| pubmed-article:21814590 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21814590 | lifeskim:mentions | umls-concept:C0524910 | lld:lifeskim |
| pubmed-article:21814590 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:21814590 | pubmed:dateCreated | 2011-8-4 | lld:pubmed |
| pubmed-article:21814590 | pubmed:abstractText | The goal of antiviral therapy for patients with chronic hepatitis C virus (HCV) infection is to attain a sustained virologic response (SVR), which is defined as undetectable serum HCV-RNA levels at 6 months after the cessation of treatment. Major improvements in antiviral therapy for chronic hepatitis C have occurred in the past decade. The addition of ribavirin to interferon-alfa therapy and the introduction of pegylated interferon (PEG-IFN) have substantially improved SVR rates in patients with chronic hepatitis C. The optimization of HCV therapy with PEG-IFN and ribavirin continues to evolve. Studies are ongoing that use viral kinetics to tailor therapy to an individual's antiviral response and determine the ideal length of treatment to maximize the chance of SVR. Improved SVR can be achieved with new specific inhibitors that target the HCV NS3/4A protease and the NS5B polymerase. Several long-term follow-up studies have shown that SVR, when achieved, is associated with a very low risk of virologic relapse. Furthermore, antiviral therapy can reduce the morbidity and mortality rates associated with chronic hepatitis C by reducing fibrosis progression, the incidence of cirrhosis, and hepatocellular carcinoma. | lld:pubmed |
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