important consequence of the global epidemic of obesity, is a common indication of orthotopic liver transplantation in the western world. Currently, NAFLD is the fourth most common indication of liver transplantation in the United Stated with prediction for increase demand of liver transplantation for NAFLD cirrhosis in the next two decades to exceed that of liver transplantation for chronic hepatitis C virus infection. Given the advances in the efficacy and tolerability of immunosuppressive agents which have reduced the incidence of chronic rejection, long-term survival rates after liver transplantation have remarkably improved. Today, long-term graft loss and death after liver transplantation are commonly related to age-related complications, such as cardiovascular disease. Features of metabolic syndrome including obesity, hypertension, hyperglycemia and dyslipidemia are very prevalent and almost universal after liver transplantation. These metabolic derangements are intricately associated with cardiovascular events and have emerged as the leading cause of morbidity and mortality after liver transplantation. In addition, the international epidemic of obesity has negatively impacted the liver transplant candidacy. Because obesity is associated with poor postoperative outcome, many transplant centers decline liver transplantation for morbidly obese individuals above certain level of body mass index.
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PMID:Metabolic syndrome and liver transplantation. 2103 47

Non-alcoholic fatty liver disease (NAFLD) encompasses a range of liver histology severity and outcomes in the absence of chronic alcohol use. The mildest form is simple steatosis in which triglycerides accumulate within hepatocytes. A more advanced form of NAFLD, non-alcoholic steatohepatitis (NASH), includes inflammation and liver cell injury, progressive to cryptogenic cirrhosis. Although prevalence in children is very difficult to establish, NAFLD is probably the most common cause of liver disease in preadolescent and adolescent groups. Over the last two decades the rise in the prevalence rates of overweight and obesity likely explains the NAFLD epidemic worldwide. NAFLD is strongly associated with abdominal obesity, type 2 diabetes, and dyslipidemia, and most patients have evidence of insulin resistance. Thus, NAFLD shares many features of the metabolic syndrome, a highly atherogenic condition, and its presence could signify a substantial cardiovascular risk. Accurate diagnosis and staging of NAFLD requires liver biopsy. The development of non-invasive surrogate markers and the advancement in imaging technology will aid in the screening of large populations at risk for NAFLD. While the optimal treatment has yet to be determined, lifestyle modification through diet and exercise should be attempted in children diagnosed with NAFLD. This review outlines current understanding, recent advances and challenges on pediatric NAFLD for both clinicians and researchers. Key words: Fatty liver.
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PMID:[Pediatric non-alcoholic fatty liver disease: recent advances and challenges]. 2104 70


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