dc.creator | Arrese, Marco | |
dc.creator | Riquelme, Arnoldo | |
dc.creator | Soza, Alejandro | |
dc.date.accessioned | 2024-01-10T13:13:55Z | |
dc.date.accessioned | 2024-05-02T18:31:52Z | |
dc.date.available | 2024-01-10T13:13:55Z | |
dc.date.available | 2024-05-02T18:31:52Z | |
dc.date.created | 2024-01-10T13:13:55Z | |
dc.date.issued | 2010 | |
dc.identifier | 10.1016/S1665-2681(19)31735-1 | |
dc.identifier | 1665-2681 | |
dc.identifier | MEDLINE:20714007 | |
dc.identifier | https://doi.org/10.1016/S1665-2681(19)31735-1 | |
dc.identifier | https://repositorio.uc.cl/handle/11534/78354 | |
dc.identifier | WOS:000280885700019 | |
dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/9270553 | |
dc.description.abstract | Insulin resistance (IR) is a common pathophysiological condition where higher-than-normal concentrations of insulin are needed to maintain a normal glycemia and adequate glucose utilization in insulin target tissues. A high proportion (50-80%) of patients chronically infected with the hepatitis C virus (HCV) exhibit evidence of IR. Basic and clinical studies have disclosed a complex bidirectional relationship between IR and HCV infection that has important clinical implications. HCV infection may promote IR through direct viral-dependent mechanisms or due to activation of the inflammatory response resulting in increased production of Tumor Necrosis Factor-alpha and other cytokine-related molecules. These abnormalities may act synergistically with pre-existing metabolic risk factors and result in the development of hepatic steatosis and type 2 diabetes mellitus (T2DM) which are frequently found in the setting of HCV infection. Moreover, in addition to underlying metabolic abnormalities leading to its development hepatic steatosis also exhibit genotype-specific pathogenic mechanisms. A number of studies have shown that hepatic steatosis is associated to fibrosis progression in patients with HCV and that IR has a negative impact on the response rates to interferon-a-based therapy. Thus, modification of these factors through life-style changes or pharmacological agents may represent an undervalued specific target of therapy aiming to improve sustained virological response rates and reduce HCV related-morbidity and mortality. | |
dc.language | en | |
dc.publisher | ELSEVIER ESPANA | |
dc.rights | acceso abierto | |
dc.subject | Fatty liver | |
dc.subject | Insulin | |
dc.subject | Diabetes | |
dc.subject | Metabolic syndrome | |
dc.subject | SUSTAINED VIROLOGICAL RESPONSE | |
dc.subject | FATTY LIVER-DISEASE | |
dc.subject | COMBINATION THERAPY | |
dc.subject | VIRUS-INFECTION | |
dc.subject | HEPATOCELLULAR-CARCINOMA | |
dc.subject | PEGYLATED INTERFERON | |
dc.subject | PEGINTERFERON | |
dc.subject | FIBROSIS | |
dc.subject | PIOGLITAZONE | |
dc.subject | IMPACT | |
dc.title | Insulin resistance, hepatic steatosis and hepatitis C: A complex relationship with relevant clinical implications | |
dc.type | artículo | |