New protease inhibitors and direct-acting antivirals for hepatitis C: interferon's long goodbye: Table 1

Dusheiko, Geoffrey; Wedemeyer, Heiner

doi:10.1136/gutjnl-2012-302910

Cited by 23 publications

(16 citation statements)

References 54 publications

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“…Recently, direct‐acting antiviral agents (DAA) are under investigation, including protease inhibitors, RNA polymerase inhibitors, and nonstructure protein 5A and 5B inhibitors. Currently, the triple therapy with the first‐generation protease inhibitors (PI) and SOC can increase the SVR rates from 40% to 70% in naive patients, and from 20% to 65% in treatment‐experienced patients with G‐1 infection [59,60]. The emergence of DAA provides another window through which to view the interaction between CHC and IR.…”

Section: Future Perspectivesmentioning

confidence: 99%

Glucose abnormalities in hepatitis C virus infection

Huang¹,

Yu²,

Yu³

et al. 2012

The Kaohsiung J of Med Scie

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Hepatitis C virus (HCV) infection is one of the most important causes of cirrhosis and hepatocellular carcinoma and has a tremendous impact on public health worldwide. HCV is both hepatotropic and lymphotropic. Replication of HCV in diseased extrahepatic organs and tissues may either trigger latent autoimmunity or induce autoimmune disorders. In addition to established liver injury, type 2 diabetes mellitus (T2DM) is an important feature of extrahepatic metabolic disorders which is attributed to HCV infection. It also has some impact on the disease activity, disease course, clinical outcomes, and treatment efficacy of antiviral therapy. Previous experimental and clinical findings have highly suggested that HCV per se is diabetogenic. The cause-effect interaction between a common endocrine disorder and an infectious disease is an important issue to elucidate. Although the precise mechanisms whereby HCV infection leads to insulin resistance (IR) and glucose abnormalities are not entirely clear, it differs from the usual pathogenesis of T2DM in those with non-HCV liver diseases. This review initially highlights epidemiological and pathophysiological studies addressing the mutual link between chronic HCV infection (CHC) and T2DM. The characteristics of glucose abnormalities in this special population are depicted from the current evidence. The mutual roles of IR and CHC with respect to the prediction of treatment efficacy, how treatment response affects IR, and the role of pancreatic beta cell function in the entire suite are discussed. With the rapid progression of antiviral therapy for CHC in the past decade, we have also listed some points of future perspective in this issue.

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Section: Future Perspectivesmentioning

confidence: 99%

Glucose abnormalities in hepatitis C virus infection

Huang¹,

Yu²,

Yu³

et al. 2012

The Kaohsiung J of Med Scie

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“…1 2 The treatment outcome for difficult to cure patients, such as those chronically infected with HCV genotype 1 (HCV-1), has remarkably improved following the addition of the oral HCV protease inhibitors (PI) boceprevir (BOC) or telaprevir (TVR) to PR therapy. [3][4][5] While eradication of HCV by PI+PR therapy is expected to greatly extend treatment success rates, resulting in a reduced risk of liver-Open Access Scan to access more free content…”

Section: Introductionmentioning

confidence: 99%

Safety and on-treatment efficacy of telaprevir: the early access programme for patients with advanced hepatitis C

Colombo

Fernández

Abdurakhmanov

et al. 2013

Gut

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Background and aimSevere adverse events (AEs) compromise the outcome of direct antiviral agent-based treatment in patients with advanced liver fibrosis due to HCV infection. HEP3002 is an ongoing multinational programme to evaluate safety and efficacy of telaprevir (TVR) plus pegylated-interferon-α (PEG-IFNα) and ribavirin (RBV) in patients with advanced liver fibrosis caused by HCV genotype 1 (HCV-1).Methods1782 patients with HCV-1 and bridging fibrosis or compensated cirrhosis were prospectively recruited from 16 countries worldwide, and treated with 12 weeks of TVR plus PEG-IFN/RBV, followed by 12 or 36 weeks of PEG-IFN and RBV (PR) alone dependent on virological response to treatment and previous response type.Results1587 patients completed 12 weeks of triple therapy and 4 weeks of PR tail (53% cirrhosis, 22% HCV-1a). By week 12, HCV RNA was undetectable in 85% of naives, 88% of relapsers, 80% of partial responders and 72% of null responders. Overall, 931 patients (59%) developed grade 1–4 anaemia (grade 3/4 in 31%), 630 (40%) dose reduced RBV, 332 (21%) received erythropoietin and 157 (10%) were transfused. Age and female gender were the strongest predictors of anaemia. 64 patients (4%) developed a grade 3/4 rash. Discontinuation of TVR due to AEs was necessary in 193 patients (12%). Seven patients died (0.4%, six had cirrhosis).ConclusionsIn compensated patients with advanced fibrosis due to HCV-1, triple therapy with TVR led to satisfactory rates of safety, tolerability and on-treatment virological response with adequate managements of AEs.

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“…About 150 million people worldwide have persistent HCV infection . Significant improvements have been achieved in treating hepatitis C with the development of direct‐acting anti‐virals (DAAs) . First‐generation DAAs, the protease inhibitors (PIs), telaprevir (TVR) and boceprevir (BOC), were approved for treatment of chronic HCV genotype 1 infection in 2011.…”

Section: Introductionmentioning

confidence: 99%

Detection of low HCV viraemia by repeated HCV RNA testing predicts treatment failure to triple therapy with telaprevir

Maasoumy

Cobb

Bremer

et al. 2013

Aliment Pharmacol Ther

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SUMMARY BackgroundEarly on-treatment virological response is one of the most important predictors for sustained virological response (SVR) to treatment of chronic hepatitis C virus (HCV) genotype 1 infection with triple therapy including HCV protease inhibitors (PI). Treatment duration (24 vs. 48 weeks) is based on HCV RNA results at weeks 4 and 12 of PI therapy when HCV RNA must be 'undetectable' to allow shorter therapy.

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New protease inhibitors and direct-acting antivirals for hepatitis C: interferon's long goodbye: Table 1

Cited by 23 publications

References 54 publications

Glucose abnormalities in hepatitis C virus infection

Glucose abnormalities in hepatitis C virus infection

Safety and on-treatment efficacy of telaprevir: the early access programme for patients with advanced hepatitis C

Detection of low HCV viraemia by repeated HCV RNA testing predicts treatment failure to triple therapy with telaprevir

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