Short‐term prolongation of pegylated interferon and ribavirin therapy for genotype 1b chronic hepatitis C patients with early viral response

Ikeda, Hiroki; Suzuki, Michihiro; Okuse, Chiaki; Yamada, Noriko; Okamoto, Masaaki; Kobayashi, Minoru; Nagase, Yoshihiko; Takahashi, Hideaki; Matsunaga, Koutarou; Matsumoto, Nobuyuki; Itoh, Fumio; Yotsuyanagi, Hiroshi; Koitabashi, Yu; Yasuda, Kiyomi; Iino, Shiro

doi:10.1111/j.1872-034x.2009.00523.x

Cited by 14 publications

(11 citation statements)

References 18 publications

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“…Another decision tree model includes viral factors, such as the interferon sensitivity determining region (ISDR) and the amino acid sequence of the HCV core protein (Core 70), as well as host factors, such as age, serum LDL cholesterol and hepatic fibrosis 75 . The ISDR is a stretch of 40 amino acids in the nonstructural 5A (NS5A) region of HCV and substitutions in ISDR are closely associated with SVR 77–82 . In contrast, amino acid substitutions at positions 70 and 91 of the core region have been reported to be associated with non‐virological response to therapy 70,83,84 .…”

Section: Serum Cholesterol Levels and Treatment Efficacymentioning

confidence: 99%

“…Cholesterol and HCV infection 699 closely associated with SVR. [77][78][79][80][81][82] In contrast, amino acid substitutions at positions 70 and 91 of the core region have been reported to be associated with nonvirological response to therapy. 70,83,84 The overall rate of SVR was only 44% in patients with a low number of substitutions in ISDR (0-1) but was increased 83% in selected subgroups of younger patients (<60 years) with the wild-type sequence at Core amino acid 70, and higher concentrations of LDL cholesterol (3120 mg/dL).…”

Section: Serum Cholesterol Levels and Treatment Efficacymentioning

confidence: 99%

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Cholesterol and chronic hepatitis C virus infection

Honda¹,

Matsuzaki²

2011

Hepatology Research

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Cholesterol is an essential molecule for the life cycle of the hepatitis C virus (HCV). This review focuses on the roles of cholesterol in HCV infection and introduces HCV events related to cholesterol metabolism and applications for cholesterol metabolism as a therapeutic target. HCV appears to alter host lipid metabolism into its preferable state, which is clinically recognized as steatosis and hypocholesterolemia. While hepatic fatty acid and triglyceride syntheses are upregulated in chronic hepatitis C patients, no direct evidence of increased hepatic de novo cholesterol biosynthesis has been obtained. Impaired VLDL secretion from hepatocytes is suggested to increase intracellular cholesterol concentrations, which may lead to hypocholesterolemia. Clinically, lower serum cholesterol levels are associated with lower rates of sustained virological responses (SVR) to pegylated-interferon plus ribavirin therapy, but the reason remains unclear. Clinical trials targeting HMG-CoA reductase, the rate-limiting enzyme in the cholesterol biosynthetic pathway, are being conducted using statins. Anti-HCV actions by statins appear to be caused by the inhibition of geranylgeranyl pyrophosphate synthesis rather than their cholesterol lowering effects. Other compounds that block various steps of cholesterol metabolic pathways have also been studied to develop new strategies for the complete eradication of this virus.

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Section: Serum Cholesterol Levels and Treatment Efficacymentioning

confidence: 99%

Section: Serum Cholesterol Levels and Treatment Efficacymentioning

confidence: 99%

Cholesterol and chronic hepatitis C virus infection

Honda¹,

Matsuzaki²

2011

Hepatology Research

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“…We discarded 415 nonrelevant records and retrieved full texts of 37 potentially relevant papers. We excluded: 10 reviews regarding the optimal treatment of infections caused by different HCV genotypes [20][21][22][23][24][25][26][27][28][29], 1 case series with 9 subjects [30], 3 studies that evaluated 24- vs. 48-week treatment of HCV genotype 1 infection in patients showing RVR [12][31][32], 1 study that compared rapid responders with slow responders [33]. Furthermore, we excluded 1 letter [34], 5 studies on long-term therapy with standard interferon [35][36][37][38][39], 3 studies on HCV/HIV co-infected patients [40][41][42], 2 non-randomized studies [43][44], 1 study in which patients in the extended therapy group were treated with low dose peginterferon or ribavirin [45].…”

Section: Resultsmentioning

confidence: 99%

Optimal Duration of Treatment for HCV Genotype 1 Infection in Slow Responders: A Meta-Analysis

Alavian¹,

Tabatabaei

Behnava

et al. 2011

Hepat Mon

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BackgroundA head-to-head comparison of the 72-week and 48-week anti-HCV therapies in slow responders with genotype 1 infection has been performed in several randomized clinical trials (RCTs).ObjectivesThis review aimed at summarizing and pooling the results of these studies.Materials and MethodsRCTs that had evaluated the 72-week vs. 48-week anti-HCV therapy (peginterferon and ribavirin) in slow responders with HCV genotype 1 infection were systematically identified. A meta-analysis was performed using the random effects model. Heterogeneity in results was assessed on the basis of the Q statistics, and publication bias was evaluated by using Harbord’s modified test. The end point was set as a sustained virological response (SVR).ResultsData of 1206 subjects were retrieved from 7 studies. A total of 631 patients had received extended therapy. Slow virological responders who received the 72-week therapy had a significantly higher probability of achieving SVR than their counterpartswho received the 48-week therapy [RR = 1.44 (95% CI, 1.20–1.73)]. With regard to publication biases, the heterogeneity in funnel plots was not significant (P = 0.19, I2 = 30%, PHarbord = 0.1).ConclusionOur meta-analysis showed that the 72-week therapy with peginterferon and ibavirin is significantly superior to the standard 48-week therapy in slow responders th HCV genotype 1 infection.

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“…showed that extended therapy with IFN‐α monotherapy for 24 weeks following PEG IFN and RBV combination therapy was effective for patients with cEVR 16 . In addition, short‐term extension of PEG IFN and RBV combination therapy for cEVR patients up to 60 weeks in genotype 1 CH‐C patients has been reported to achieve an 80.5% SVR rate 17 . In the present study, the SVR rate of female cEVR patients with initial HCV RNA negativity at treatment week 12 and then treated for 52–64 weeks was not significantly higher than those treated for 48 weeks because of the small number of patients.…”

Section: Discussionmentioning

confidence: 99%

Treatment extension may benefit female genotype 1 chronic hepatitis C patients with complete early virological response to peginterferon‐alpha‐2b and ribavirin combination therapy

Nishimura

Yamaguchi

Hashimoto

et al. 2012

Hepatology Research

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Short‐term prolongation of pegylated interferon and ribavirin therapy for genotype 1b chronic hepatitis C patients with early viral response

Abstract: The results indicate that short-treatment extension of PEG IFN plus RBV treatment protocols in EVR patients can improve overall SVR rates.

Cited by 14 publications

References 18 publications

Cholesterol and chronic hepatitis C virus infection

Cholesterol and chronic hepatitis C virus infection

Optimal Duration of Treatment for HCV Genotype 1 Infection in Slow Responders: A Meta-Analysis

Treatment extension may benefit female genotype 1 chronic hepatitis C patients with complete early virological response to peginterferon‐alpha‐2b and ribavirin combination therapy

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