Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonalcoholic fatty liver disease (NAFLD) has become one of the most prevalent liver diseases in the Western world. NAFLD represents a wide spectrum of histologic subgroups, with nonalcoholic steatohepatitis as the most aggressive form. The risk of developing NAFLD is strongly associated with metabolic syndrome and insulin resistance. The pathogenesis of NAFLD is a multiple-hit process resulting from hepatic fat deposition that is related to several conditions, including insulin resistance and central obesity. Additional hits, such as oxidative stress or adipocytokines produced by white adipose tissue, can further enhance liver damage leading to nonalcoholic steatohepatitis or fibrosis. Although NAFLD is often the primary liver disease of metabolic conditions, it can also exacerbate other liver diseases such as hepatitis C (HCV); indeed, more than 50% of patients with HCV have hepatic steatosis. Hepatic steatosis can be related to host factors (e.g., obesity, metabolic syndrome or insulin resistance) or to the genotype of virus (e.g., HCV genotype 3). Increasing evidence suggests that hepatic steatosis, insulin resistance and obesity in the setting of HCV have a negative impact on the efficacy of treatment and hepatic progression of fibrosis.
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PMID:Interaction of metabolic syndrome, nonalcoholic fatty liver disease and chronic hepatitis C. 1907 56

Non-alcoholic fatty liver disease (NAFLD), a spectrum of liver disease ranging from simple steatosis to non-alcoholic steatohepatitis, is increasingly recognized as the hepatic manifestation of metabolic syndrome and is an important cause of liver-related morbidity and mortality. It is among the most common forms of liver disease. NAFLD reflects abnormal partitioning of fat, such that fat deposition is increased in the liver, and provides a link between NAFLD and the metabolic syndrome, a constellation of metabolic disorders that can also be associated with visceral fat or central adiposity. Together, the features of the metabolic syndrome presage overt diabetes and increase cardiovascular risk. Hepatitis C virus (HCV) appears to exacerbate the metabolic syndrome by eliciting increased insulin resistance (IR) and promoting truncal obesity. Moreover, the concomitant presence of HCV and NAFLD is associated with an increased likelihood of diabetes, hypertension and/or hypertriglyceridaemia. Metabolic abnormalities have been shown to influence response to treatment such that the presence of IR or obesity reduces the likelihood of a sustained virological response (SVR); conversely, SVR has been demonstrated to ameliorate IR and improve beta-cell function. Clinically, these data suggest that attention must be paid not only to optimizing antiviral response but also to screening for and treatment of the various components of the metabolic syndrome.
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PMID:Metabolic syndrome, non-alcoholic fatty liver disease and hepatitis C virus: impact on disease progression and treatment response. 1918 68

Abnormal accumulation of fat in the liver (steatosis) is commonly observed in hepatitis C virus (HCV) infection, and the severity of steatosis has been well correlated with the degree of hepatic fibrosis. In patients with chronic HCV infection, steatosis may occur in conjunction with other metabolic risk factors such as insulin resistance and the metabolic syndrome. This was observed primarily in patients infected with non-genotype 3 virus. Otherwise, in HCV-infected patients, especially those infected with genotype 3a, reductions in total cholesterol as well as high-density lipoprotein and low-density lipoprotein cholesterol are observed compared with matched controls, and the normalization of these parameters appears to be an important correlate of the response to antiviral therapy. In that setting, the pathogenic mechanisms involved in HCV-induced steatosis are mediated in large part by the HCV core protein, whose expression is associated with lipid droplet accumulation, changes in lipogenic gene expression and/or the activity of lipogenic proteins, and effects on mitochondrial oxidative function. The importance of genes such as peroxisome proliferator-activated receptor-alpha and the proteasome activator PA28-gamma in HCV-mediated steatosis has been elucidated from studies in genetically altered mice, and the manipulation of these and other pathways may provide an avenue for therapeutic intervention.
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PMID:Hepatitis C virus, steatosis and lipid abnormalities: clinical and pathogenic data. 1918 70

Metabolic steatosis or non-alcoholic fatty liver (NAFLD) is the most common cause of chronic liver injury in Western countries. Histological signs of necroinflammation, indicating the presence of non-alcoholic steatohepatitis (NASH), are present in 20-30% of cases. While steatosis on its own has a benign course, NASH may be associated with fibrosis and may progress to cirrhosis, terminal liver failure and hepatocellular carcinoma. NAFLD is closely associated with the metabolic syndrome, its prevalence reaching 50-90% in obese patients. The clinical impact of NAFLD has been demonstrated in large cohort studies by the overprevalence of cirrhosis and hepatocellular carcinoma in obese and diabetic patients. In terms of survival, liver disease is the third most common cause of mortality in patients with NAFLD. When associated with other causes of liver disease such as alcohol consumption or hepatitis C infection, metabolic steatosis may be a major risk factor for disease progression.
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PMID:Definition and natural history of metabolic steatosis: clinical aspects of NAFLD, NASH and cirrhosis. 1919 23

