Comparison of Clevudine and Entecavir for Treatment-naive Patients With Chronic Hepatitis B Virus Infection

Yoon, Eileen L.; Yim, Hyung Joon; Lee, Hyun Jung; Kim, Jeong Han; Jung, Eun Suk; Kim, Ji Hoon; Seo, Yeon Seok; Yeon, Jong Eun; Lee, Hong Sik; Um, Soon Ho; Byun, Kwan Soo

doi:10.1097/mcg.0b013e31821f8bdf

Cited by 18 publications

(18 citation statements)

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“…Previously published research has focused on the comparative clinical effectiveness [18][19][20][21][22][23] and/or costeffectiveness 24-28 of oral antiviral agents in the treatment of CHB.…”

Section: Discussionmentioning

confidence: 99%

Adherence, persistence, healthcare utilization, and cost benefits of guideline-recommended hepatitis B pharmacotherapy

Han

Jing²,

Mena³

et al. 2012

Journal of Medical Economics

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Section: Discussionmentioning

confidence: 99%

Adherence, persistence, healthcare utilization, and cost benefits of guideline-recommended hepatitis B pharmacotherapy

Han

Jing²,

Mena³

et al. 2012

Journal of Medical Economics

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“…However, two patients developed increase of CPK, and one of them experienced muscle weakness. Muscle-related problems have been reported in CHB patients receiving CLV previously 20–23. Incidence of the myopathy related to CLV varied 2.9% to 14.6%, and it became a major drawback of CLV in clinical use 20–23.…”

Section: Discussionmentioning

confidence: 99%

“…Muscle-related problems have been reported in CHB patients receiving CLV previously 20–23. Incidence of the myopathy related to CLV varied 2.9% to 14.6%, and it became a major drawback of CLV in clinical use 20–23. Especially, long term administration of CLV could be the one of the risk factor for its development 21,23.…”

Section: Discussionmentioning

confidence: 99%

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Management of Clevudine-Resistant Chronic Hepatitis B: A Multicenter Cohort Study

et al. 2017

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Background/AimsData are lacking regarding the management of chronic hepatitis B (CHB) with resistance to clevudine (CLV). This study evaluated the efficacy of different rescue therapies for CLV-resistant CHB.MethodsPatients with CLV-resistant CHB were enrolled in the cohort, and all patients developed virologic breakthrough during CLV therapy and had confirmed-genotypic resistance to CLV (rtM204I mutation) before enrollment.ResultsOf the 107 patients, 12 received adefovir (ADV), 21 received a CLV plus ADV combination (CLV+ADV), 34 received a lamivudine plus ADV combination (LAM+ADV), and 40 received entecavir (ETV) therapy for 48 weeks. The CLV+ADV group had the lowest hepatitis B virus (HBV) DNA level (p<0.0001) and showed the greatest reduction of HBV DNA levels from baseline compared to all other groups (p=0.004) at week 48. HBV DNA was undetectable (<70 IU/mL) in 0%, 57.1%, 21.2%, and 27.5% (p=0.003) of the patients in each group, respectively, at week 48. At the end of the study, the mean alanine transaminase (ALT) level, rate of ALT normalization, and rate of hepatitis B envelope antigen loss or seroconversion did not differ between groups.ConclusionsCLV+ADV combination therapy in patients with CLV-resistant CHB more effectively suppresses HBV replication than ETV, ADV, or LAM+ADV therapy.

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“…Clevudine however was associated with a higher virologic breakthrough rate and clinical myopathy [Shin et al 2011]. This was further correlated in a 2-year follow up [Yoon et al 2011].MIV-210 a prodrug of 3′-fluoro-2′,3′-dideoxyguanosine has been shown with woodchuck hepatitis virus to produce a rapid virological response and is currently undergoing further phase II trials [Michalak et al 2009]. …”

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Therapeutic advances in the management of chronic hepatitis B infection

Brooks

Gelson

Rushbrook

2013

Therapeutic Advances in Chronic Disease

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Hepatitis B virus (HBV) is a small nonenveloped DNA virus that is a member of the Hepadnaviridae family. Chronic HBV infection is estimated to effect more than 350 million people worldwide with over 2 billion people being exposed to the virus. Risk factors for chronic infection include age of exposure to the virus, concurrent immunosuppression and HIV infection. Individuals chronically infected are 200 times more likely to develop hepatocellular carcinoma (HCC) than uninfected individuals and are at risk of developing cirrhosis and the risks of decompensated liver disease. This article focuses on the recent therapeutic advances that reduce the risk of developing these complications, those that prevent the spread of HBV and strategies for the prevention of post-liver-transplantation recurrence of HBV. (cccDNA). Replication of the HBV genome is an error-prone mechanism. Owing to an overlapping of the ORFs of the viral products, mutations in one opening frame can cause an amino acid substitution in a different viral protein product [Cheng et al. 2012]. Keywords: chronic infection, hepatitis B, treatmentUtilization of the host cellular transcription/translation machinery leads to production of the viral particle as well as noninfectious spherical and filamentous subviral particles (SVPs) that only contain the small HBV S protein. HBV immunity and HBV viral escapeHepatocellular injury in HBV is immune-mediated, with human leukocyte antigen (HLA) class I restricted CD8 cells recognizing HBV peptide fragments processed and presented on hepatocytes. Direct cell killing by CD8 cytotoxic T lymphocytes then occurs, in association with noncytolytic inhibition of virus replication. However, the activation of the CD8+ T-cell adaptive immune response only occurs once the innate immune system has recognized HBV along with assistance from activated CD4+ T cells. Several studies have highlighted the role of type 1 interferon (IFN) in the production of the antiviral state in acute HBV [Fletcher et al. 2012], with Toll-like receptors (TLRs) [Tjwa et al. 2012] mediating the production of IFN. HBeAg has been shown to induce a tolerogenic effect by acting as an immune decoy for the core antigen and also by downregulating cell signalling suppressing TLR-induced IFN beta activation [Visvanathan et al. 2007]. By mechanisms that are as-yet unclear, HBV-infected cells have been shown to have downregulation of signal transducer and activator of transcription-1, thereby reducing the antiviral state further [Lutgehetmann et al. 2011]. HBeAg is not alone in its immunomodulatory effects: Protein X downregulates mitochondrial antiviral signalling [Bouchard et al. 2003] by suppressing the retinoic acid inducible gene I (RIG-I) [Civril et al. 2011;Luo et al. 2011] and SVPs have been shown in vitro to inhibit TLR-9 mediated IFN alpha production by dendritic cells [Xie et al. 2009]. HBeAg seroconversion is predictive of a substantial reduction in HBV DNA levels, a decrease in intrahepatic inflammation and improved prognosis [Chen et al. 20...

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Comparison of Clevudine and Entecavir for Treatment-naive Patients With Chronic Hepatitis B Virus Infection

Abstract: Although both drugs showed potent antiviral activity, entecavir showed better virologic response at 24 months, primarily owing to treatment failures in the clevudine group that were associated with development of drug resistance and muscle-related problems.

Cited by 18 publications

References 33 publications

Adherence, persistence, healthcare utilization, and cost benefits of guideline-recommended hepatitis B pharmacotherapy

Adherence, persistence, healthcare utilization, and cost benefits of guideline-recommended hepatitis B pharmacotherapy

Management of Clevudine-Resistant Chronic Hepatitis B: A Multicenter Cohort Study

Therapeutic advances in the management of chronic hepatitis B infection

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