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| 1 | Subclinical abnormal glucose tolerance is a predictor of death in liver cirrhosis显示文摘AIM:To determine if subclinical abnormal glucose tolerance(SAGT)has influence on survival of non-diabetic patients with liver cirrhosis.METHODS:In total,100 patients with compensatedliver cirrhosis and normal fasting plasma glucose were included.Fasting plasma insulin(FPI)levels were measured,and oral glucose tolerance test(OGTT)was performed.According to OGTT results two groups of patients were formed:those with normal glucose tolerance(NGT)and those with SAGT.Patients were followed every three months.The mean follow-up was932 d(range of 180-1925).Survival was analyzed by the Kaplan-Meyer method,and predictive factors of death were analyzed using the Cox proportional hazard regression model.RESULTS:Of the included patients,30 showed NGT and70 SAGT.Groups were significantly different only in age,INR,FPI and HOMA2-IR.Patients with SAGT showed lower 5-year cumulated survival than NGT patients(31.7%vs 71.6%,P=0.02).Differences in survival were significant only after 3 years of follow-up.SAGT,Child-Pugh B,and high Child-Pugh and Model for EndStage Liver Disease(MELD)scores were independent predictors of death.The causes of death in 90.3%of cases were due to complications related to liver disease.CONCLUSION:SAGT was associated with lower survival.SAGT,Child-Pugh B,and high Child-Pugh and MELD scores were independent negative predictors of survival. | Diego García-Compeán Joel Omar Jáquez-Quintana Fernando Javier Lavalle-González José Alberto González-González Linda Elsa Mu?oz-Espinosa Jesús Zacarías Villarreal-PérezEndocrinology Service and Department of Internal Medicine University Hospital 'Dr. José E. González' and Medical School Universidad Autónoma de Nuevo León Monterrey 64320 México Héctor J Maldonado-Garza | 2014 | World Journal of Gastroenterology2014，20，22： | 12 |
| 2 | Chronic hepatitis C virus infection and atherosclerosis: Clinical impact and mechanisms显示文摘Hepatitis C virus(HCV)infection represents a major health issue worldwide due to its burden of chronic liver disease and extrahepatic manifestations including cardiovascular diseases,which are associated with excess mortality.Analysis of published studies supports the view that HCV infection should be considered a risk factor for the development of carotid atherosclerosis,heart failure and stroke.In contrast,findings from studies addressing coronary artery disease and HCV have yielded conflicting results.Therefore,meta-analytic reviews and prospective studies are warranted.The pathogenic mechanisms connecting HCV infection,chronic liver disease,and atherogenesis are not completely understood.However,it has been hypothesized that HCV may promote atherogenesis and its complications through several direct and indirect biological mechanisms involving HCV colonization and replication within arterial walls,liver steatosis and fibrosis,enhanced and imbalanced secretion of inflammatory cytokines,oxidative stress,endotoxemia,mixed cryoglobulinemia,perturbed cellular and humoral immunity,hyperhomocysteinemia,hypo-adiponectinaemia,insulin resistance,type 2 diabetes and other components of the metabolic syndrome.Understanding these complex mechanisms is of fundamental importance for the development of novel therapeutic approaches to prevent and to treat vascular complications in patients with chronic HCV infection.Currently,it seems that HCV clearance by interferon and ribavirin treatment significantly reduces non-liver-related mortality;moreover,interferon-based treatment appears to decrease the risk of ischemic stroke. | Luigi E Adinolfi Rosa Zampino Luciano Restivo Amedeo Lonardo Barbara Guerrera Aldo Marrone Fabio Nascimbeni Anna Florio Paola Loria | 2014 | World Journal of Gastroenterology2014，20，13： | 6 |
| 3 | Hepatitis C virus and metabolic disorder interactions towards liver damage and atherosclerosis显示文摘Hepatitis C virus(HCV)is one of the main causes of liver disease worldwide,and alterations of glucose metabolism have reached pandemic proportions in western countries.However,the frequent coexistence between these two conditions is more than simply coincidental,since HCV can induce insulin resistance through several mechanisms.Indeed,the virus interferes with insulin signaling both directly and indirectly,inducing the production of pro-inflammatory cytokines.Furthermore,the entire viral life cycle has strict interconnections with lipid metabolism,and HCV is responsible for a'viral'steatosis which is frequently superimposed to a'metabolic'one.Several evidences suggest that HCV-induced metabolic disorders contribute both to the evolution of liver fibrosis and,likely,to the progression of the other disorders which are typically associated with altered metabolism,in particular atherosclerosis.In the present review,we will examine in depth the links between HCV infection and insulin resistance,liver steatosis and diabetes,and analyze the impact of these interactions on the progression of liver fibrosis and atherosclerosis.Special attention will be focused on the highly debated topic of the relationship between HCV infection and cardiovascular disease.The available clinical literature on this item will be broadly reviewed and all the mechanisms possibly implied will be discussed. | Umberto Vespasiani-Gentilucci Paolo Gallo Antonio De Vincentis Giovanni Galati Antonio Picardi | 2014 | World Journal of Gastroenterology2014，20，11： | 5 |
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