The natural history of chronic hepatitis C has been defined in several retrospective and prospective studies conducted in the last 20 years. These studies have clearly demonstrated that the outcome of chronic hepatitis C virus infection is profoundly influenced by a variety of cofactors and comorbidities. Many of the cofactors that affect the course of liver disease in hepatitis C also have a significant influence on the result of antiviral therapy. Unfortunately, comorbidities that have been shown to negatively influence the course and outcome of liver disease often reduce the chance of achieving a sustained virological response with pegylated interferon (PEG-IFN) and ribavirin treatment. The most important and frequent comorbidity influencing the course of chronic hepatitis C and the response to antiviral therapy is represented by the metabolic syndrome, and by the associated state of insulin resistance. Other comorbidities that have a negative influence on the progression of hepatitis C and on the response to antiviral therapy include excess alcohol intake, human immunodeficiency virus and hepatitis B virus co-infection and a number of conditions that reduce the benefit of therapy by affecting negatively compliance and/or adherence to adequate PEG-IFN or ribavirin doses.
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PMID:What are the comorbidities influencing the management of patients and the response to therapy in chronic hepatitis C? 1920 61

We evaluated the prevalence and the risk factors for gallstone disease in patients with chronic hepatitis C infection. We investigated 453 consecutively admitted patients with chronic infection with hepatitis C virus (HCV) (cirrhosis excluded) and 879 patients without liver disease (October 2006-April 2007). Gallstone disease was diagnosed if gallstones were present at ultrasonography or if there had been a previous cholecystectomy. Variables evaluated were age, gender, gallstone heredity, body mass index, waist circumference, parity, serum lipids, fatty liver, arterial hypertension, diabetes mellitus and metabolic syndrome (International Diabetes Federation criteria). Informed consent was obtained from all patients. We found that 88 of 453 (19%) patients with chronic HCV hepatitis (age 50.1 +/- 11.7 years) and 153 of 879 (17%) controls (age 60.6 +/- 12.6 years) had gallstone disease (GD). Abdominal obesity (OR = 2.108, 95% CI 1.287-3.452) and steatosis (OR = 3.699, 95% CI 2.277-6.008) were risk factors for GD in HCV patients. Gallstone heredity, dyslipidaemia, type 2 diabetes mellitus and metabolic syndrome increased the risk for GD in controls vs HCV patients. Our study shows that even HCV patients with chronic hepatitis but not cirrhosis have an increased prevalence of gallstones. Compared with controls, gallstones are present in HCV patients at a younger age and are associated with central obesity and liver steatosis, but not with gallstone heredity, dyslipidaemia, diabetes mellitus or metabolic syndrome. Although we could not establish a temporal relationship, the association between HCV infection and gall stone disease is real and appears to be causally linked, at least in predisposed individuals (obese and with liver steatosis).
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PMID:Hepatitis C virus infection is a risk factor for gallstone disease: a prospective hospital-based study of patients with chronic viral C hepatitis. 1948 79

Metabolic syndrome (MS) is a complicated disorder associated with a high risk of future development of micro- and macrovascular complications. The extrahepatic manifestations of hepatitis C virus (HCV) infection can include multiple metabolic abnormalities. However, the extent, severity, and characteristics of MS in HCV-infected patients have rarely been investigated in community-based settings. This study aimed to determine the difference in prevalence and distribution of the components of MS between HCV-infected patients and healthy controls. Multipurpose mass screening of adults was conducted in an HCV-endemic area of Southern Taiwan. Clinical profiles in terms of anthropometric data and MS components, as well as viral hepatitis markers, were assessed. Two hundred and thirty-seven adults (94 males; mean age, 55.5 +/- 10.8 years) were recruited. The prevalence of anti-HCV seropositivity was 39.2% (93/237). The prevalence of MS was higher in the HCV-infected individuals (24.7%, 23/93) than in the control, uninfected subjects (13.2%, 19/144, p = 0.02). In terms of MS components, HCV-infected subjects had a higher prevalence of high waist circumference (51.6% vs. 25.7%, p < 0.001) and hypertension (58.1% vs. 36.8%, p = 0.001) than controls. Multivariate logistic regression analysis demonstrated that anti-HCV positivity was significantly associated with MS (odds ratio, 6.4; 95% confidence interval, 1.82-22.84; p = 0.004). HCV infection was associated with a higher prevalence of MS. Determination of MS in patients with HCV infection could therefore be indicated.
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PMID:Hepatitis C virus infection and metabolic syndrome---a community-based study in an endemic area of Taiwan. 1956 Sep 94

