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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 a chronic liver disease that can progress to cirrhosis and hepatocellular carcinoma. NAFLD has been associated with obesity and other features of the metabolic syndrome, including insulin resistance, impaired glucose tolerance, and dyslipidemia. As a result, and with a lack of other effective treatments, weight loss achieved through lifestyle modifications (diet and exercise) has been promoted as the standard treatment. However, there is very little empiric evidence to support the effectiveness of weight loss for NAFLD. This article reviews the current literature on the effects of weight loss achieved through lifestyle modification or medications on NAFLD. To date, there have been no randomized controlled trials of weight loss interventions on hepatic pathology. Only three published trials (N = 89 subjects), which include a comparison group, have been published. These studies suggest improvement in liver enzymes and/or hepatic pathology; however, direct between group comparisons are lacking. Four small, nonrandomized studies (N = 59 subjects) have evaluated the effect of weight loss achieved with medications (4 of orlistat, 1 of sibutramine) on NAFLD. These suggest some improvement in liver enzymes and histopathology. Finally, a brief review of observational studies on the association between NAFLD pathology or liver enzymes and diet composition suggests a possible role for the manipulation of macronutrients and/or micronutrients in NAFLD treatment. In summary, there is little empiric evidence to support the role of weight loss achieved through lifestyle modification or medication in the treatment of NAFLD. Rigorously conducted, randomized controlled trials are needed in this area.
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PMID:Weight loss as a treatment for nonalcoholic fatty liver disease. 1654 Jul 66

The management of nonalcoholic fatty liver has been limited by a paucity of well-conducted studies that are of sufficient duration and quality to determine the outcome, which is best defined by liver biopsy. The mainstays, diet and physical activity plus behavioral modifications, are not always successful, particularly in the very obese. Although it is intuitive to expect that weight loss should diminish steatosis, only limited evidence exists that liver enzymes improve with reduction in body weight. The available pharmacologic therapy has focused on the two limbs of the pathogenetic basis for nonalcoholic steatohepatitis (NASH), insulin resistance and oxidative stress, but with quite limited success. Neither behavioral, nor dietary, nor drug therapy has been particularly effective either in obesity or NASH. In the severely obese, the fatty liver and its stages often have progressed to NASH or cirrhosis even before contemplating therapy. In the severely obese, the best therapeutic modality is bariatric surgery, which is safe and has been successful in producing a 61% weight loss overall. The result is improvement in diabetes mellitus, the metabolic syndrome, and presumably its sequelae. Early reports (and procedures) were attended with dramatic weight loss but markedly aggravated the inflammatory liver disease. In recent trials with more modest weight loss and less malnutrition, bariatric surgery reduced the fat, inflammation, and even the fibrosis in well-documented NASH. These promising procedures will undoubtedly increase and constitute the major therapeutic modality for those who are severely obese.
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PMID:Bariatric surgery: a promising solution for nonalcoholic steatohepatitis in the very obese. 1654 Jul 67

Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease that has been shown to progress to cirrhosis and hepatocellular carcinoma. This article reviews the prevalence of NAFLD and the factors associated this disorder, and with the more advanced stages of NAFLD, including nonalcoholic steatohepatitis (NASH) and fibrosis. In the general population, the estimated prevalence ranges from 3% to 24%, with most estimates in the 6% to 14% range. NAFLD is extremely common among patients undergoing bariatric surgery, ranging from 84% to 96%. In these patients, 25% to 55% have NASH, 34% to 47% have fibrosis, and 2% to 12% have bridging fibrosis or cirrhosis. NAFLD appears to be most strongly associated with obesity, and insulin resistance states including diabetes and with other features of the metabolic syndrome, such as high triglycerides and low HDL. It appears to be more common in men, and it increases with increasing age and after menopause. Some data suggest that Mexican Americans are more likely to have NAFLD and blacks are less likely compared with non-Hispanic whites. More advanced stages of NAFLD are associated with older age, higher body mass index, diabetes, hypertension, high triglycerides, and/or insulin resistance. An AST/ALT ratio greater >1 may also indicate more severe disease. Although hepatocellular carcinoma can occur in the setting of NAFLD, the risk factors for hepatocellular carcinoma in the setting of NAFLD have not been established. More prospective studies are needed to determine the true risk factors for the development and progression of NAFLD to help identify patients at highest risk who might benefit from treatment trials.
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PMID:The epidemiology of nonalcoholic fatty liver disease in adults. 1654 Jul 68

Non-alcoholic fatty liver disease (NAFLD) is now recognized as one of the most important causes of chronic liver disease in Western Countries, and is the hepatic manifestation of metabolic syndrome. The prevalence of NAFLD has increased with the global epidemic of obesity and type 2 diabetes mellitus. The pathophysiological hallmark of NAFLD is insulin resistance, associated with mediators of oxidative stress and inflammatory cytokines. Although simple steatosis by itself is generally benign, patients with histologically proven non-alcoholic steatohepatitis (NASH) can progress to cirrhosis. Hepatitis C (HCV) is another common cause of liver disease with some potential for progression to cirrhosis. Steatosis is present in almost 50% of patients infected by HCV. Hepatic steatosis in the setting of another liver disease (such as HCV) is associated liver disease progression. In particular, significant fibrosis is observed in patients with HCV whose liver biopsies show significant steatosis or superimposed NASH. This article reviews the host and viral factors potentially involved in the interaction between NAFLD and HCV. These factors include mediators of metabolic syndrome such as adipokines, inflammatory cytokines, factors associated with oxidative stress, lipid peroxidation products, as well as apoptosis and hepatic stellate cell activation with the resultant deposition of extracellular matrix. In addition to the mediators of metabolic syndrome (host factors), hepatic steatosis can be influenced by viral factors. The most important viral factor is HCV genotype 3, which has been independently associated with hepatic steatosis. Finally, superimposed NAFLD and visceral fat are associated with lower response rates to antiviral therapy in non-genotype 3 patients. Furthermore, viral clearance is associated with the resolution of hepatic steatosis in HCV genotype 3 but not other HCV genotypes. In these genotypes, hepatic steatosis and its impact on response to therapy are related to metabolic syndrome. Thus, the management of obesity and metabolic syndrome in patients with chronic hepatitis C may be important for reducing the risk of progression as well as improving the efficacy of antiviral therapy.
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PMID:Non-alcoholic fatty liver disease and hepatitis C infection. 1655 85

The management of nonalcoholic fatty liver has been limited by a paucity of well-conducted studies that are of sufficient duration and quality to determine the outcome, which is best defined by liver biopsy. The mainstays, diet and physical activity plus behavioral modifications, are not always successful, particularly in the very obese. Although it is intuitive to expect that weight loss should diminish steatosis, only limited evidence exists that liver enzymes improve with reduction in body weight. The available pharmacologic therapy has focused on the two limbs of the pathogenetic basis for nonalcoholic steatohepatitis (NASH), insulin resistance and oxidative stress, but with quite limited success. Neither behavioral, nor dietary, nor drug therapy has been particularly effective either in obesity or NASH. In the severely obese, the fatty liver and its stages often have progressed to NASH or cirrhosis even before contemplating therapy. In the severely obese, the best therapeutic modality is bariatric surgery, which is safe and has been successful in producing a 61% weight loss overall. The result is improvement in diabetes mellitus, the metabolic syndrome, and presumably its sequelae. Early reports (and procedures) were attended with dramatic weight loss but markedly aggravated the inflammatory liver disease. In recent trials with more modest weight loss and less malnutrition, bariatric surgery reduced the fat, inflammation, and even the fibrosis in well-documented NASH. These promising procedures will undoubtedly increase and constitute the major therapeutic modality for those who are severely obese.
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PMID:Bariatric Surgery: A Promising Solution for Nonalcoholic Steatohepatitis in the Very Obese. 1667 25

Recent advances in molecular genetics have led to a better understanding of hereditary iron overload syndromes, of which the most frequent are recessive HFE-hemochromatosis and, to a much lesser extent, dominant ferroportin disease. Acquired iron overload syndromes can be related to metabolic syndrome (insulin resistance syndrome), end-stage cirrhosis, or hematological disorders such as thalassemia and refractory anaemia.
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PMID:[Human hepatic iron overload syndromes]. 1673 93

Non-alcoholic fatty liver disease is considered a component of the metabolic syndrome associated with obesity. Problems still exist concerning non-alcoholic fatty liver disease patients in clinical practice, for example: (a) how to diagnose non-alcoholic fatty liver disease and its type; (b) how to select patients candidate to treatment; (c) how to treat selected patients. Non-alcoholic fatty liver disease includes steatosis and non-alcoholic steatohepatitis, but only non-alcoholic steatohepatitis evolves into cirrhosis and the absolute risk of mortality for non-alcoholic fatty liver disease is low. As yet, no tools, other than liver biopsy, are available to differentiate the various types of non-alcoholic fatty liver disease. Many drugs are, currently, under study to treat non-alcoholic fatty liver disease, even if well-performed trials are until necessary to define the best treatment. At the moment, the entity of the problem and the characteristics of patients frequently put the physician, in clinical practice, to choose the therapeutic approach arbitrarily which is considered more effective for each individual patient. Probably the future will consider the possibility of treating non-alcoholic fatty liver disease with more than one drug, by considering the various aspects and degree of this syndrome. Actually each physician should select the individual treatment on the basis of his/her knowledge and experience, by never forgetting the old saying 'primum non nocere'. However, the epidemiological entity of the problem, the characteristics of the patients, generally young, the frequent lack of clinical evidence of involvement of the liver, are all the factors that require vast well-performed clinical trials in order to define the best therapeutic approach for each individual patient.
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PMID:Treatment of patients with non-alcoholic fatty liver disease: current views and perspectives. 1675 Jun 61

Nonalcoholic fatty liver disease (NAFLD), including simple steatosis and nonalcoholic steatohepatitis (NASH), is commonly associated with metabolic syndrome. Many of NASH patients do not have subjective symptoms. The NASH is often found by routine health checkups etc. It is difficult to distinguish the simple steatosis and the NASH by transaminase level. It is reported that 25% of the NASH patient progress to cirrhosis in a decade. However, there is no study by a lot of patients concerning the prognosis of the NASH, and further studies will be required in the future.
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PMID:[Clinical features of NASH]. 1676 18

Nonalcoholic fatty liver disease (NAFLD) encompasses a histological spectrum ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) that may progress eventually to cirrhosis. Any clinically useful serum biomarkers have never been reported to distinguish patients with NASH from those with simple steatosis. The serum CRP concentration, formerly used as a marker of acute-phase reaction, has been revealed to be a strong predictor of coronary event after the introduction of the high-sensitivity assay method. Patients with metabolic syndrome also have been reported to have higher high-sensitivity CRP(hs-CRP) concentration. We showed patients with more active form of NASH (grade2-3) have higher concentration of hs-CRP than those with quiescent form of NASH (grade1) or simple steatosis. hs-CRP may be a promising biomarker for screening of NASH, a hepatic manifestation of metabolic syndrome.
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PMID:[High-sensitivity C-reactive protein (hs-CRP): a promising biomarker for the screening of non-alcoholic steatohepatitis (NASH)]. 1676 21


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