Hepatocellular carcinoma (HCC) is the most rapidly increasing cause of cancer death in the United States. Although many risk factors for HCC are well defined, including hepatitis B virus (HBV), hepatitis C virus (HCV), and alcohol, most series have indicated that 5% to 30% of patients with HCC lack a readily identifiable risk factor for their cancer. The majority of "cryptogenic" HCC in the United States is attributed to nonalcoholic fatty liver disease (NAFLD), a hepatic manifestation of the metabolic syndrome. The metabolic syndrome is a constellation of problems that includes insulin resistance, obesity, hypertension, and hyperlipidemia. Increasingly, components of the metabolic syndrome are being linked to various forms of cancer with respect to both increased risk of disease and worsened outcome. In this review, the authors focused on the relation between metabolic syndrome and HCC. They investigated the increased risks of HCC among individuals with features of metabolic syndrome, potentially worsened cancer outcomes in these patients, possible pathogenic mechanisms to explain these relations, and treatment options for those with NAFLD and its progressive counterpart, nonalcoholic steatohepatitis. It is predicted that metabolic syndrome will lead to large increases in the incidence of HCC over the next decades. A better understanding of the relation between these 2 diseases ultimately should lead to improved screening and treatment options for patients with HCC.
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PMID:Metabolic syndrome and hepatocellular carcinoma: two growing epidemics with a potential link. 1983 57

The hepatitis C virus (HCV) induces lipid accumulation in vitro and in vivo. The pathogenesis of steatosis is due to both viral and host factors. Viral steatosis is mostly reported in patients with genotype 3a, whereas metabolic steatosis is often associated with genotype 1 and metabolic syndrome. Several molecular mechanisms responsible for steatosis have been associated with the HCV core protein, which is able to induce gene expression and activity of sterol regulatory element binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor gamma (PPARgamma), increasing the transcription of genes involved in hepatic fatty acid synthesis. Steatosis has been also implicated in viral replication. In infected cells, HCV core protein is targeted to lipid droplets which serve as intracellular storage organelles. These studies have shown that lipid droplets are essential for virus assembly. Thus, HCV promotes steatosis as an efficient mechanism for stable viral replication. Chronic HCV infection can also induce insulin resistance. In patients with HCV, insulin resistance is more strongly associated with viral load than visceral obesity. HCV seems to lead to insulin resistance through interference of intracellular insulin signalling by HCV proteins, mainly, the serine phosphorylation of insulin receptor-1 (IRS-1) and impairment of the downstream Akt signalling pathway. The HCV core protein interferes with in vitro insulin signalling by genotype-specific mechanisms, where the role of suppressor of cytokine signal 7 (SOCS-7) in genotype 3a and mammalian target of rapamycin (mTOR) in genotype 1 in IRS-1 downregulation play key roles. Steatosis and insulin resistance have been associated with fibrosis progression and a reduced rate of sustained response to peginterferon plus ribavirin.
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PMID:Steatosis and insulin resistance in hepatitis C: a way out for the virus? 1985 93

1. Despite methodological problems in estimating the true incidence of new-onset diabetes (NODM), it is generally accepted that this is a common complication of liver transplantation (LT), with the mean reported incidence varying between 7% and 30%. 2. The main predictors of post-LT NODM are ethnicity, a family history of diabetes, age > 45 years, glucose intolerance prior to LT, central obesity, metabolic syndrome, use of corticosteroids over a long period, use of tacrolimus, and hepatitis C infection. 3. NODM is associated with impaired long-term graft function and reduced survival. Diabetes is among the main risk factors for coronary heart disease, cerebrovascular disease, and peripheral occlusive arterial disease in transplant recipients. 4. The management of NODM includes the therapeutic and preventive steps taken in patients with type 2 diabetes. Little information exists on the use of antidiabetic compounds in transplant recipients. Some studies have suggested that LT recipients with NODM may benefit from a conversion to cyclosporine through improved glucose metabolism.
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PMID:Long-term outcomes of liver transplantation: diabetes mellitus. 1987 23


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